Abstract

The effects of 6-hydroxydopamine (6-HDA) on hemodynamic function were assessed in pithed male Sprague-Dawley rats prepared for continuous measurement of cardiac output by electromagnetic flowmetry. One week after 6-HDA administration, 100 mg/kg s.c., blood pressure increments elicited by electrical stimulation of the lumbar sympathetic outflow (0.25-8.0 Hz) were reduced significantly (P less than .01), whereas heart rate responses were normal. The reduction in blood pressure responses was due to an attenuation of increases in both cardiac output (P less than .01) and total peripheral resistance (P less than .02). Cardiac output responses were reduced exclusively due to a fall in stroke volume inasmuch as heart rate increases were not altered by 6-HDA. Furthermore, the reduction in neurally mediated cardiac output increases by 6-HDA appeared to result from impaired sympathetic control of inotropic activity. This conclusion was supported by the observation that pretreatment with the beta adrenergic receptor antagonist, nadolol, markedly decreased cardiac output responses in control animals, but did not further attenuate cardiac output increases in 6-HDA-treated rats. However, after nadolol a substantial cardiac output response remained that was equivalent in 6-HDA-treated and control rats. This remaining response may be accounted for by venous constriction and because there was no difference in the cardiac output increases in the two groups after nadolol it appears that neural control of venoconstriction was not impaired by 6-HDA. Thus results of the present study indicate that at 1 week after 6-HDA treatment noradrenergic control of resistance vessels and cardiac inotropism are reduced significantly.(ABSTRACT TRUNCATED AT 250 WORDS)