Effects of anesthesia on carotid sinus reflex control of arterial hemodynamics in the dog

1980 ◽  
Vol 239 (5) ◽  
pp. H681-H691 ◽  
Author(s):  
R. H. Cox ◽  
R. J. Bagshaw
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Peripheral Resistance ◽  
Operating Point ◽  
Set Point ◽  
Arterial Hemodynamics ◽  
Pulsatile Pressure ◽  
Reflex Gain ◽  
Reflex Control

The detailed characteristics of the carotid sinus reflex control of regional pressure-flow relations were compared in dogs anesthetized with chloralose, pentobarbital, or halothane. The carotid sinuses were isolated and perfused under conditions of controlled pulsatile pressure. Pressure and flow were measured in the ascending aorta and the celiac, mesenteric, renal, and iliac artery. Mean arterial pressure and peripheral resistance were highest under chloralose and lowest under halothane. For cardiac output this relation was reversed. Set point values of reflex gain and overall range of control were similar under chloralose and halothane and lowest under pentobarbital. These results were found both before and after bilateral cervical vagotomy. Operating point values of regional resistance were generally largest with chloralose and smallest with halothane. Operating point sensitivities of regional resistances were generally smallest under pentobarbital and similar under chloralose and halothane. Vagotomy was associated with increases in set point values of mean arterial pressure, set point gain, and overall range of control under all three anesthetics. With chloralose as a reference, halothane does not depress cardiovascular reflex mechanisms. Carotid sinus reflexes under halothane were as sensitive and well maintained as they were under chloralose. These reflexes were significantly depressed under pentobarbital compared with chloralose.

Baroreceptor reflex cardiovascular control in mongrel dogs and racing greyhounds

1985 ◽  
Vol 249 (3) ◽  
pp. H655-H662 ◽  
Author(s):  
R. H. Cox ◽  
R. J. Bagshaw ◽  
D. K. Detweiler
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Open Loop ◽  
Baroreceptor Reflex ◽  
Operating Point ◽  
Baroreflex Control ◽  
Pulsatile Pressure ◽  
Carotid Sinus Baroreflex ◽  
Before And After

The open-loop carotid sinus baroreflex control of arterial pressure-flow relations were compared in mongrel dogs and racing greyhounds (GH) anesthetized with alpha-chloralose. The carotid sinuses were bilaterally isolated and perfused under controlled pressure. Pulsatile pressure and flow were simultaneously measured in the ascending aorta, the celiac, superior mesenteric, left renal, and right iliac arteries. Open-loop set point values of mean arterial pressure were higher in GH before and after vagotomy. Reflex gains were similar before vagotomy but lower in GH after vagotomy. The overall range of control of arterial pressure was the same before vagotomy but smaller in GH after vagotomy. The variation of mean arterial pressure with mean carotid sinus pressure in GH was shifted toward higher pressure levels similar to resetting. The overall effects of vagotomy on carotid sinus baroreceptor reflex responses were smaller in GH. Operating point values of regional resistance were generally smaller in GH. Operating point sensitivities of regional resistance were the same except for the iliac bed, which was more sensitive in GH. These results document significant regional differences in the baroreceptor control of regional hemodynamics between mongrels and greyhounds that could contribute to altered responses especially to "hypertensive" perturbations.

Pulsatile vs. mean component of baroreflex compensation for posthemorrhage hypotension

1988 ◽  
Vol 254 (6) ◽  
pp. H1074-H1080
Author(s):  
T. Yamazaki ◽  
M. J. Brunner ◽  
K. Sagawa
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Aortic Pressure ◽  
Open Loop ◽  
Feedback Condition ◽  
Carotid Baroreflex ◽  
Pulsatile Pressure ◽  
Mean Pressure ◽  
Pressure Feedback

We studied the influence of pulsatile pressure and mean arterial pressure signals on the restoration of arterial pressure after 10% hemorrhage in seven anesthetized dogs. After transection of the aortic nerve, a quick 10% hemorrhage was repeated under four different sinus conditions: condition 1, carotid sinus pressure depulsated and fixed at a level equal to the prehemorrhage level (no feedback); condition 2, pulsatile component of aortic pressure fed back to the carotid sinus with a fixed mean pressure (pulsatile feedback); condition 3, depulsated mean aortic pressure fed back (mean pressure feedback); condition 4, both pulsatile and mean pressure fed back (pulsatile plus mean component feedback). The restoration of arterial pressure in condition 2 was not significantly different from that in condition 1, but there was greater restoration in conditions 3 and 4. At 1.5 min posthemorrhage, the open-loop gains calculated from the restoration values were nearly zero for the pulsatile feedback only, 2.8 +/- 0.8 for mean arterial pressure feedback, and 1.5 +/- 0.3 for pulsatile and mean pressure feedback. These results indicate that the pulsatile component of the carotid baroreflex contributes minimally to the restoration of arterial pressure after 10% hemorrhage in the anesthetized dog.

Arterial pressure-flow relationships in hypertensive dogs: effect of carotid sinus baroreflex

1993 ◽  
Vol 265 (3) ◽  
pp. H986-H992
Author(s):  
M. J. Brunner ◽  
G. G. Bishop ◽  
K. Shigemi ◽  
J. P. Freeman ◽  
D. Chung
Keyword(s):  
Arterial Pressure ◽  
Carotid Sinus ◽  
Peripheral Resistance ◽  
Coefficient Of Determination ◽  
Experimental Hypertension ◽  
Baroreflex Control ◽  
Pressure Flow ◽  
Hypertensive Group ◽  
Carotid Sinus Baroreflex ◽  
Reflex Gain

The effect of the carotid sinus baroreflex reflex on arterial pressure-flow relationships was studied in Goldblatt hypertensive and normotensive dogs on cardiopulmonary bypass. Dogs were anesthetized with pentobarbital sodium, vagotomized, and the carotid sinuses were isolated at controlled carotid sinus pressures (CSP). The mean arterial pressure-flow relationships were measured at different levels of CSP. The arterial pressure-flow relationship was found to be linear except at extreme levels of flow. The slopes derived from the linear regression of the pressure-flow relationships [total peripheral resistance (TPR)] were 1.466 +/- 0.111 and 0.786 +/- 0.13 mmHg.ml-1 x min.kg at CSP of 50 and 200 mmHg in the normotensive group and 1.758 +/- 0.183 and 0.937 +/- 0.114 mmHg.ml-1 x min.kg at CSP of 50 and 250 mmHg in the hypertensive group. The increases in slope measured when CSP was decreased from saturation to threshold were 0.68 mmHg.ml-1 x min.kg (187% increase) in the normotensive group and 0.82 mmHg.ml-1 x min.kg (188% increase) in the hypertensive group. Zero-flow arterial pressures at CSP of 50, 125, and 200 mmHg were found to be 23.1 +/- 2.9, 21.7 +/- 2.2, and 17.1 +/- 1.8 mmHg in the normotensive group and 28.4 +/- 2.2, 23.8 +/- 1.5, and 20.0 +/- 1.2 mmHg in the hypertensive group. A nonlinear model fit was found to give a significantly better fit [coefficient of determination (r2) = 0.932 linear, 0.956 nonlinear] of the arterial pressure-flow relationships. We conclude that, in experimental hypertension, carotid baroreflex control of TPR is shifted to a higher operating point without any reduction in overall reflex gain.

Effects of pulsations on carotid sinus control of regional arterial hemodynamics

1980 ◽  
Vol 238 (2) ◽  
pp. H182-H190 ◽  
Author(s):  
R. H. Cox ◽  
R. J. Bagshaw
Keyword(s):  
Carotid Sinus ◽  
Peripheral Resistance ◽  
Aortic Pressure ◽  
Operating Point ◽  
Systemic Hemodynamic ◽  
Arterial Hemodynamics ◽  
Hemodynamic Variables ◽  
Anesthetized Dogs ◽  
Mean Aortic Pressure ◽  
Sinus Pressure

Studies were conducted in halothane-anesthetized dogs to evaluate the interaction of mean and pulsatile components of carotid sinus perfusion pressure on the control of regional pressure-flow relations. Pressure and flow were measured simultaneously in the ascending aorta, celiac, mesenteric, renal, and iliac arteries. The carotid sinuses were bilaterally isolated and perfused under controlled conditions. Mean (CSP) and pulsatile components (CSPP) of carotid sinus pressure were varied systemically. Values of mean aortic pressure (AP) at the operating point (AP = CSP) decreased with increasing CSPP (127 +/- 5 at CSPP = 0 to 103 +/- 5 at CSPP = 60). Reflex gains at the operating point also decreased with increasing CSPP (-1.35 +/- 0.16 for CSPP = 0 to -0.92 +/- 0.18 for CSPP = 60). Changes in cardiac output and peripheral resistance nonuniformly contributed to these responses, with the former predominating at low CSPP and the later at high CSPP. Operating-point values of regional resistance generally decreased with increasing CSPP but to different degrees in the various beds. With increasing CSPP amplitude, regional resistance sensitivity at the operating point (i.e., slope) increased in the celiac and decreased in the mesenteric, renal, and iliac vascular beds. Separate changes in mean and pulsatile components of carotid sinus pressure about the normal operating point produce quantitatively similar changes in systemic hemodynamic variables.

Reflex Control of Renin Release in Essential Hypertension

1978 ◽  
Vol 54 (3) ◽  
pp. 217-222 ◽  
Author(s):  
G. Mancia ◽  
G. Leonetti ◽  
Laura Terzoli ◽  
A. Zanchetti
Keyword(s):  
Essential Hypertension ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Carotid Sinus ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Release ◽  
Tissue Pressure ◽  
Reflex Control

1. The reflex control of renin release was studied in subjects with essential hypertension by comparing the effects of a variable-pressure neck chamber and head-up tilting. 2. Increase in carotid sinus transmural pressure (obtained by reducing tissue pressure outside the carotid sinus by 34 ± 3 mmHg) decreased mean arterial pressure by 16 ± 2 mmHg, but did not reduce significantly the renal venous—arterial difference in plasma renin activity. Likewise decrease in carotid sinus transmural pressure (obtained by increasing tissue pressure outside the carotid sinus by 39 ± 2 mmHg) increased mean arterial pressure by 14 ± 3 mmHg, but caused only a very slight increase in the renal venous—arterial difference in plasma renin activity. 3. Passive tilting reduced mean arterial pressure by 9 ± 1 mmHg. In this circumstance the renal venous—arterial difference in plasma renin activity increased significantly and markedly. 4. It is concluded that in essential hypertension the carotid sinus baroreceptors, though active in blood pressure control, do not exert a major influence on renin release. In these patients reflex increase of renin during tilting is apparently mediated through other receptors than those in the carotid sinuses.

Depressed responsiveness of the carotid sinus reflex in conscious newborn animals

1979 ◽  
Vol 237 (1) ◽  
pp. H40-H43 ◽  
Author(s):  
S. F. Vatner ◽  
W. T. Manders
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Peripheral Resistance ◽  
Carotid Baroreceptor ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid ◽  
Baroreceptor Reflexes ◽  
Newborn Animals

The responsiveness of the carotid sinus reflex was evaluated by comparing the effects of bilateral carotid occlusion (BCO) in conscious adult dogs and puppies on measurements of arterial pressure, cardiac output, heart rate, and calculations of total peripheral resistance (TPR). In eight adult dogs, BCO increased mean arterial pressure by 57 +/- 6%, TPR by 48 +/- 5%, and heart rate by 45 +/- 15%. In puppies, BCO induced smaller increases (P less than 0.05) in mean arterial pressure (30 +/- 5%) and TPR (29 +/- 4%), while heart rate did not change. After elimination of opposing vagal and aortic baroreceptor reflexes, the differences in responses to BCO of mean arterial pressure and TPR between adults and newborns were even greater. Thus, the carotid baroreceptor reflex appears to be depressed in the newborn when compared with the fully developed reflex in the normal, conscious adult.

Angiotensin II induces insulin resistance independent of changes in interstitial insulin

1999 ◽  
Vol 277 (5) ◽  
pp. E920-E926 ◽  
Author(s):  
Joyce M. Richey ◽  
Marilyn Ader ◽  
Donna Moore ◽  
Richard N. Bergman
Keyword(s):  
Insulin Resistance ◽  
Heart Rate ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Glucose Uptake ◽  
Peripheral Resistance ◽  
Glucose Turnover ◽  
Ang Ii

We set out to examine whether angiotensin-driven hypertension can alter insulin action and whether these changes are reflected as changes in interstitial insulin (the signal to which insulin-sensitive cells respond to increase glucose uptake). To this end, we measured hemodynamic parameters, glucose turnover, and insulin dynamics in both plasma and interstitial fluid (lymph) during hyperinsulinemic euglycemic clamps in anesthetized dogs, with or without simultaneous infusions of angiotensin II (ANG II). Hyperinsulinemia per se failed to alter mean arterial pressure, heart rate, or femoral blood flow. ANG II infusion resulted in increased mean arterial pressure (68 ± 16 to 94 ± 14 mmHg, P < 0.001) with a compensatory decrease in heart rate (110 ± 7 vs. 86 ± 4 mmHg, P < 0.05). Peripheral resistance was significantly increased by ANG II from 0.434 to 0.507 mmHg ⋅ ml−1⋅ min ( P < 0.05). ANG II infusion increased femoral artery blood flow (176 ± 4 to 187 ± 5 ml/min, P < 0.05) and resulted in additional increases in both plasma and lymph insulin (93 ± 20 to 122 ± 13 μU/ml and 30 ± 4 to 45 ± 8 μU/ml, P < 0.05). However, glucose uptake was not significantly altered and actually had a tendency to be lower (5.9 ± 1.2 vs. 5.4 ± 0.7 mg ⋅ kg−1⋅ min−1, P > 0.10). Mimicking of the ANG II-induced hyperinsulinemia resulted in an additional increase in glucose uptake. These data imply that ANG II induces insulin resistance by an effect independent of a reduction in interstitial insulin.

PGE2 does not act at carotid sinus to raise arterial pressure in conscious sheep

1983 ◽  
Vol 245 (6) ◽  
pp. H1007-H1012
Author(s):  
B. A. Breuhaus ◽  
J. E. Chimoskey
Keyword(s):  
Carotid Artery ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Pressor Response ◽  
Direct Action ◽  
Peripheral Resistance ◽  
External Carotid Artery ◽  
External Carotid ◽  
Conscious Sheep ◽  
Female Sheep

Conscious chronically instrumented adult female sheep were used to determine whether direct action of prostaglandin E2 (PGE2) on the carotid sinus baroreceptors contributes to the pressor response observed during infusion of PGE2 into the common carotid artery (CCA). During infusion of PGE2 into the CCA caudal to an intact carotid sinus, into the CCA caudal to a denervated carotid sinus, and into the external carotid artery, mean arterial pressure (MAP) rose 17, 22, and 17 mmHg, respectively (P less than 0.01). Heart rate (HR) rose 6, 6, and 8 beats/min, respectively (P less than 0.05). Cardiac output (CO) was also measured by indicator dilution using indocyanine green. In these experiments with infusion of PGE2 into the external carotid artery, MAP rose 15 mmHg (P less than 0.01), HR increased 6 beats/min (P less than 0.05), CO did not change, and total peripheral resistance (TPR) increased 23% (P less than 0.01). With infusion of PGE2 past a denervated carotid sinus, MAP rose 20 mmHg (P less than 0.01), HR rose 4 beats/min (P less than 0.05), CO did not change, and TPR increased 29% (P less than 0.01). There were no statistically significant differences in MAP or HR responses when PGE2 was infused past an intact carotid sinus, past a denervated carotid sinus, or beyond the carotid sinus. There is no evidence that direct action of PGE2 on carotid sinus baroreceptors either augments or inhibits the observed pressor effect of intracarotid PGE2. Intracarotid PGE2 acts rostral to the carotid sinus to increase MAP, HR, and TPR in conscious sheep.

Carotid sinus control of pulsatile hemodynamics in halothane-anesthetized dogs

1980 ◽  
Vol 238 (3) ◽  
pp. H294-H299
Author(s):  
R. H. Cox ◽  
R. J. Bagshaw
Keyword(s):  
Arterial Pressure ◽  
Carotid Sinus ◽  
Open Loop ◽  
Hydraulic Power ◽  
Set Point ◽  
Hemodynamic Variables ◽  
Vascular Impedance ◽  
Mean Pressure ◽  
Anesthetized Dogs ◽  
Sinus Pressure

The open-loop characteristics of the carotid sinus baroreceptor reflex control of pulsatile arterial pressure-flow relations were studied in halothane-anesthetized dogs. Pressures and flows were measured in the ascending aorta, the celiac, mesenteric, renal, and iliac arteries and were used to compute values of regional vascular impedance and hydraulic power. The carotid sinuses were bilaterally isolated and perfused under conditions of controlled mean pressure with a constant sinusoidal component. Measurements were made with the vagi intact and after bilateral vagotomy. Maximum values of open-loop gain averaged -0.78 +/- 0.08 before and -1.42 +/- 0.20 after vagotomy. Vagotomy produced significant increases in the variation of all hemodynamic variables with carotid sinus pressure that were nonuniformly affected in the various regional vascular beds. Aortic and regional vascular impedance showed significant variations with carotid sinus pressure that were augmented by vagotomy. Aortic impedance exhibited a minimum at the normal set point. These results indicate that a) carotid sinus baroreflexes are well preserved with halothane anesthesia, b) thoracic baroreceptor-mediated reflexes exert significant hemodynamic effects on systemic hemodynamics around normal set point values of arterial pressure, c) systemic baroreceptors exert control over large as well as small vessel properties, and d) the baroreceptor-mediated reflexes produce significant influences on hydraulic power and its components.

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