To assess cardiac sympathetic nervous function in diabetics, the heart rates attained following a pharmacological dose of intravenous atropine, were studied under N20, isoflurane anaesthesia in diabetics (n = 2 I) and nondiabetics (n = 30). A tropine-induced heart rate in diabetics was significantly lower than that in nondiabetics (95 + 14 (SD) bpm vs 109 +-12 bpm, P < 0.001) and were closely related to preoperative orthostatic diastolic blood pressure change (r = 0.60, P < 0.01). There was some correlation between the atropineinduced heart rate and preoperative P < 0.05 Accepted for publication 21st August, 1990 Sudden deaths without autopsy evidence of myocardial infarction have been described in diabetics with cardiovascular autonomic neuropathy.~ Recently, severe perioperative bradycardia and hypotension 2-4 as well as cardiac standstill 5 were reported in diabetics with orthostatic hypotension under well-monitored circumstances where such episodes are not normally expected to occur. The bradycardia was refractory to atropine and ephedrine, suggesting that cardiac sympathetic nerves in addition to the sympathetic innervation to blood vessels and cardiac parasympathetic nerves may have been damaged in these patients. [2][3][4] In diabetics the resting heart rate correlates inversely with RR-variation, 6 and the decrease in RR-variation is related to damage to cardiac parasympathetic nerves. 7 The degree of tachycardia depends on the relative severity of damage to the cardiac parasympathetic and sympathetic nervous systems. As cardiac sympathetic nerve damage progresses, the tachycardia tends to lessen and ultimately results in a fixed heart rate that is equal to the intrinsic rate of the heart. 8 A recent longitudinal study in diabetics demonstrated an initial increase and a subsequent decline in resting heart rate related to the deterioration of cardiovascular autonomic nervous function. 9 Current autonomic function tests, however, do not assess cardiac sympathetic neuropathy, I~ and its natural history has remained unclear.The peripheral interactions that occur between cardiac parasympathetic and sympathetic postganglionic fibres, i.e., accentuated antagonism and reciprocal excitation, are so complex that observed responses to administered autonomic drugs are difficult to interpret. J~'12 However, the interactions are abolished either by anticholinergic or 13-adrenergic antagonists, II't2 and the pharmacological denervation of the heart results in a moderate tachycardia, which is unresponsive to stimuli, ta. 14 The surgical denervation of the heart, i.e., a transplanted heart, responds similarly. ~4'15 Thus, under basal conditions, heart rate resulting from pharmacological blockade of the cardiac parasympathetic nervous system is expected to reflect unopposed cardiac sympathetic tone. We therefore studied the heart rate attained following a pharmacological dose of atropine in anaesthetized diabetics and its relationship CAN J ANAESTH 1991 / 38:l/pp20-3
