Effect of carotid sinus baroreceptor reflex on hepatic and splenic vascular capacitance in vagotomized dogs

1994 ◽  
Vol 266 (4) ◽  
pp. H1528-H1533 ◽  
Author(s):  
C. Risoe ◽  
W. Tan ◽  
O. A. Smiseth
Keyword(s):  
Volume Change ◽  
Carotid Sinus ◽  
Portal Pressure ◽  
Baroreceptor Reflex ◽  
Volume Changes ◽  
Splenic Volume ◽  
Vascular Volume ◽  
Vascular Compliance ◽  
Vascular Capacitance ◽  
Sinus Pressure

Mechanisms of how baroreflex activation changes splanchnic vascular volumes were studied in eight vagotomized dogs, anesthetized by chloralose/urethan. Hepatic and splenic vascular volume changes were determined from organ dimensions by sonomicrometry. Pulsatile carotid sinus pressure (CSP) in isolated and separately perfused carotid sinuses was changed among 200, 120, and 40 mmHg. Lowering CSP from 120 to 40 mmHg significantly decreased both hepatic and splenic vascular volume (at similar portal pressure) by 1.9 +/- 0.5 and 1.8 +/- 0.6 ml/kg body wt, respectively. Increasing CSP from 120 to 200 mmHg tended to increase regional vascular volumes (P = NS). The combined volume change of liver and spleen between CSP 40 and 200 mmHg was 4.2 +/- 0.6 ml/kg body wt (P < 0.001). Pressure-volume (dimension) curves at high, low, and baseline CSP were determined to separate active and passive mechanisms of vascular volume changes. Changes in CSP did not change regional vascular compliance. Low CSP significantly decreased unstressed liver and unstressed splenic volume by 3.3 +/- 0.9 and 1.9 +/- 0.5 ml/kg body wt, respectively. These results indicate that liver and spleen both contribute to blood volume mobilization by vasoconstriction during low CSP and that the carotid sinus baroreceptor reflex modulates hepatic and splenic vascular capacitance by changing unstressed volume rather than by changing vascular compliance.

Splanchnic vascular capacitance and positive end-expiratory pressure in dogs

1991 ◽  
Vol 70 (2) ◽  
pp. 818-824 ◽  
Author(s):  
C. Risoe ◽  
C. Hall ◽  
O. A. Smiseth
Keyword(s):  
Blood Volume ◽  
Venous Pressure ◽  
Portal Venous Pressure ◽  
Central Blood Volume ◽  
Positive End Expiratory Pressure ◽  
Splenic Volume ◽  
Vascular Volume ◽  
Vascular Capacitance ◽  
Anesthetized Dogs ◽  
Blood Volumes

We have investigated the effect of positive end-expiratory pressure ventilation (PEEP) on regional splanchnic vascular capacitance. In 12 anesthetized dogs hepatic and splenic blood volumes were assessed by sonomicrometry. Vascular pressure-diameter curves were defined by obstructing hepatic outflow. With 10 and 15 cmH2O PEEP portal venous pressure increased 3.1 +/- 0.3 and 5.1 +/- 0.4 mmHg (P less than 0.001) while hepatic venous pressure increased 4.9 +/- 0.4 and 7.3 +/- 0.4 mmHg (P less than 0.001), respectively. Hepatic blood volume increased (P less than 0.01) 3.8 +/- 0.9 and 6.3 +/- 1.4 ml/kg body wt while splenic volume decreased (P less than 0.01) 0.8 +/- 0.2 and 1.3 +/- 0.2 ml/kg body wt. The changes were similar with closed abdomen. The slope of the hepatic vascular pressure-diameter curves decreased with PEEP (P less than 0.01), possibly reflecting reduced vascular compliance. There was an increase (P less than 0.01) in unstressed hepatic vascular volume. The slope of the splenic pressure-diameter curves was unchanged, but there was a significant (P less than 0.05) decrease in unstressed diameter during PEEP. In conclusion, hepatic blood volume increased during PEEP. This was mainly a reflection of passive distension due to elevated venous pressures. The spleen expelled blood and thus prevented a further reduction in central blood volume.

Alpha- and beta-adrenergic mechanisms in the control of vascular capacitance by the carotid sinus baroreflex system

1994 ◽  
Vol 267 (1) ◽  
pp. H201-H210 ◽  
Author(s):  
K. Shigemi ◽  
M. J. Brunner ◽  
A. A. Shoukas
Keyword(s):  
Adrenergic Receptor ◽  
Carotid Sinus ◽  
Venous Pressure ◽  
Systemic Circulation ◽  
Adrenergic System ◽  
Beta Adrenergic ◽  
Vascular Volume ◽  
Adrenergic Mechanisms ◽  
Vascular Capacitance ◽  
Carotid Sinus Baroreflex

We examined the active and passive contributions of the alpha- and beta-adrenergic receptor mechanisms to the changes in systemic vascular capacitance caused by the carotid sinus baroreflex system in anesthetized, vagotomized dogs. The carotid sinuses were isolated from the systemic circulation and perfused with controlled pressures. To determine the changes in vascular capacitance, a constant flow, constant venous pressure cardiopulmonary bypass was used. The changes in unstressed vascular volume were calculated when carotid sinus pressure was reduced from 200 to 50 mmHg without any adrenergic receptor antagonist, with either an alpha- (phentolamine) or a beta- (propranolol) antagonist and then with both. The reflex change in unstressed vascular volume in the systemic circulation (22.6 +/- 9.0 ml/kg without any antagonist) was reduced by 72% with phentolamine, by 35% with propranolol, and by 73% with both antagonists. Our results suggest that the alpha-adrenergic mechanisms contribute significantly to active changes in systemic venous capacity. In addition, the beta-adrenergic system has very little effect on active changes in venous vessels but does contribute to the overall capacity changes by dilating the hepatic outflow resistance when the carotid sinus baroreflex system is activated.

Rapid resetting of the carotid baroreceptor reflex in the cat

1981 ◽  
Vol 241 (6) ◽  
pp. H802-H806 ◽  
Author(s):  
D. L. Kunze
Keyword(s):  
Carotid Sinus ◽  
Blood Pressure Response ◽  
Systemic Blood Pressure ◽  
Baroreceptor Reflex ◽  
Reflex Response ◽  
Carotid Baroreceptor ◽  
Depressor Reflex ◽  
Sinus Pressure ◽  
Anesthetized Cat

The carotid baroreceptor depressor reflex of the chloralose-anesthetized cat was examined to determine the role of the prevailing carotid pressure in determining the threshold, gain, and range of operation of the reflex response. After the pressure of an isolated perfused carotid sinus was held at 80 mmHg for 20 min the threshold pressure necessary to elicit the reflex systemic blood pressure response was 78 +/- 2.9 (SE) mmHg (n = 5). When carotid pressure was maintained for 20 min at 120 and 160 mmHg the threshold rose to 113 +/- 2.9 and 126 +/- 3.0 mmHg, respectively. The resetting of the threshold to a stable value upon elevating or reducing carotid sinus pressure was accomplished within 15—;20 min. The entire range of operation of the reflex response was shifted to higher carotid pressures as the holding pressure was elevated. The midrange gain of the response was unchanged at the three holding pressures tested. These findings indicate that the carotid baroreceptor reflex need not operate over a fixed range but that the range may be rapidly adjustable to the prevailing pressure. When arterial pressure is sustained at a level that is elevated or depressed from normal the carotid baroreceptor reflex acutely resets to operate in the range of the prevailing pressure with a threshold that has moved toward the prevailing pressure.

Left ventricular reflex control of venous return and systemic vascular capacitance in dogs

1988 ◽  
Vol 66 (1) ◽  
pp. 112-118 ◽  
Author(s):  
Sumio Hoka ◽  
Zeljko J. Bosnjak ◽  
Jeanne L. Seagard ◽  
Daniel Siker ◽  
Barbara W. Palmisano ◽  
...  
Keyword(s):  
Blood Volume ◽  
Venous Return ◽  
Carotid Sinus ◽  
Left Ventricular ◽  
Sodium Pentobarbital ◽  
Systemic Blood ◽  
Nerve Activity ◽  
Efferent Nerve ◽  
Vascular Capacitance ◽  
Sinus Pressure

The reflex effects of left ventricular distension on venous return, vascular capacitance, vascular resistance, and sympathetic efferent nerve activity were examined in dogs anesthetized with sodium pentobarbital. In addition, the interaction of left ventricular distension and the carotid sinus baroreftex was examined. Vascular capacitance was assessed by measuring changes in systemic blood volume, using extracorporeal circulation with constant cardiac output and constant central venous pressure. Left ventricular distension produced by balloon inflation caused a transient biphasic change in venous return; an initial small increase was followed by a late relatively large decrease. Left ventricular distension increased systemic blood volume by 3.8 ± 0.6 mL/kg and decreased systemic blood pressure by 27 ± 2 mmHg (1 mmHg = 133.3 Pa) at an isolated carotid sinus pressure of 50 mmHg. These changes were accompanied by a simultaneous decrease in sympathetic efferent nerve activity. When the carotid sinus pressure was increased to 125 and 200 mmHg, these responses were attenuated. It is suggested that left ventricular mechanoreceptors and carotid baroreceptors contribute importantly to the control of venous return and vascular capacitance.

β-Adrenoceptors in vascular capacitance responses to unloading of carotid baroreceptors in anesthetized dogs

1997 ◽  
Vol 273 (4) ◽  
pp. H1713-H1718
Author(s):  
F. Karim ◽  
S. M. Poucher
Keyword(s):  
Constant Pressure ◽  
Carotid Sinus ◽  
Adrenoceptor Antagonist ◽  
Vascular Capacitance ◽  
Anesthetized Dogs ◽  
Loading And Unloading ◽  
Pressure Changes ◽  
Capacitance Response ◽  
Sinus Pressure

The role of β- and α-adrenoceptors in the total vascular capacitance responses to changing pressure in vascularly isolated carotid sinuses of anesthetized and atropinized dogs was investigated. A change in vascular capacitance was determined by measuring the shift of blood in and out of a reservoir that was connected to the aorta and maintained at a constant pressure. Changes in carotid sinus pressure from 135 to 57 mmHg and back to 137 mmHg resulted in a rapid vascular capacitance response of ∼30 ml in the absence of adrenoceptor antagonists. Administration of a β2-adrenoceptor antagonist (ICI-118551) caused a significant enhancement of the capacitance responses to similar decreases and increases in carotid sinus pressure (∼130%). Administration of a β1-adrenoceptor antagonist (CGP-20712A) did not cause any further enhancement of the responses. However, an α-blocker (phentolamine) reduced the responses by 75%. The results suggest that in the presence of a β2-adrenoceptor antagonist vascular capacitance responses to loading and unloading of baroreceptors are greatly enhanced and that patients suffering from orthostatic syncope may benefit from this kind of drug.

Changes in canine cardiac function and venous return curves by the carotid baroreflex

1986 ◽  
Vol 251 (2) ◽  
pp. H288-H296 ◽  
Author(s):  
A. S. Greene ◽  
A. A. Shoukas
Keyword(s):  
Arterial Pressure ◽  
Cardiac Function ◽  
Venous Return ◽  
Carotid Sinus ◽  
Baroreceptor Reflex ◽  
Primary Mechanism ◽  
Carotid Baroreflex ◽  
Carotid Sinus Baroreflex ◽  
Anesthetized Dogs ◽  
Sinus Pressure

Venous return curves and cardiac function relationships were simultaneously determined in 10 pentobarbital-anesthetized dogs at three different isolated carotid sinus pressures. Changing carotid sinus pressure (CSP) between 50 and 200 mmHg produced large changes in the zero flow intercept of the venous return curves from 15.37 +/- 0.97 to 11.94 +/- 1.36 mmHg (P less than 0.001) but no change in slope. These changes in the intercept of the venous return curve were due to alterations in systemic vascular capacity caused by the carotid sinus baroreceptor reflex. Changes in the cardiac function curve with baroreceptor pressure were masked by concomitant changes in arterial pressure afterload; however, when arterial pressure was controlled, there was a significant change in the slope of the cardiac function curve from 60.32 +/- 26.9 to 37.06 +/- 13.31 ml X min-1 X kg-1 X mmHg-1 as CSP was changed from 50 to 200 mmHg. We conclude that changes in vascular capacity are the primary mechanism responsible for changes in cardiac output during activation of the carotid sinus baroreflex.

Raphe neurons with sympathetic-related activity: baroreceptor responses and spinal connections

1984 ◽  
Vol 246 (3) ◽  
pp. R338-R348 ◽  
Author(s):  
S. F. Morrison ◽  
G. L. Gebber
Keyword(s):  
Spinal Cord ◽  
Carotid Sinus ◽  
Phase Relationship ◽  
Baroreceptor Reflex ◽  
Type I ◽  
Type Ii ◽  
Antidromic Activation ◽  
Reflex Arc ◽  
Sinus Pressure ◽  
Raphe Neurons

We have previously used spike-triggered averaging to identify cat medullary raphe neurons with activity locked to the 2- to 6-cycles/s rhythm in sympathetic nerve discharge (SND) [Am. J. Physiol. 243 (Regulatory Integrative Comp. Physiol. 12): R49-R59, 1982]. In the present study, we classified such cat raphe neurons on the bases of their spinal connections and responses to baroreceptor reflex activation. Type I neurons, comprising 139 of 190 raphe units with activity related to inferior cardiac SND, were excited when carotid sinus pressure was elevated. The majority of these neurons were located in nucleus raphe pallidus. A time-controlled collision test for antidromic activation revealed that the axons of approximately one-third of type I neurons terminated in the sympathetic intermediolateral nucleus (IML) after coursing through the dorsolateral funiculus (DLF) of the spinal cord. The axons of the remaining type I neurons did not project to the spinal cord. It is suggested that type I raphe neurons are involved in mediating sympathoinhibition at spinal and supraspinal levels. Importantly, type I unit discharge remained locked to SND when the phase relationship between baroreceptor afferent and sympathetic efferent activities was disrupted. Thus type I neurons are not simple interneurons in the afferent limb of the baroreceptor reflex arc. Apparently they also receive input from the generator of the 2- to 6-cycles/s rhythm in SND. Type II raphe neurons (n = 51) were inhibited when carotid sinus pressure was elevated. Although the axons of these neurons coursed through the spinal DLF, they did not terminate in IML. Whether type II neurons subserve a sympathoexcitatory function remains to be determined.

Interaction of carotid chemoreceptor and baroreceptor reflexes in anesthetized dogs

1988 ◽  
Vol 254 (1) ◽  
pp. R1-R10 ◽  
Author(s):  
M. J. Brunner ◽  
A. Wallace ◽  
C. L. MacAnespie
Keyword(s):  
Significant Interaction ◽  
Response Curve ◽  
Carotid Sinus ◽  
Baroreceptor Reflex ◽  
Reflex Response ◽  
Linear Portion ◽  
Baroreceptor Reflexes ◽  
Anesthetized Dogs ◽  
Simultaneous Activation ◽  
Sinus Pressure

Interaction between baroreceptors and chemoreceptors during simultaneous activation of the reflexes was studied in eight pentobarbital sodium-anesthetized vagotomized dogs. The carotid sinus reflexogenic area was isolated and perfused at controlled carotid sinus pressure (CSP), PO2, and PCO2. Random combinations of CSP, PO2, and PCO2 were delivered to the carotid sinus. Results were analyzed by multiple linear regression. For the arterial pressure response, increasing CO2 resulted in an upward shift of the baroreceptor reflex response curve and an increased slope of the linear portion of the curve. The heart rate-CSP curve was also shifted upward by CO2, with the effect being greatest at high levels of CSP. The respiratory frequency-CO2 relationship had an increased slope and was shifted upward when CSP was decreased. The responses of tidal volume and ventilation (VE) depended on all three inputs. At any level of PO2, decreasing CSP resulted in a parallel shift of the VE-CO2 relationship. The results indicate that there is a significant interaction between chemoreceptor and baroreceptor reflex sensitivities.

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