ISSN:
1432-2013
Keywords:
Pressoreceptors
;
Cardiac Output
;
Blood Pressure
;
Autoregulation
;
Sympatholytics
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Summary Flow velocity in the ascending aorta and aortic blood pressure were recorded continuously in healthy conscious dogs. Using implanted pneumatic cuffs the effect of bilateral carotid occlusion on heart rate, stroke volume, cardiac output, peak velocity, maximum acceleration, blood pressure, and total peripheral resistance (T.P.R.) was studied in the resting animal. Following carotid occlusion heart rate rose within 3–4 sec by 13 beats/min; during the steady state it exceeded the control by 8 beats/min. Cardiac output closely followed heart rate, since stroke volume decreased slightly (3–4%), mainly because of the elevated aortic pressure. During the first 3–4 sec cardiac output increased by 10–15% reaching a steady state level 8% above control. The initial fast increase of cardiac output caused mean aortic pressure to rise rapidly, while T.P.R. transiently decreased. Subsequently T.P.R. rose, causing a secondary slow increase of pressure. During the steady state blood pressure was elevated by 27 mm Hg (26%), T.P.R. by 12.1 mm Hg×l−1×min (20%). Maximum acceleration did not change with heart rate and was hardly affected (−1.5%) by the pressure rise. Peak velocity was little influenced by heart rate; it decreased by 7% mainly because of the elevated aortic pressure. β-blockade (0.5 mg/kg propranolol) affected T.P.R. only during control (+18%), but did not modify the time course of the reflex and its steady state changes. α-blockade (5.0 mg/kg phenoxybenzamine) decreased aortic mean pressure (5 mm Hg) and T.P.R. (7%) during control. Following carotid occlusion T.P.R. rose by the same amount, but much more slowly. Starting from the lower control the same pressure level was now obtained by a higher reflex increase of heart rate and cardiac output. It is concluded that the initial pressor response is initiated by an increase of cardiac output mediated by vagal inhibition. The secondary rise of blood pressure is predominantly caused by an increase of T.P.R. due to autoregulation in some vascular beds. The higher stroke work during the reflex is not accomplished by an increased contractility due to sympathetic activation.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00586859
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