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THE BLOOD LEVELS OF GLUCAGON, CORTISOL, AND INSULIN FOLLOWING THE INJECTION OF VENOM BY THE SCORPION (Mesobuthus tamulus concanesis, POCOCK) IN DOGS

Abstract

Severe envenoming was induced in two groups of experimental dogs after subcutaneous (SQ) injection of venom of the scorpion (Mesobuthus tamulus concanesis, Pocock) (3.0 and 3.5 mg/kg body weight). The circulating levels of blood sugar, insulin, glucagon, and cortisol were assayed at 0, and 30, 60, 90 and 120 min after venom injection. There was an increase in the circulating levels of blood sugar, insulin, glucagon, and cortisol following envenoming. Scorpion envenoming causes an autonomic storm resulting in a massive release of catecholamines, angiotensin II, glucagon, and cortisol accompanied by changes in insulin secretion. The rise in the counter-regulatory hormones (glucagon, cortisol, and catecholamines) oppose the anabolic actions of insulin resulting in a variety of clinical manifestations. These changes may lead to a syndrome of fuel-energy deficits and to an inability of the vital organs to utilise the existing metabolic substrates, ultimately resulting in multisystem organ failure (MSOF) and death.

scorpion envenoming; insulin; glucagon; cortisol; Mesobuthus tamulus concanesis


Mesobuthus tamulus concanesis, POCOCK) IN DOGS

K. RADHA KRISHNA MURTHY

CORRESPONDENCE TO: K. RADHA KRISHNA MURTHY - Professor of Physiology, Seth G.S. Medical College and K.E.M. Hospital, Parel, Mumbai 400 012, India., L. HAGHNAZARI

1 Department of Physiology, Seth G.S. Medical College and K.E.M. Hospital, Parel, Mumbai 400 012, India.

ABSTRACT: Severe envenoming was induced in two groups of experimental dogs after subcutaneous (SQ) injection of venom of the scorpion (Mesobuthus tamulus concanesis, Pocock) (3.0 and 3.5 mg/kg body weight). The circulating levels of blood sugar, insulin, glucagon, and cortisol were assayed at 0, and 30, 60, 90 and 120 min after venom injection. There was an increase in the circulating levels of blood sugar, insulin, glucagon, and cortisol following envenoming.

Scorpion envenoming causes an autonomic storm resulting in a massive release of catecholamines, angiotensin II, glucagon, and cortisol accompanied by changes in insulin secretion. The rise in the counter-regulatory hormones (glucagon, cortisol, and catecholamines) oppose the anabolic actions of insulin resulting in a variety of clinical manifestations. These changes may lead to a syndrome of fuel-energy deficits and to an inability of the vital organs to utilise the existing metabolic substrates, ultimately resulting in multisystem organ failure (MSOF) and death.

KEY WORDS: scorpion envenoming, insulin, glucagon, cortisol, Mesobuthus tamulus concanesis.

INTRODUCTION

Scorpion envenoming is a major health hazard in rural areas worldwide (29). The different mechanisms by which scorpion envenoming causes the death of the scorpion sting victims is not clearly known. Severe scorpion envenoming results in an autonomic storm which leads to a massive release of catecholamines (1,2,9-11), suppressed insulin secretions (16,23,24), and an increase in angiotensin II (28) levels. Angiotensin II stimulates the release of catecholamines, thereby synergising and amplifying each other's actions, and these may act, at least in part, at similar sites (7). We have already suggested that there could also be a rise in glucagon and cortisol secretions in severe scorpion envenoming. The elevated levels of the counter-regulatory hormones (glucagon, glucocorticoids, and catecholamines) oppose the anabolic actions of insulin resulting in fuel-energy deficits and an inability of the vital organs to utilise the existing metabolic substrates, which causes multisystem organ failure (MSOF), resulting in death. We demonstrate here the effects of scorpion venom on the circulating levels of blood sugar, insulin, glucagon, and glucocorticoids in experimental animals.

MATERIALS AND METHODS

A total of 21 healthy mongrel dogs of either sex (weight 8 ± 2 kg) were used in this study. After an overnight fast, the animals were anaesthetised with thiopentone sodium (35 mg/kg). The lyophilised red scorpion (Mesobuthus tamulus concanesis, Pocock) (earlier called Buthus tamulus) venom was purchased from Haffkine's Institute, Mumbai, India. Venom in saline (3.0 mg/kg) was given to a group of 9 dogs by subcutaneous injection (SQ). Blood was collected at 0, and 30, 60, 90, and 120 min following venom injection and processed for glucose (6) and insulin levels. Venom in saline (3.5 mg/kg) was given to the other 12 dogs. The blood from these animals was collected before venom administration and after 60 and 120 min. The blood samples were processed for blood glucose (6) and radioimmunoassay of insulin, glucagon, and cortisol. The radioimmunoassay kits were obtained from Diagnostic Products Corporation, Los Angeles, USA The results were statistically analysed using paired Student 't' test (3).

RESULTS

After envenoming (either 3.0 mg/kg or 3.5 mg/kg), the dogs showed several behavioural changes. These changes were: profuse thick ropy mucus salivary secretion, increased lacrimation, watery secretions from the nostrils, distended abdomen, increased frequency of urination, ejaculation, passing of stools (sometimes stained with either bile or blood), skeletal muscle fasciculations, clonus and tetany-like muscle contractions, irregular respiration, protrusion of eyeballs, and widely dilated pupils not reacting to light.

Table 1 shows the changes observed in blood glucose and insulin levels in the group of 9 experimental dogs before venom injection and after 30, 60, 90, and 120 min. There was an increase in blood sugar following venom injection. However, insulin levels fell 60 min and increased 90 min following envenoming.

Table 2 shows the changes in blood glucose, insulin, glucagon, and glucocorticoid levels in the group of 12 experimental dogs before venom injection, and after 60 and 120 min. These increased levels were significant when compared to the values obtained before venom injection in the same animals.

DISCUSSION

India harbours 99 species of scorpions, but not all scorpion stings result in victim death. Only 45 of these species, members of the Buthidae family, can cause fatalities. Elsewhere the most venomous species also belong to the Buthidae family: Androctonus from Algeria, Leiurus quinquestriatus from Israel and Jordan, Centruroides from Mexico, Buthus occitanus from Jordan, Tityus serrulatus from Brazil, Parabuthus from South Africa, Buthus occitanus from Sahara, Tityus trinitatis from Trinidad, and Centruroides sculpturatus from North America and many other countries (28). In spite of zoological differences resulting in venoms of differing chemical structure, the symptomatology following human envenomation is quite similar (28). The effect of the venom depends on the age of the offending scorpion, the season of the year, and the size (age and weight) of the victim (30).

The behavioural changes observed in the experimental animals following envenoming confirmed our earlier reports (19,22) and indicated an autonomic (sympathetic and parasympathetic) and neuro-muscular over-activity. The rise in the blood glucose levels observed in this study (Tables 1, 2) could be due to increased glycogenolysis stimulated by increased catecholamines (1,2,9-11,28), glucagon, cortisol, and changes in insulin secretion. The results of hyperglycaemia due to scorpion envenoming were in accordance with earlier work (16,18,19,24,27).

TABLE 1.
Changes in blood glucose and insulin levels in anaesthetised dogs injected with 3 mg/kg of scorpion venom (Mean ± S. E. D.)
TABLE 2.
Changes in blood glucose and hormonal levels in anaesthetised dogs injected with 3.5 mg/kg of scorpion venom. (Mean ± S.E.D)

In previous studies, intravenous injection of venom by the scorpion (Mesobuthus tamulus concanesis, Pocock) (4 mg/kg) in experimental dogs resulted in a suppressed insulin secretion (16,20,21,22), and subcutaneous injection of scorpion venom (3 mg/kg) in dogs resulted in suppression of insulin secretion 30 min after venom injection, and elevated insulin levels 60 min after venom injection (27). In this study, both insulin and blood glucose were found to be higher after 60 and after 120 min of venom injection (Table 2). These results confirmed the previous findings (12,27).

Inhibition of insulin release (15) and stimulation of glucagon secretion (14) by toxin from Leiurus quinquestriatus scorpion venom in rat pancreatic islets had already been demonstrated. These investigations (14,15) have suggested that norepinephrine release from sympathetic nerve endings is probably much greater when stimulated by scorpion venom toxin than by physiologic stimulation. Further, Johnson et al.(14,15) reported that the large release of glucagon caused by scorpion venom toxin suggests that norepinephrine released from the adrenergic nerve terminals of the pancreas may be a more effective stimulus to glucagon secretion than norepinephrine reaching the pancreas through the general circulation.

Glucocorticoids can also be released following stress or injury (8), as observed in this study. The sympatho-adrenal axis primarily serves to maintain the pressure flow relationship necessary for organ perfusion. Thus, during the "ebb phase", the insulin levels are reduced and with the onset of hypermetabolism, characteristic of the "flow phase", the hormonal environment is changed (8).

The presence of increased circulating levels of any one of these catabolic hormones that is glucagon, glucocorticoids, or catecholamines in a normal individual result in only minimal alterations in the metabolism and circulation (8). However, in the presence of increased circulating levels of all three catabolic counter-regulatory hormones, the effects of these hormonal actions are synergistic and sustained hepatic glucose production is observed (8). Thus, it appears that the simultaneous elaboration of the counter-regulatory hormones is partly responsible for the pathogenesis of a variety of clinical and biochemical manifestations following scorpion envenoming. This could be the reason for glycogenolysis in the atria, ventricle, liver, and skeletal muscles (4,5,21,22,24), hyperglycaemia (21,22,24 ), lipolysis and its products (18,22,23,24,27), increased protein breakdown products under the catabolic influence of the counter-regulatory hormones, and a simultaneous suppressed insulin secretion or insulin resistance.

Hyperinsulinism observed in this study could be equated with insulin resistance. Insulin resistance could be caused by a change in the receptor membrane, a change in hormone-receptor binding characteristics, or a change in post-receptor events (13,17).

Increased secretions of glucagon, cortisol, and catecholamines along with simultaneous reduction in insulin levels or insulin resistance stimulate glycogenolysis in skeletal muscle and promotes lactate production. Thus, under the conditions existing in scorpion envenoming, lactate is produced but not utilised contributing to lactic acidosis (22).

With the disturbed carbohydrate metabolism, dissimilation of fat is incomplete, since 'fats burn in the flame of carbohydrates' leading to ketosis (22) and this is aggravated by low glycogen content in the liver (4,5,22-24).

Insulin administration reversed the haemodynamic changes and pulmonary oedema in children and adults stung by venomous scorpions (25,31,32). Insulin administration in adult respiratory distress syndrome (ARDS) patients with multisystem organ failure (MSOF) following septic shock resulted in normal biochemical profile, radiological clearance of lungs, and clinical improvement (26). This could be due to insulin favouring glycogen deposition, inhibiting glycogenolysis and promoting glycogenesis, suppressing the mobilisation of fatty acids from adipose tissue, and promoting lipogenesis. Insulin administration following scorpion envenoming reversed the ECG and metabolic changes in experimental animals (19,21,24) as well as in scorpion sting victims (25,31,32) reducing angiotensin II levels (20), glycogenesis, and lipogenesis (22,25).

Severe scorpion envenoming is thus a syndrome of fuel-energy deficits and an inability of the vital organs to utilise the existing metabolic substrates. This ultimately may result in multisystem organ failure (MSOF) and death. These changes are brought about by a massive release of catecholamines, angiotensin II, glucagon, glucocorticoids, and either insulin deficiency, suppressed insulin secretion, or insulin resistance.

ACKNOWLEDGEMENTS

The authors thank the financial assistance from Indian Council of Medical Research, New Delhi (Task - Force Research Project No. 46/6/90 - B M S - 1). This research was conducted at Department of Physiology, L.T.M. Medical College, Sion, Mumbai, India.

REFERENCES

01 AMARAL CFS., REZENDE NA. Both cardiogenic and non-cardiogenic factors are involved in the pathogenesis of pulmonary oedema after scorpion envenoming. Toxicon, 1997, 35, 997-8.

02 AMARAL CFS., BARBOSA AJA., LEITE VHR. TAFURI WL., REZENDE NA. Scorpion sting-induced pulmonary oedema: evidence of increased alveolocapillary membrane permeability. Toxicon, 1994, 32, 999-1003.

03 BAHN AK. Basic medical statistics. New York: Grune & Stratton, 1975. 145p.

04 BALASUBRAMANIAM P., RADHA KRISHNA MURTHY K. Abnormal cardiovascular and electrocardiographic profiles and cardiac glycogen content in rabbits injected with scorpion venom. Indian J. Physiol. Pharmacol., 1981, 25, 351-5.

05 BALASUBRAMANIAM P., RADHA KRISHAN MURTY K. Liver glycogen depletion in acute myocardititis produced by scorpion venom ( Buthus tamulus ). Indian Heart J., 1984, 36, 101-3.

06 BITTNER DL., MANNING J. Automation in analytical chemistry. New York: White Plains, 1967, 1, 33.

07 DOUGLAS WW. Polypeptides, angiotensin, plasma kinins and others. In: DOUGLAS WW. The Pharmacological Basis of Therapeutics. 7.ed. New York: MacMillan, 1985.

08 DOUGLAS WW. Homeostasis: body changes in trauma and surgery. In: SABISTON DC. JR. Ed. .Textbook of surgery. Philadelphia: WB Saunders, 1986, 23-37.

09 FREIRE-MAIA L., CAMPOS JA. On the treatment of the cardiovascular manifestations of scorpion envenoming. Toxicon, 1987, 25, 125-131.

10 GUERON M., OVSYSHCHER I. What is the treatment for the cardiovascular manifestations of scorpion envenomation? Toxicon, 1987, 25, 121-4.

11 GUERON M., YAROM R. Cardiovascular manifestations of scorpion sting. Chest, 1970, 57, 156-62.

12 ISMAIL M., ABD-ELSALAM MA. Are the toxicological effects of scorpion envenomation related to tissue venom concentration? Toxicon, 1987, 26, 233-9.

13 IZZO JR. JL. Insulin resistance, is it truly the link? Am. J. Med., 1991, suppl. 2A, 217-65.

14 JOHNSON DG., ENSINCK JW. Stimulation of glucagon secretion by scorpion toxin in the perfused rat pancreas. Diabetis, 1976, 25, 645-9.

15 JOHNSON DG., HENRY DP., MOSS Y., WILLIAMS RH. Inhibition of insulin release by scorpion toxin in the pancreatic islets. Diabetes, 1975, 25, 198-201.

16 RADHA KRISHNA MURTHY K., ANITA AG. Reduced insulin secretion in acute myocarditis produced by scorpion (Buthus tamulus) venom. Indian Heart J., 1986, 38, 467-9.

17 RADHA KRISHAN MURTHY K., HASE NK. Scorpion envenoming and the role of insulin. Toxicon, 1994, 32, 1041-4.

18 RADHA KRISHNA MURTHY K., MEDH JD. Increase in serum free fatty acids, phospholipids and reduction in total cholesterol in acute myocarditis produced by scorpion (Buthus tamulus) venom. Indian Heart J., 1986, 38, 369-72.

19 RADHA KRISHNA MURTHY K., YEOLEKAR ME. Electrocardiographic changes in acute myocarditis produced by scorpion (Buthus tamulus) venom. Indian Heart J., 1986, 38, 206-10.

20 RADHA KRISHNA MURTHY K., VAKIL AE. Elevation of angiotensin levels in dogs by Indian red scorpion (Buthus tamulus) venom & its reversal by administration of insulin + tolazoline. Indian J. Med. Res., 1988, 88, 376-9.

21 RADHA KRISHNA MURTHY K., ANITA AG., DAVE BN., BILLIMORIA FR. Erythrocyte Na+-K+ ATPase activity inhibition and increase in red cell fragility in experimental myocarditis produced by Indian red scorpion venom. Indian J. Med. Res., 1988, 88, 536-40.

22 RADHA KRISHNA MURTHY K., VAKIL AE., YEOLEKAR ME., VAKIL YE. Reversal of metabolic & electrocardiographic changes induced by Indian red scorpion (Buthus tamulus) venom by administration of insulin, alpha blocker & sodium bicarbonate. Indian J. Med. Res., 1988, 88, 450-7.

23 RADHA KRISHNA MURTHY K., ZOLPHAGHRIAN H., MEDH JD., KUDALKAR JA., YEOLEKAR ME., PANDIT SP., KHOPKAR M., DAVE KN., BILLIMORIA FR. Disseminated intravascular coagulation and disturbances in carbohydrate and fat metabolism in acute myocarditis produced by scorpion (Buthus tamulus) venom. Indian J. Med. Red., 1988, 87, 318-25.

24 RADHA KRISHNA MURTHY K., VAKIL AE., YEOLEKAR ME. Insulin administration reverses the metabolic and electrocardiographic changes in acute myocarditis induced by Indian red scorpion (Buthus tamulus) venom in experimental dogs. Indian Heart J., 1990, 42, 35-42.

25 RADHA KRISHNA MURTHY K., SHENOI LR., VAIDYANATHAN P., KELKAR K., SHARMA N., NEETA B., RAO S., MEHTA MN. Insulin reverses haemodynamic changes and pulmonary oedema in children stung by the Indian red scorpion Mesobuthus tamulus concanesis, Pocock. Ann. Trop. Med. Parasitol, 1991, 85, 651-7.

26 RADHA KRISHNA MURTHY K., BHAMBURE NM., ABHYANKAR NY., PHADKE AY., SOMAN SS., SHAH AS., DESHMUKH SN. Insulin administration in adult respiratory distress syndrome following septic shock. Indian Pract., 1992, 45, 641-4.

27 RADHA KRISHNA MURTHY K., KANKONKAR RC., ZARE AM., MALATHI A., BALASUBRAMANIAM P., YEOLEKAR ME. Reversal of metabolic and electrocardiographic changes by scorpion antivenin administration in experimental myocarditis induced by Indian red scorpion (Buthidae family) venom. Recent Adv. Toxinol. Res., 1992, 2, 70-83.

28 SOFER S., GUERON M. Cardiovascular effects of scorpion envenomation. Recent Adv. Toxinol. Res., 1992, 2, 20-49

29 TIKADER BK., BASTWADE DB. The fauna of India scorpion, Scorpionida, Arachnida. Calcutta: Zoological Survey of India, 1983, 3, 1-686.

30 TIWARI AK., DESHPANDE SB. Toxicity of scorpion (Buthus tamulus) venom in mammals. Toxicon, 1993, 31, 1619-22.

31 USHA KIRAN P. A retrospective study on treatment of red scorpion stings. Vijayawada: The Andhra Pradesh University of Health Sciences, 1996. (MD Thesis)

32 YUGANDHAR B. Clinical study of scorpion sting with special reference to insulin glucose treatment. Vijayawada: The Andhra Pradesh University of Health Sciences, 1995. (M.D. Thesis).

  • 01 AMARAL CFS., REZENDE NA. Both cardiogenic and non-cardiogenic factors are involved in the pathogenesis of pulmonary oedema after scorpion envenoming. Toxicon, 1997, 35, 997-8.
  • 02 AMARAL CFS., BARBOSA AJA., LEITE VHR. TAFURI WL., REZENDE NA. Scorpion sting-induced pulmonary oedema: evidence of increased alveolocapillary membrane permeability. Toxicon, 1994, 32, 999-1003.
  • 04 BALASUBRAMANIAM P., RADHA KRISHNA MURTHY K. Abnormal cardiovascular and electrocardiographic profiles and cardiac glycogen content in rabbits injected with scorpion venom. Indian J. Physiol. Pharmacol., 1981, 25, 351-5.
  • 05 BALASUBRAMANIAM P., RADHA KRISHAN MURTY K. Liver glycogen depletion in acute myocardititis produced by scorpion venom ( Buthus tamulus ). Indian Heart J, 1984, 36, 101-3.
  • 06 BITTNER DL., MANNING J. Automation in analytical chemistry. New York: White Plains, 1967, 1, 33.
  • 07 DOUGLAS WW. Polypeptides, angiotensin, plasma kinins and others. In: DOUGLAS WW. The Pharmacological Basis of Therapeutics 7.ed. New York: MacMillan, 1985
  • 08 DOUGLAS WW. Homeostasis: body changes in trauma and surgery. In: SABISTON DC. JR. Ed. .Textbook of surgery. Philadelphia: WB Saunders, 1986, 23-37.
  • 09 FREIRE-MAIA L., CAMPOS JA. On the treatment of the cardiovascular manifestations of scorpion envenoming. Toxicon, 1987, 25, 125-131.
  • 10 GUERON M., OVSYSHCHER I. What is the treatment for the cardiovascular manifestations of scorpion envenomation? Toxicon, 1987, 25, 121-4.
  • 11 GUERON M., YAROM R. Cardiovascular manifestations of scorpion sting. Chest, 1970, 57, 156-62.
  • 12 ISMAIL M., ABD-ELSALAM MA. Are the toxicological effects of scorpion envenomation related to tissue venom concentration? Toxicon, 1987, 26, 233-9.
  • 13 IZZO JR. JL. Insulin resistance, is it truly the link? Am. J. Med, 1991, suppl. 2A, 217-65.
  • 14 JOHNSON DG., ENSINCK JW. Stimulation of glucagon secretion by scorpion toxin in the perfused rat pancreas. Diabetis, 1976, 25, 645-9.
  • 15 JOHNSON DG., HENRY DP., MOSS Y., WILLIAMS RH. Inhibition of insulin release by scorpion toxin in the pancreatic islets. Diabetes, 1975, 25, 198-201.
  • 16 RADHA KRISHNA MURTHY K., ANITA AG. Reduced insulin secretion in acute myocarditis produced by scorpion (Buthus tamulus) venom. Indian Heart J, 1986, 38, 467-9.
  • 17 RADHA KRISHAN MURTHY K., HASE NK. Scorpion envenoming and the role of insulin. Toxicon, 1994, 32, 1041-4.
  • 18 RADHA KRISHNA MURTHY K., MEDH JD. Increase in serum free fatty acids, phospholipids and reduction in total cholesterol in acute myocarditis produced by scorpion (Buthus tamulus) venom. Indian Heart J., 1986, 38, 369-72.
  • 19 RADHA KRISHNA MURTHY K., YEOLEKAR ME. Electrocardiographic changes in acute myocarditis produced by scorpion (Buthus tamulus) venom. Indian Heart J, 1986, 38, 206-10.
  • 20 RADHA KRISHNA MURTHY K., VAKIL AE. Elevation of angiotensin levels in dogs by Indian red scorpion (Buthus tamulus) venom & its reversal by administration of insulin + tolazoline. Indian J. Med. Res, 1988, 88, 376-9.
  • 21 RADHA KRISHNA MURTHY K., ANITA AG., DAVE BN., BILLIMORIA FR. Erythrocyte Na+-K+ ATPase activity inhibition and increase in red cell fragility in experimental myocarditis produced by Indian red scorpion venom. Indian J. Med. Res, 1988, 88, 536-40.
  • 22 RADHA KRISHNA MURTHY K., VAKIL AE., YEOLEKAR ME., VAKIL YE. Reversal of metabolic & electrocardiographic changes induced by Indian red scorpion (Buthus tamulus) venom by administration of insulin, alpha blocker & sodium bicarbonate. Indian J. Med. Res, 1988, 88, 450-7.
  • 23 RADHA KRISHNA MURTHY K., ZOLPHAGHRIAN H., MEDH JD., KUDALKAR JA., YEOLEKAR ME., PANDIT SP., KHOPKAR M., DAVE KN., BILLIMORIA FR. Disseminated intravascular coagulation and disturbances in carbohydrate and fat metabolism in acute myocarditis produced by scorpion (Buthus tamulus) venom. Indian J. Med. Red., 1988, 87, 318-25.
  • 24 RADHA KRISHNA MURTHY K., VAKIL AE., YEOLEKAR ME. Insulin administration reverses the metabolic and electrocardiographic changes in acute myocarditis induced by Indian red scorpion (Buthus tamulus) venom in experimental dogs. Indian Heart J, 1990, 42, 35-42.
  • 25 RADHA KRISHNA MURTHY K., SHENOI LR., VAIDYANATHAN P., KELKAR K., SHARMA N., NEETA B., RAO S., MEHTA MN. Insulin reverses haemodynamic changes and pulmonary oedema in children stung by the Indian red scorpion Mesobuthus tamulus concanesis, Pocock. Ann. Trop. Med. Parasitol, 1991, 85, 651-7.
  • 26 RADHA KRISHNA MURTHY K., BHAMBURE NM., ABHYANKAR NY., PHADKE AY., SOMAN SS., SHAH AS., DESHMUKH SN. Insulin administration in adult respiratory distress syndrome following septic shock. Indian Pract., 1992, 45, 641-4.
  • 27 RADHA KRISHNA MURTHY K., KANKONKAR RC., ZARE AM., MALATHI A., BALASUBRAMANIAM P., YEOLEKAR ME. Reversal of metabolic and electrocardiographic changes by scorpion antivenin administration in experimental myocarditis induced by Indian red scorpion (Buthidae family) venom. Recent Adv. Toxinol. Res., 1992, 2, 70-83.
  • 28 SOFER S., GUERON M. Cardiovascular effects of scorpion envenomation. Recent Adv. Toxinol. Res., 1992, 2, 20-49
  • 29 TIKADER BK., BASTWADE DB. The fauna of India scorpion, Scorpionida, Arachnida. Calcutta: Zoological Survey of India, 1983, 3, 1-686.
  • 30 TIWARI AK., DESHPANDE SB. Toxicity of scorpion (Buthus tamulus) venom in mammals. Toxicon, 1993, 31, 1619-22.
  • 31 USHA KIRAN P. A retrospective study on treatment of red scorpion stings. Vijayawada: The Andhra Pradesh University of Health Sciences, 1996 (MD Thesis)
  • 32 YUGANDHAR B. Clinical study of scorpion sting with special reference to insulin glucose treatment. Vijayawada: The Andhra Pradesh University of Health Sciences, 1995. (M.D. Thesis).
  • CORRESPONDENCE TO:
    K. RADHA KRISHNA MURTHY - Professor of Physiology, Seth G.S. Medical College and K.E.M. Hospital, Parel, Mumbai 400 012, India.
  • Publication Dates

    • Publication in this collection
      16 Apr 1999
    • Date of issue
      1999
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