Why the study?
Does the absence of ventricular innervation prevent the vasodepressor reflex during central hypovolaemia in cardiac transplant patients?
Does the absence of ventricular innervation prevent the vasodepressor reflex during central hypovolaemia in cardiac transplant patients?
Left ventricular mechanoreceptors may not be the primary afferent trigger for syncope, as denervated hearts in transplant patients exhibit similar vasodepressor responses to hypovolemia as healthy controls.
Similar hypovolaemia tolerance despite denervation suggests non-ventricular triggers for vasodepressor reflex; hypothesis-generating, should not yet change practice.
To determine whether activation of the left ventricular C-fibre mechanoreceptors initiates the vasodepressor reflex that often causes syncope, we exposed six orthotopic cardiac transplant patients and six matched, healthy control subjects to progressively increasing lower body negative pressure until the onset of vasodepressor responses. 2. There was no significant difference (P = 0.78) between the central hypovolaemia tolerances of the cardiac transplant and the control groups. 3. The decrease in systolic blood pressure before the onset of vasodepressor reflexes was greater in the cardiac transplant group. The cardiac transplant group did not maintain diastolic blood pressure during central hypovolaemia. From baseline to the onset of vasodepression, there were no differences in leg circumference, forearm blood flow and forearm vascular resistance responses between the two groups. 4. We conclude that the left ventricular mechanoreceptors may not be the primary afferent trigger for syncope.
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Lightfoot et al. (1993) studied this question.
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