The effects of an intravenous infusion of 1 |xg/kg/min nitroglycerin were studied on systemic arterial properties in nine acutely instrumented dogs. Aortic impedance and pulse-wave velocity were calculated from measured pressure and flow signals collected during random ventricular pacing. Central aortic diameter was simultaneously determined with ultrasonic dimension crystals. Mean blood pressure was maintained constant to avoid the confounding effects of passive, pressure-induced changes in vascular properties. Nitroglycerin both reduced the amplitude of peripheral vascular reflections and delayed the return of these reflections to the aortic root. This reflection delay was manifested as a consistent leftward shift in both impedance modulus and phase. The magnitude of this reflection delay could not be entirely accounted for on the basis of the measured changes in average pulse-wave velocity along the aorta. ; 2) increased arterial compliance, as determined by both the rate of aortic diastolic pressure decay and pressure-diameter relations in peripheral arteries 6 ; and 3) decreased magnitude of arterial pulse-wave reflections. -3This study used an acute canine preparation to further define the effects of nitroglycerin on systemic arterial properties. We measured the effects of intravenous nitroglycerin on aortic impedance, diameter, and pulse-wave velocity (PWV). The use of spectral analysis techniques, in conjunction with random cardiac pacing, allowed us to determine the impedance spectrum with a frequency resolution as small as 0.1 Hz. Our results indicate that nitroglycerin has significant effects on both the magnitude and timing of peripheral vascular reflections. Materials and Methods In Vivo MethodsNine mongrel dogs (body weight 17-23 kg) were anesthetized with a combination of pentobarbital and fentanyl (initial dose: 12 mg/kg pentobarbital and 50 u.g/kg fentanyl; subsequent infusion: 1.1 mg/kg/hr and 15 u,g/kg/hr, respectively). Instrumentation in all dogs included a nonconstricting ultrasonic flow probe (model T-101, Transonic Systems, Ithaca, New York) in the ascending aorta, a Millar pressure catheter (Houston, Texas) in the ascending aorta, inserted through the right common carotid artery, and a central venous pressure catheter passed through the femoral vein. The Millar catheter was positioned at the same level as the aortic flow probe by palpating the catheter tip within the aorta. Additional instrumentation in seven dogs included a second Millar catheter in the femoral artery, inserted and attached with a nonocclusive purse-string suture, and a pair of ultrasonic crystals on the aortic arch (5-HHz crystals connected to a sonomicrometer; model 401, Schuessler, Cardiff by the Sea, California). These ultrasonic crystals, used to measure aortic diameter, were attached to opposing sides of the aortic adventitia with either fine sutures (tied to a flexible woven backing sheet) and/or a small amount of cyanoacrylate glue.7 Permanent atrioventricular block was produced in all dogs by injection of 40% ...
Four physiological mechanisms are known to be important for recovery of arterial pressure (AP) after acute hemorrhage. These are the sino-aortic baroreflex (SA), the vagally mediated cardiopulmonary baroreflex (CP), the renin-angiotensin system (RA), and the vasopressin system (VP). We evaluated in anesthetized rabbits the relative importance of these mechanisms by repeating rapid, 10% arterial hemorrhage (6.5 ml/kg) once before and once after eliminating one of them and comparing the posthemorrhage hypotension. The study was conducted in two series. In the first series, we randomly grouped 24 rabbits into four groups, i.e., a sinoaortic baroreceptor-denervated group (SA) a vagotomized group (CP), a renin-angiotensin-blocked group (RA), and a vasopressin-blocked group (VP). In control conditions, AP fell to 88% at 2 min and 92% at 6 min after completing the hemorrhage. Significantly greater hypotension (e.g., 74% at 6 min) occurred only in the SA group. In the second series, we randomly classified 18 rabbits into three groups, i.e., an autonomic ganglion-blocked group (AB) plus a RA group and a VP group as before. Hypotension significantly greater than control (68% opposed to 91% at 6 min) occurred only in the AB group. We submit that as far as restoration of arterial pressure after rapid, mild hemorrhage in the rabbit is concerned, the arterial baroreceptor reflex system plays a far more important role than the vagally mediated cardiopulmonary baroreflex, the vasopressin system, or the renin-angiotensin system triggered directly by a fall in renal arterial pressure.
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