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Myogenic origin of the hypotension induced by rapid changes in posture in awake dogs following autonomic blockade

Department of Integrative Physiology, The University of Iowa, Iowa City, Iowa

Submitted 9 June 2008 ; accepted in final form 13 October 2008

The "push-pull" effect denotes the reduced tolerance to +G_z (hypergravity) when +G_z stress is preceded by exposure to hypogravity, i.e., fractional, zero, or negative G_z. The purpose of this study was to test the hypothesis that an exaggerated, myogenically mediated rise in leg vascular conductance contributes to the push-pull effect, using heart level arterial blood pressure as a measure of G tolerance. The approach was to impose control (30 s of 30° head-up tilt) and push-pull (30 s of 30° head-up tilt immediately preceded by 10 s of –15° head-down tilt) gravitational stress after administration of hexamethonium (5 mg/kg) to inhibit autonomic ganglionic neurotransmission in seven dogs. Cardiac output or thigh level arterial pressure (myogenic stimulus) was maintained constant by computer-controlled ventricular pacing. The animals were sedated with acepromazine and lightly restrained in lateral recumbency on a tilt table. Following the onset of head-up tilt, the magnitude of the fall in heart level arterial pressure from baseline was –11.6 ± 2.9 and –17.1 ± 2.2 mmHg for the control and push-pull trials, respectively (P < 0.05), when cardiac output was maintained constant. Over 40% of the exaggerated fall in heart level arterial pressure was attributable to an exaggerated rise in hindlimb vascular conductance (P < 0.05). Maintaining thigh level arterial pressure constant abolished the exaggerated rise in hindlimb blood flow. Thus a push-pull effect largely attributable to a myogenically induced rise in leg vascular conductance occurs when autonomic function is inhibited.

tilt; gravitational stress; orthostatic intolerance; atrioventricular block

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