SciELO - Scientific Electronic Library Online

 
vol.54 issue3Volume and pressure of tracheal tube cuffs filled with air or nitrous oxideGastric emptying after oral contrast for abdominal tomography: report of six cases author indexsubject indexarticles search
Home Pagealphabetic serial listing  

Services on Demand

Article

Indicators

Related links

Share


Revista Brasileira de Anestesiologia

Print version ISSN 0034-7094

Rev. Bras. Anestesiol. vol.54 no.3 Campinas May/June 2004

http://dx.doi.org/10.1590/S0034-70942004000300008 

SCIENTIFIC ARTICLE

 

Effects of pneumoperitoneum on renal hemodynamics and function of dogs under volume and pressure-controlled ventilation*

 

Efectos del pneumoperitonio sobre la hemodinámica y función renal de perros ventilados con volumen y presión controlados

 

 

Armando Vieira de Almeida, TSA, M.D.I; Eliana Marisa Ganem, TSA, M.D.II

IPós-Graduando (Doutorado) do Programa de Pós-Graduação em Anestesiologia da FMB UNESP. Bolsista CAPES
IIProfessora Adjunta Livre-Docente do CET/SBA do Departamento de Anestesiologia da Faculdade de Medicina de Botucatu, UNESP

Correspondence

 

 


SUMMARY

BACKGROUND AND OBJECTIVES: There are no studies associating ventilatory mode effects on renal repercussions during pneumoperitoneum. This study aimed at evaluating pneumoperitoneum-induced renal hemodynamics and function changes in dogs under volume and pressure controlled ventilation.
METHODS: This study involved 16 dogs anesthetized with sodium thiopental and fentanyl, which were divided in two groups: Group 1: volume controlled; and Group 2: pressure controlled, both submitted to 10 and 15 mmHg pneumoperitoneum. The following parameters were evaluated: renal blood flow, renal vascular resistance, sodium para-aminohippurate clearance, plasma sodium, plasma potassium, plasma osmolality, creatinine clearance, filtration fraction, urinary volume, urinary clearance, osmolar clearance, free water clearance, sodium clearance, sodium urinary excretion, sodium fractional excretion, potassium clearance, potassium urinary excretion and potassium fractional excretion. Data were collected in 4 moments: M1 before pneumoperitoneum, M2, 30 minutes after 10 mmHg pneumoperitoneum, M3, 30 minutes after 15 mmHg pneumoperitoneum, M4, 30 minutes after pneumoperitoneum deflation.
RESULTS: Sodium para-aminohippurate and creatinine clearance remained constant for both groups throughout the experiment. Plasma sodium and potassium were not changed. There has been potassium clearance and fractional excretion decrease as from M2 in both groups.
CONCLUSIONS: Ventilatory modes have not promoted renal hemodynamic differences between groups. Pneumoperitoneum, by compressing renal parenchyma, may have determined changes in potassium reabsorption and/or secretion.

Key Words: ANIMAL: dog; SURGERY, Abdominal: videolaparoscopic; VENTILATION: mechanical controlled


RESUMEN

JUSTIFICATIVA Y OBJETIVOS: No existen estudios que asocien los efectos determinados por las modalidades ventilatorias a las repercusiones renales durante el pneumoperitonio. El objetivo de este trabajo fue evaluar las alteraciones en la hemodinámica y función renal determinadas por el pneumoperitonio en perros con ventilación a volumen y presión controlados.
MÉTODO: Dieciséis perros anestesiados con tiopental sódico y fentanil fueron divididos en Grupo 1, volumen controlado y Grupo 2, presión controlada y sometidos a pneumoperitonio de 10 y 15 mmHg. Fueron estudiados flujo sanguíneo renal, resistencia vascular renal, depuración de para-aminohipurato de sodio, sodio plasmático, potasio plasmático, osmolalidad plasmática, depuración de creatinina, fracción de filtración, volumen urinario, osmolalidad urinaria, depuración osmolar, depuración de agua libre, depuración de sodio, excreción urinaria de sodio, excreción fraccionaria de sodio, depuración de potasio, excreción urinaria de potasio, excreción fraccionaria de potasio. Los datos fueron colectados en 4 momentos. M1, antes del pneumoperitonio; M2, 30 minutos después pneumoperitonio con 10 mmHg; M3, 30 minutos después pneumoperitonio con 15 mmHg; M4, 30 minutos después de la deflación del pneumoperitonio.
RESULTADOS: Las depuraciones de para-aminohipurato de sodio y creatinina permanecieron constantes en ambos grupos durante el experimento. Los valores plasmáticos del sodio y del potasio no se alteraron. Ocurrió diminución a partir de M2 de la depuración y de la excreción fraccionaria de potasio en ambos grupos.
CONCLUSIONES: Las modalidades ventilatórias no determinaron diferencias en la hemodinámica renal entre los grupos estudiados. El pneumoperitonio, ocasionando compresión del parenquima renal, puede tener determinado alteraciones en la reabsorción y/o secreción del potasio.


 

 

INTRODUCTION

Increased abdominal pressure promoted by pneumoperitoneum as well as intraoperative patients' positioning may affect several organs and systems during videolaparoscopic surgeries.

Compression of renal parenchyma, arteries and veins during pneumoperitoneum peaks with oliguria 1. When intra-abdominal pressure increases from 0 to 20 mmHg, renal vascular resistance increases 555% and glomerular filtration rate decreases 25% 2.

Renal changes are also associated to neuroendocrine system activation 3,4. High plasma vasopressin 3-5, rennin 4,6-9 and endothelin 10 concentrations have been observed during pneumoperitoneum. The increase of these substances in plasma induces vasoconstriction and contributes for systemic vascular resistance increase.

Rennin-angiotensin-aldosterone system activation leads to angiotensin II-mediated renal vasoconstriction promoting medulla blood flow shift to renal cortex, worsening renal perfusion 8.

When mechanical ventilation is installed, internal chest pressure variations change pre and afterload, which may affect cardiovascular hemodynamics 11 and renal hemodynamics and function, especially in severely ill patients. Added to this, there is IAP increase which, depending on clinical conditions and patients' positioning, may determine major changes in established ventilatory parameters which, as a consequence, may lead to hemodynamic changes.

Oliguria is a common event during pneumoperitoneum, evidencing not yet explained renal homeostasis changes. This study aimed at correlating two ventilatory modes - volume and pressure controlled - to renal hemodynamics and function changes in dogs submitted to 10 and 15 mmHg pneumoperitoneum.

 

METHODS

After the Animal Experiment Ethics Committee approval, 16 adult mixed-breed dogs of both genders, weighing 15 to 23 kg and supplied by the Experimental Animals Facility, Botucatu Campus, Universidade Estadual Paulista Julio de Mesquita Filho were evaluated.

Exclusion criteria were unhealthy-looking animals. Dogs were randomly distributed in two experimental groups of 8 animals according to the ventilatory mode:

Group 1 (G1) - Volume controlled ventilation;
Group 2 (G2) - Pressure controlled ventilation.

After 12-hour fasting with free access to water, animals were weighed, anesthetized with intravenous 15 mg.kg-1 sodium pentobarbital and 15 µg.kg-1 fentanyl and placed in the supine position on Claude Bernard's device, when they were ventrally measured from nose to anus. Using this distance and weight in kg, body surface was estimated through normal physiological data tables.

Then, animals were intubated with 38 tube with low pressure and high compliance cuff to install mechanical ventilation. Animals were ventilated with 100% oxygen. Group 1, with volume controlled ventilation by Ohmeda's anesthesia machine and monitored by Datex-Engstrom's AS/3 device, received tidal volume enough to maintain PETCO2 (end tidal CO2) between 35 and 45 mmHg. Group 2, with pressure controlled ventilation by Ohmeda's anesthesia machine and monitored by Datex-Engstrom's AS/3 device, was ventilated with enough pressure to maintain PETCO2 between 35 and 45 mmHg. PETCO2 was measured by expired air sample collection close to the Y piece of the respiratory circuit. Respiratory rate was initially established in 10 movements per minute for both groups. To help artificial ventilation, pancuronium was administered in the initial dose of 0.07 mg.kg-1 and additional dose of 0.008 mg.kg-1.

Right and left femoral veins and right and left femoral arteries were dissected and catheterized with polyethylene catheters introduced 2 to 3 cm. Left femoral vein catheter received 6 mL.kg-1.h-1 lactated Ringer's solution controlled by Abbott Laboratories (USA) "Anne"® microprocessed pump, and sodium thiopental (100 µg.kg-1.min-1) and fentanyl (0.1 µg.kg-1.min-1) continuous infusion.

Intravenous creatinine (30 mg.kg-1) and sodium para-aminohippurate (4 mg.kg-1) prime was administered 30 minutes after lactated Ringer's solution infusion. Then, creatinine (0.6 g%) and PAH (0.24 g%) continuous infusion in lactated Ringer's was installed until experiment completion, being administered 0.6 mg creatinine and 0.24 mg PAH per minute/kg, with infusion controlled by "Anne" microprocessed pump.

Left femoral artery catheter edge was connected to blood pressure reading module of the Datex-Engstrom's AS/3 device. Right femoral artery catheter was used to collect arterial blood.

After right cervical region tricotomy, right external jugular vein was dissected for Swan-Ganz catheter insertion according to Gouvea et al. 12 technique.

Peritoneal cavity was accessed with the help of approximately 5 cm surgical incision on medial abdominal wall region, through which a 12G polyethylene catheter was inserted under direct view followed by surgical plane suture. Catheter edge was connected to the inflating device and pneumoperitoneum was achieved with CO2. Intra-abdominal 10 mmHg and 15 mmHg pressures were reached and maintained by the pressure and flow control module. Peritoneal cavity was deflated after disconnecting the catheter from the inflating device, followed by mild abdominal cavity compression.

Uretral catheterization was achieved with polyvinyl tube and vesical emptying was obtained with mild suprapubic compression.

For clearance periods (30 minutes), urine was collected in graded pipettes. In the middle of the procedure, 5 mL venous blood were collected in centrifuge tubes with heparin.

The following parameters: renal blood flow, renal vascular resistance, PAH clearance, plasma sodium, plasma potassium, plasma osmolality, creatinine clearance, filtration fraction, urinary volume, urinary osmolality, osmolar clearance, free water clearance, sodium clearance, sodium urinary excretion, sodium fractional excretion, potassium clearance, potassium urinary excretion and potassium fractional excretion were obtained in the following moments after PAH and creatinine prime injection:

M1 - 60 minutes after PAH and creatinine prime injection and immediately before 10 mmHg pneumoperitoneum;

M2 - 90 minutes after PAH and creatinine prime injection, 30 minutes after 10 mmHg pneumoperitoneum and immediately before 15 mmHg pneumoperitoneum;

M3 - 120 minutes after PAH and creatinine prime injection, 30 minutes after 15 mmHg pneumoperitoneum and immediately before pneumoperitoneum deflation;

M4 - 150 minutes after PAH and creatinine prime injection, 30 minutes after pneumoperitoneum deflation and immediately before animals' sacrifice.

For vasopressin dosage, 5 mL venous blood were collected in refrigerated and heparin-containing centrifuge tubes, in the following moments:

M1' - immediately before 10 mmHg pneumoperitoneum;

M2' - 15 minutes after 10 mmHg pneumoperitoneum;

M3' - 15 minutes after 15 mmHg pneumoperitoneum;

M4' - 15 minutes after pneumoperitoneum deflation.

Vasopressin was dosed by the radioimmunoassay technique using Arginine Vasopressin Radioimmunoassay DSL-1800 Kit.

At experiment completion animals were sacrificed with 10 mL intravenous injection of 19.1% potassium chloride.

For statistical analysis, Profile Analysis was used for Morrison's hypothesis test 13. In all tested hypotheses, calculated F statistics were considered significant when p < 0.05.

 

RESULTS

Statistical analysis of PAH clearance (Figure 1) and renal blood flow (Figure 2) has shown no differences between groups among moments throughout the experiment.

Statistical analysis of renal vascular resistance has shown that it has been significantly lower in Group 1, however without differences among moments throughout the experiment for both groups (Figure 3).

Plasma sodium and potassium were similar for both groups with stable values throughout the procedure (Figure 4 and 5).

Similarly, plasma osmolality and creatinine clearance were similar for both groups with stable values throughout the procedure (Figure 6 and 7).

Filtration fraction was also similar for both groups with significant decrease in M2 and remaining like that until experiment completion (Figure 8).

Urinary volume has been stable throughout the experiment for both groups, but Group1 had significantly higher values as compared to Group 2 (Figure 9).

Urinary osmolality was also similar for both groups with significant decrease throughout the procedure (Figure 10).

There has been no variation in osmolar clearance among moments in both groups, however Group 1 had higher values as compared to Group 2 (Figure 11).

Free water clearance has increased throughout the experiment for both groups (Figure 12).

Sodium clearance, sodium urinary excretion and sodium fractional excretion were similar for both groups without variations throughout the experiment. Group 1, however, had significantly higher values as compared to Group 2 (Figure 13, 14 and 15).

Potassium clearance was similar for both groups with significant decrease in M2 and remaining like that until experiment completion. Group 1 values were significantly higher as compared to Group 2 (Figure 16).

Potassium urinary excretion was similar for both groups and remained stable throughout the experiment. Group 1 values were significantly higher as compared to Group 2 (Figure 17).

Potassium fractional excretion was similar for both groups and has decreased in M2 remaining like that until experiment completion (Figure 18).

 

DISCUSSION

Pneumoperitoneum-induced intra-abdominal pressure (IAP) increase promotes systemic changes, the magnitude of which is directly related to IAP values used.

In patients with impaired renal function, be it acute or chronic, these may be major changes since there is often diuresis decrease during pneumoperitoneum.

Venous and arterial compression, added to parenchymal compression and hormonal changes, lead to decreased diuresis 14. This is even observed in patients without any evidence of histological changes or renal tubular injury. In general, there is no diuresis and renal function impairment after peritoneal cavity deflation 15.

An experimental study with dogs has observed 63% decrease in urinary output and 26% decrease in renal blood flow when kidneys were under 15 mmHg IAP compression 1. However, when IAP was above 20 mmHg, there has been 75% decrease in glomerular filtration and anuria was observed with 40 mmHg IAP, values which have not changed with increased hydration 2.

In a swine model submitted to different IAP values during 4 hours, it has been observed that pressures equal to or above 15 mmHg have decreased cardiac output, urinary output, renal venous blood flow and creatinine clearance. These changes were not associated to permanent injuries or histological renal changes 16.

Clinical and experimental studies on renal function and pneumoperitoneum are not uniform as to the volume of fluid to be administered, and vary 2 to 15 mL.kg-1.h-1. Oliguria does not seem to be affected by hydration 16-19.

In our study, animals have received 6 mL.kg-1.h-1 hydration, aiming at keeping them hydrated and preventing hyper-hydration and dehydration.

High blood CO2 values may increase plasma rennin activity, plasma catecholamines, aldosterone and vasopressin concentrations during laparoscopic surgeries 6,20,21. As a result of this hormonal stimulation there is renal vasoconstriction with decreased renal blood flow and glomerular filtration 22.

The fast systemic vascular resistance increase after pneumoperitoneum has been correlated to hormonal changes with increased plasma rennin 6,7,9 and vasopressin 3,18,23 activity.

SR 4925 - a vasopressin antagonist - has inhibited systemic vascular resistance increase 23. So, vasopressin has a major role in hemodynamic regulation during pneumoperitoneum 23,24.

As to catecholamines, there is no temporal relationship between their plasma concentration increase and systemic vascular resistance and mean blood pressure increase 24.

In our study, blood CO2 values and vasopressin concentrations have remained within physiological limits. Renal vascular resistance has not changed throughout the experiment for both groups, but Group 1 values were higher as compared to Group 2 and this fact was related to the characteristics of the studied group.

In favorable hemodynamic conditions there is increase in renal blood flow, renal plasma flow and filtration fraction with increased cardiac output and decreased peripheral resistance; in fact, there is a decrease in filtration fraction, that is, the rate between glomerular filtration rate and renal plasma flow, showing that increased renal plasma flow was proportionally higher that glomerular filtration rate 25.

So, filtration fraction decrease observed in our study, where there has been cardiac index increase and systemic vascular resistance decrease 26, would be a consequence of increased renal plasma flow.

In extracellular fluids, sodium cation and the two major anions following it, chloride and bicarbonate, are responsible for 90% solutes in this compartment 25. So, it is possible to estimate plasma osmolality through sodium plasma concentrations.

Plasma osmolality remains virtually unchanged due to the integration hypothalamic-hypophysial-renal and antidiuretic hormone, which is critical for the maintenance of such stability 27. Plasma sodium has not significantly changed in both groups throughout the experiment with stable plasma osmolality and vasopressin plasma values.

Positive pressure ventilation may promote cardiac output and blood pressure decrease in situations such as hypovolemia and increased intra-thoracic pressure, as it is the case with pneumoperitoneum 28,29.

Cardiac output and blood pressure decrease leads to renal blood flow decrease, rennin-angiotensin-aldosterone system activation and higher sodium and water absorption, changing plasma osmolality.

Our study has not observed cardiac index, mean blood pressure 26 and renal blood flow changes in both groups, thus not expecting influences in plasma osmolality, which has remained stable throughout the procedure and was not influenced by pneumoperitoneum, hydration or mechanical ventilation.

Most remarkable event triggered by IAP increase on kidneys is diuresis decrease 1,8,17,19,30. It is related to vasopressin plasma concentration increase 3,8,23 and to mechanical compression of renal parenchyma, renal artery, renal vein and inferior vena cava, triggering negative effects on renal blood flow and renal function.

Diuresis is increased when there is extracellular volume expansion 25, natriuretic hormone release 31, stretching receptors and atrial pressure stimulation 32 and preload increase.

Mechanical ventilation, for determining intra-thoracic pressure increase and, as a consequence, decreased venous return and cardiac output, may stimulate vasopressin release and atrial natriuretic factor inhibition. Our study, however, has not observed cardiac index decrease 26 or changes in plasma vasopressin values for both groups.

Vasopressin, which plays a major role in renal perfusion and water reabsorption has not changed in our study, and IAP has not exceeded 15 mmHg for one hour. These factors, associated to our hydration pattern with maintenance of normovolemia may have contributed for the maintenance of diuresis throughout the procedure for both groups. Higher Group 1 values would be individual characteristics and in line with higher mean blood pressure values of this group.

Considering that there has been normovolemia, hemodynamic stability and no changes in plasma vasopressin values for both groups, it is possible to conclude that the lack of significant changes in plasma sodium, sodium clearance, sodium urinary excretion and sodium fractional excretion was a reflex of hemodynamic stability promoted by ventilatory modes.

It is known that structural polarity of proximal tubule cells is essential for the primary function of the selective reabsorption of molecules in the tubular fluid, and that it is changed during renal ischemia 33. Changes in Na, K-ATPase pump position are responsible for high sodium excretion fractions characteristic of the urine of patients with post-ischemia acute renal failure 34.

It has to be highlighted that there has been no renal sodium excretion in any moment for both groups, but in analyzing absolute sodium clearance, sodium urinary excretion and sodium fractional excretion values it was possible to infer that there has been a trend toward a decrease in their values for both groups throughout the experiment, what adds to urinary osmolality decrease and free water clearance increase.

So, trends to sodium clearance and urinary and fractional excretion decrease could reveal mild renal function involvement triggered by IAP increase, leading to parenchymal compression and promoting possible changes in tubular absorption and secretion.

Higher values for these attributes in Group 1 could be a reflex of higher mean blood pressure values observed in G1 25,26.

As to potassium, it is believed that almost everything that is filtered is reabsorbed and that potassium excreted by the urine is originated from tubular secretion. When tubular fluid reaches the distal tubule, 85% to 95% of filtered potassium have already been absorbed and excreted concentrations and amounts in final urine have no major variations 35.

Potassium excretion regulation is influenced by its plasma and cellular concentrations which, when increased, also act on adrenal aldosterone secretion, which stimulates sodium reabsorption and potassium excretion, without a mandatory coupling between these cell absorption and excretion mechanisms 36.

Potassium secretion in the distal tubule may increase as a function of fluids overload and luminal flow increase 36. Volume expansion is able to decrease plasma rennin activity with consequent decrease in aldosterone production and lower potassium excretion. Increased intratubular flow decreases potassium luminal concentration, favoring the passive ionic movement of the cell to the tubular lumen toward the ion gradient.

There is an inverse correlation between acid and potassium secretion in the acid-base balance. Alkaloid states lead to higher potassium excretion; as opposed, potassium excretion is decreased in acid states 36. Plasma pH and potassium ratio is such that for each 0.1 pH unit increase or decrease, there is 0.63 mEq.L-1 plasma potassium decrease or increase.

Ventilatory modes used have determined pH values decrease, which was more evident in Group 1 and could peak with lower potassium clearance and fractional excretion.

Positive pressure ventilation may act on potassium through aldosterone's hormonal action, inducing higher sodium reabsorption and potassium excretion. This, however, was not observed since potassium fractional excretion has not increased, showing that ventilatory modes have not interfered with rennin-angiotensin-aldosterone system.

In a clinical trial with patients submitted to laparoscopic cholecystectomy, there have been no changes in potassium fractional excretion 37. However, in swine submitted to pneumoperitoneum, increased potassium plasma concentrations were observed 16,38. In both studies, plasma concentrations were below values potentially able to trigger arrhythmias.

Potassium serum concentrations have not changed in our study. However, potassium clearance and fractional excretion have decreased as from pneumoperitoneum, and potassium urinary excretion tended to decrease in both groups. Higher potassium clearance and fractional excretion in Group 1 was probably due to higher mean blood pressure levels in this group.

It is possible that there has been no aldosterone influence in potassium handling since there has been no increase in sodium reabsorption, which would lead to ion excretion. Since hemodynamic parameters have remained stable, animals' volume status was enough to not influence tubular flow.

Although potassium plasma concentrations have not changed, some factors, such as renal parenchymal compression determined by increased IAP and/or arterial pH decrease, may have contributed for lower ion clearance and fractional excretion observed in both groups as from M2, as a consequence of its higher reabsorption and/or lower secretion. Water transport is always secondary to other solutes transport by purely physical-chemical mechanisms. In most distal nephron segments, water transport is modulated by antidiuretic hormone or vasopressin 39.

The ratio between solutes excretion and water may be studied considering that urinary volume is made up of "two waters" - one to contain all solutes (osmoles) excreted by urine and the other "water" to be excreted as such, pure and solute-free 40.

Decreased urinary osmolality observed after pneumoperitoneum might have been a consequence of lower potassium ion clearance and excretion added to a trend to lower sodium ion clearance and excretion.

Higher free water clearance observed as from pneumoperitoneum is also in line with decreased urinary osmolality, representing the trend to higher and solute-free urinary filtrate. Vasopressin plasma levels have remained within normal limits, what excludes the participation of the hormone in increased free water clearance.

Osmolar clearance, corresponding to plasma volume (mL) in which all osmotically active substances in the time unit are removed, was not significantly different between groups.

PAH clearance values maintenance throughout the procedure reflects stable glomerular filtration rate, thus excluding any renal function impairment secondary to pre-renal factors.

So, decreased urinary osmolality and increased free water clearance could be a consequence of renal parenchyma involvement as a consequence of IAP increase, which would compress kidneys and lead to changes in nephrons absorption and secretion ability.

So, it is possible to conclude from our experiment that, among different variables which could have determined changes in renal hemodynamics and function, ventilatory modes have not led to systemic changes able to determine renal function involvement. It could be inferred that renal parenchyma compression determined by increased intra-abdominal pressure could have been responsible for changes in renal potassium excretion.

 

REFERENCES

01. Razvi HA, Fields D, Vargas JC et al - Oliguria during laparoscopic surgery: evidence for direct renal parenchymal compression as an etiologic factor. J Endourol, 1996;10:1-4.        [ Links ]

02. Harman PK, Kron IL, Mclachlan HD et al - Elevated intra-abdominal pressure and renal function. Ann Surg, 1982;196:594-597.        [ Links ]

03. Punnonen R, Viinamaki O - Vasopressin release during laparoscopy: role of increased intra-abdominal pressure. Lancet, 1982;1:175-176.        [ Links ]

04. Joris JL, Noirot DP, Legrand MJ et al - Hemodynamic changes during laparoscopic cholecystectomy. Anesth Analg, 1993;76:1067-1071.        [ Links ]

05. Ortega A, Peters J, Incarbone R et al - A prospective randomized comparison of the metabolic and stress hormonal responses of laparoscopic and open cholecystectomy. J Am Coll Surg, 1996;183:249-256.        [ Links ]

06. Koivusalo AM, Kellokumpu I, Scheinin M et al - Randomized comparison of the neuroendocrine response to laparoscopic cholecystectomy using either conventional or abdominal wall lift techniques. Br J Surg, 1996;83:1532-1536.        [ Links ]

07. O'leary E, Hubbard K, Tormey W et al - Laparoscopic cholecystectomy: haemodynamic and neuroendocrine response after pneumoperitoneum and changes in position. Br J Anaesth, 1997;76:640-644.        [ Links ]

08. Koivusalo AM, Kellokumpu I, Ristkari S et al - Splanchnic and renal deterioration during and after laparoscopic cholecystectomy: a comparation of the carbon dioxide pneumoperitoneum and the abdominal wall lift method. Anesth Analg, 1997;85:886-891.        [ Links ]

09. Koivusalo AM, Kellokumpu I, Scheinin M et al - A comparison of gasless mechanical and conventional carbon dioxide pneumoperitoneum methods for laparoscopic cholecystectomy.  Anesth Analg, 1998;86:153-158.        [ Links ]

10. Hamilton BD, Chow GK, Inman SR et al - Increased intra-abdominal pressure during pneumoperitoneum stimulates endothelin release in a canine model. J Endourol, 1998;12:193-197.        [ Links ]

11. David CM - Ventilação Mecânica: Repercussões Hemodinâmicas, em: David C - Ventilação Mecânica. Rio de Janeiro, Revinter, 1996;77-86.        [ Links ]

12. Gouvea F, Ferreira E, Campos AP et al - Monitorização hemodinâmica: métodos invasivos. Rev Bras Anestesiol, 1992;42:21-41.        [ Links ]

13. Morrison DF - Multivariate Statistical Methods. New York: McGraw-Hill, 1967;338.        [ Links ]

14. Dualé C, Bolandard F, Duband P et al - Conséquences physiopathologiques de la chirurgie coelioscopique. Ann Chir, 2001;126:508-514.        [ Links ]

15. Dunn MD, McDougall EM - Renal physiology. Laparoscopic considerations. Urol Clin Norh Am, 2000;27:609-614.        [ Links ]

16. McDougall EM, Monk TG, Wolf Jr JS et al - The effect of prolonged pneumoperitoneum on renal function in an animal model. J Am Coll Surg, 1996;182:317-328.        [ Links ]

17. Chang DT, Kirsch AJ, Sawczuk IS - Oliguria during laparoscopic surgery. J Endourol, 1994;8:349-352.        [ Links ]

18. Dolgor B, Kitano S, Yoshida T et al - Vasopressin antagonist improves renal function in a rat model of pneumoperitoneum. J Surg Res, 1998;79:109-114.        [ Links ]

19. London ET, Ho HS, Neuhaus AM et al - Effect of intravascular volume expansion on renal function during prolonged CO2 pneumoperitoneum. Ann Surg, 2000;231:195-201.        [ Links ]

20. Walder AD, Aitkenhead AR - Role of vasopressin in the haemodynamic response to laparoscopic cholecystectomy. Br J Anaesth, 1997;78:264-266.        [ Links ]

21. Corwin C, Fabrega AJ, Scott-Conner C - Neurohormonal Response to Laparoscopy and Acute Rise in Intra-Abdominal Pressure, em: Rosenthal RJ, Friedman RL, Phillips EH - The Pathophysiology of Pneumoperitoneum. Berlin, Springer, 1998;99-113.        [ Links ]

22. Diebel LN - Renal Function and Circulation under the Influence of Pneumoperitoneum, em: Rosenthal RJ, Friedman RL, Phillips EH - The Pathophysiology of Pneumoperitoneum. Berlin. Springer, 1998;62-69.        [ Links ]

23. Mann C, Boccara G, Pouzeratte Y et al - The relationship among carbon dioxide pneumoperitoneum, vasopressin release, and hemodynamic changes. Anesth Analg, 1999;89:278-283.        [ Links ]

24. Joris JL, Chiche JD, Canivet JL et al - Hemodynamic changes induced by laparoscopy and their endocrine correlates: effects of clonidine. J Am Coll Cardiol, 1998;32:1389-1396.        [ Links ]

25. Marcondes M - Regulação do Volume de Fluido Extracelular, em: Malnic G, Marcondes M - Fisiologia renal, 3ª Ed, São Paulo: EPU, 1986a;253-270.        [ Links ]

26. Almeida AV, Ganem EM, Carraretto AR et al - Alterações hemodinâmicas durante o pneumoperitônio em cães ventilados com volume e pressão controlados. Rev Bras Anestesiol, 2003;53:756-766.        [ Links ]

27. Marcondes M - Alterações do Metabolismo da Água, em: Malnic G, Marcondes M - Fisiologia renal. 3ª Ed, São Paulo: EPU, 1986b;271-82.        [ Links ]

28. Fessler HE, Brower RG, Wise RA et al - Effects of positive end-expiratory pressure on the gradient for venous return. Am Rev Respir Dis, 1991;143:19-24.        [ Links ]

29. Kotanidou A, Armaganidis A, Zakynthinos S et al - Changes in thoracopulmonary compliance and hemodynamic effect of positive end-expiratory pressure in patients with or without heart failure. J Crit Care Med, 1997;12:101-111.        [ Links ]

30. Cisek LJ, Gobet RM, Peters CA - Pneumoperitoneum produces reversible renal dysfunction in animals with normal and chronically reduced renal function. J Endourol, 1998;12:95-100.        [ Links ]

31. Rahman SN, Batt, AT, Dubose TD et al - Differentiating clinical effects of ANP in oliguric and non-oliguric ATN. J Am Soc Nephrol, 1995;6:474-475.        [ Links ]

32. Moe GM, LegaulT L, Skorechi KL - Control of Extracelular Fluid Volume and Phatophysiology of Edema Formation, em: Brenner BM, Rector FC - The Kidney, 4th Ed, Philadelphia: WB Saunders, 1991;623-676.        [ Links ]

33. Chen J, Doctor B, Mandel MJ - Cytoskeletal dissociation of ezrin during renal anoxia. Role in microvillar injury. Am J Physiol, 1994;36:784-795.        [ Links ]

34. Edelstein CL, Ling H, Schrier RW - The nature of renal cell injury. Kidney Int, 1997;51:1341-1351.        [ Links ]

35. Aires MM - Reabsorção e Secreção Tubular: Técnicas de Depuração, em: Malnic G, Marcondes M - Fisiologia Renal, 3ª Ed, São Paulo: EPU, 1986;89-111.        [ Links ]

36. Furtado MR - Balanço do Potássio e sua Regulação, em: Malnic G, Marcondes M - Fisiologia Renal, 3ª Ed, São Paulo: EPU, 1986;299-310.        [ Links ]

37. Iwase K, Takenaka H, Ishizaka T et al - Serial changes in renal function during laparoscopic cholecystectomy. Eur Surg Res, 1993;25:203-212.        [ Links ]

38. Pearson MR, Sander ML - Hyperkalaemia associated with prolonged insufflation of carbon dioxide into the peritoneal cavity. Br J Anaesth, 1994;72:602-604.        [ Links ]

39. Malnic G - Excreção Renal de Água e Eletrólitos, em: Malnic G, Marcondes M - Fisiologia Renal, 3ª Ed, São Paulo: EPU, 1986a;125-156.        [ Links ]

40. Malnic G - Concentração e Diluição Urinária, em: Malnic G, Marcondes M - Fisiologia Renal, 3ª Ed, São Paulo: EPU, 1986b;173-213.        [ Links ]

 

 

Correspondence to
Dr. Armando Vieira de Almeida
Rua Padre João Crippa, 3299/204 Bairro São Francisco
79010-180 Campo Grande, MS

Submitted for publication May 28, 2003
Accepted for publication August 25, 2003

 

 

* Received from Laboratório Experimental do CET/SBA do Departamento de Anestesiologia da Faculdade de Medicina de Botucatu (FMB UNESP), para o Programa de Pós-Graduação em Anestesiologia, Mestrado