The broad objective is to evaluate the performance of the arterial and cardiopulmonary reflex control of arterial pressure and its major determinants (cardiac output and resistance). We have emphasized quantification of interactions among reflex, humoral and mechanical regulations because systems physiology is responsible for providing such integrative information for health care.
Aim I is to quantify carotid sinus reflex control of cardiac contractility and arterial properties as after load against ventricular ejection. Left ventricular contractility is assessed by three indices, which can be obtained by changing ventricular preload over a wide range. These are slopes of the end-systolic P-V relation, stroke work vs. end-diastolic volume (ADV) relation, and maximum dP/dt vs. EDV relation. Arterial load properties are gauged by high-resolution frequency spectrum of aortic input impedance and parameters of wave reflection derived from the spectrum. Such impedance spectrum is obtained by randomly pacing the heart and applying white noise analysis to aortic pressure and flow data. Prepared for these measurements by preliminary surgery, and data are obtained at low, middle, and high carotid sinus pressures, first in sedated conscious state and then under anesthesia Aim II is to determine contributions of three mechanisms, i.e., the cardiopulmonary reflex (CPR), renin-angiotensin system, and vasopressin system to restoration of arterial pressure after 10% quick hemorrhage . In Part A, we leave only the CPR-neuroeffector mechanism and CPR- vasopressin mechanism intact, them eliminate one of them, and finally remove both while repeating the hemorrhage-transfusion three times. The posthemorrhage hypotension data at 6 in permits evaluation of individual mechanisms and interactive contributions. In Part B, we leave only the baroreflex-renin release mechanism and the renal arterial pressure-renin release mechanism intact. As in Part A, the two mechanisms are removed sequentially and their separate and interactive contributions quantified. Plasma level of AVP and renin activity are measured and correlated with arterial pressure change.
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