Effects of magnesium on isolated rabbit atria.

The cardiac effects of magnesium were studied on 40 spontaneously beating rabbit atria at 37 degrees C. Magnesium administered in doses of 30, 60, 120 and 240 mmol elicited dose dependent negative inotropic and chronotropic responses. Larger doses above 240 mmol caused complete atrial arrest. Further it was observed that propranolol with magnesium became more effective in blocking the positive chronotropic and inotropic responses to isoprenaline. The finding is interesting and suggestive that magnesium could be employed either alone or in combination with propranolol in treatment of arrhythmias which are non-responsive to propranolol.

Reduced beta adrenergic responsiveness in isolated rabbit atria during hypothermia.

Beta adrenergic agonist isoprenaline (8x10(-6)M) produced a 500% increase in inotropic and 90% increase in the chronotropic responses of isolated rabbit atria at 37 degrees C. On cooling the atria to 23 degrees C, these responses were significantly reduced to 87% and 30% respectively. Similar results were obtained with adrenaline, but isoprenaline was more potent. The positive chronotropic and inotropic responses to isoprenaline were effectively blocked by propranolol and practolol at 37 degrees C whereas at 23 degrees C these beta blockers were unable to block even minor positive responses obtained by isoprenaline at this temperature. On the contrary at 23 degrees C, phenylephrine (alpha adrenergic agonist) produced marked positive chronotropic and inotropic effects indicating enhancement of alpha adrenoceptor activity at lower temperatures. This also suggests that reduced beta receptor activity at lower temperature is not due to a generalised depression of adrenoceptors as a result of hypothermia. Rewarming of atria to 37 degrees C restored the beta adrenoceptor responsiveness to previous level. It appears that ambient temperature is important im maintaining normal beta adrenergic activity of the atria.

Hypoglycemic responses to insulin in normothermic and hyperthermic young dogs.

The present study was conducted in 10 healthy young dogs in which pattern of hypoglycemia to injected insulin (0.12 U/kg I.V.) was studied at normothermic (38.5 degrees C) and hyperthermic (42.5 degrees C) body temperatures. Average maximum fall in plasma glucose concentration from the control level was 44.3% and 53.8% in normothermic and hyperthermic dogs respectively. The hypoglycemic response to injected insulin was much greater and prolonged in hyperthermic dogs. The recovery of plasma glucose to preinjection level was also very sluggish and incomplete in these dogs. The above changes in hyperthermic animals may be due to enhanced secretion of insulin, as well as an increased sensitivity to injected insulin. The slow recovery of plasma glucose to preinjection level following insulin administration in hyperthermic dogs would indicate inefficient feedback mechanisms which normally operate to raise the plasma glucose during hypoglycemia.

Effect of hyperthermia on glucose homeostasis in young dogs. An experimental study.

Hyperthermia was produced in healthy anaesthetized young dogs by keeping them in a theromostatically controlled chamber, and the effects on blood glucose concentration were studies. The blood glucose levels decreased significantly at body temperatures of 40.5 degrees C and 42.5 degrees C. The decrease was greater at the latter temperature. Intravenous glucose tolerance tests were performed to study the rates of glucose utilization during hyperthermia. The calculated fractional rates of disappearance of glucose (Kt values) were found to be significantly higher in dogs having a body temperature of 42.4 degrees C. The cause of hypoglycemia produced at high body temperature seems to be due to an elevated insulin secretion which increases the over all utilization of glucose by the peripheral tissues. The study of time course of hyperglycemic response following intravenous glucose tolerance tests performed at high body temperature further support the possibility of an increase in insulin secretion in dogs subjected to hyperthermia.