Relative roles of heart rate and ventricular stroke volume for the regulation of cardiac output during controlled hypotension with sodium nitroprusside in man.

The effects of N-allyl clonidine (St 567, alinidine), (0.5 mg/kg i.v.) a substance with specific bradycardic action at the sinus node, were studied on a total of thirteen patients in neuroleptanaesthesia and during controlled hypotension with sodium nitroprusside (SNP). Invariably, the fall in blood pressure was associated with an increase in heart rate (20.0 +/- 4.3+; P less than 0.01), presumably due to an activation of the arterial baroreceptor reflex. Alinidine decreased heart rate to the original level but no fall in cardiac output occurred a ventricular stroke volume and the calculated left ventricular stroke work were increased compensatorily (35.9 +/- 7.2% and 35.9 +/- 6.7%, P less than 0.01, respectively). In patients who received alinidine before the onset of controlled hypotension (n = 5) SNP failed to elicit an increase in heart rate. It is concluded that in patients under neuroleptanaesthesia tachycardiac does not play an important role for the maintenance of an adequate cardiac output during controlled hypotension with SNP.