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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Regional haemodynamic control by the cardiovascular baroreceptors was examined in dogs anaesthetized with 1 + MAC halothane in oxygen (1%). The open-loop relationships between carotid sinus pressure (CSP) and regional haemodynamics in the iliac, renal, mesenteric, aortic and coeliac beds were examined before vagotomy, following vagotomy and following thoracotomy. Around the carotid sinus reflex set point, the ratio of the reflex decrease in systemic arterial pressure to an increase in CSP (reflex gain) was -0.744+/-0.089 (mean+/-SEM): the latter increased to -1.275+/-0.093 following vagotomy. Reflex resistance changes were greatest in the renal bed and least in the coeliac bed, reflecting blood flow homeostasis which was well preserved in the renal bed but minimal in the coeliac bed. Thoracotomy in the dogs in which vagotomy had been performed resulted in no significant changes in the dependent variables studied. It is concluded that, in these dogs anaesthetized with 1 + MAC of halothane, baroreceptor control of regional pressure flow relationships is well preserved.
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PMID:Baroreceptor control of regional haemodynamics during halothane anaesthesia in the dog. 87 50

The effect on mean circulatory filling pressure (MCFP) of changes in pressure within the vascularly isolated carotid sinus has been studied in anaesthetized rabbits. With the sinus exposed to arterial pressure (102 +/- 6 mm Hg; mean +/- SEM) MCFP was 6.18 +/- 0.40 mm Hg. At sinus pressures of 160 and 40 mm Hg, MCFP was 5.71 +/- 0.39 and 6.43 +/- 0.33 mm Hg respectively. The mean difference of 0.72 +/- 0.06 mm Hg between MCFP at these two sinus pressures was significant (P < 0.001). MCFP varied with blood volume when this was increased or reduced by 8%, but at each blood volume level the difference between MCFP at high and low sinus pressure remained significant (P < 0.01). The gradient for venous return, MCFP minus right atrial pressure, was altered by changes in carotid sinus pressure, being 0.60 +/- 0.12 mm Hg less at a sinus pressure of 160 mm Hg than at a sinus pressure of 40 mm Hg. This difference was significant (P < 0.01).
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PMID:The effect of carotid sinus pressure changes on mean circulatory filling pressure in the anaesthetized rabbit. 129 38

The purpose of this study was to test the hypothesis that prostaglandins released from vascular endothelial cells contribute to activation of baroreceptors during increases in arterial pressure. Baroreceptor activity was recorded from the vascularly isolated carotid sinus in rabbits anesthetized with chloralose. Baroreceptor activity was measured during ramp or step increases in nonpulsatile carotid sinus pressure over a range of 0-175 mm Hg. Exposure of the isolated carotid sinus to inhibitors of prostaglandin formation (indomethacin [n = 10] or aspirin [n = 6]) decreased baroreceptor activity significantly (p less than 0.05). The slope of the pressure-activity relation averaged 0.80 +/- 0.07 %/mm Hg (mean +/- SEM) during control measurements and 0.72 +/- 0.06 and 0.63 +/- 0.05 %/mm Hg during exposure to 10 and 20 microM indomethacin, respectively. Exposure of the carotid sinus to exogenous prostacyclin (PGI2 [n = 11]) increased baroreceptor activity significantly. The slope of the pressure-activity relation averaged 0.89 +/- 0.10, 1.09 +/- 0.09, and 1.26 +/- 0.16 %/mm Hg during control and during exposure to 10 and 20 microM PGI2, respectively. Activity returned to control after removal of PGI2 (0.89 +/- 0.12 %/mm Hg). Removal of endothelium with either a balloon catheter (n = 4) or a jet of a 95% O2-5% CO2 gas mixture (n = 6) decreased the slope of the pressure-activity relation from 0.92 +/- 0.09 to 0.56 +/- 0.08 %/mm Hg (p less than 0.05). Exposure of the denuded sinus to exogenous PGI2 (20 microM [n = 4]) restored activity (slope = 1.09 +/- 0.24 %/mm Hg). Neither indomethacin (n = 5) nor PGI2 (n = 5) nor denudation (n = 5) significantly altered the pressure-diameter relation of the carotid sinus (sonomicrometers), suggesting that the effects on baroreceptor discharge are not caused by altered stretch of the carotid sinus at a given pressure. The results suggest that prostaglandins (e.g., PGI2) released from endothelium contribute in a paracrine manner to activation of baroreceptors during increases in arterial pressure.
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PMID:Prostaglandins contribute to activation of baroreceptors in rabbits. Possible paracrine influence of endothelium. 224 1

The present study was designed to determine whether 12 wk of daily exercise alter autonomic neural control of the heart during baroreflex stimulation in healthy dogs. We studied 16 untrained and 12 endurance-trained anesthetized dogs which were instrumented to measure arterial blood pressure (AP), carotid sinus baroreceptor pressure (CBP), electrocardiogram (ECG), heart rate (HR), and R-R interval (RR). The arterial baroreflex was studied during hypertension caused by i.v. bolus infusion of phenylephrine, hypotension caused by i.v. bolus infusion of nitroprusside, and bilateral carotid occlusion (BCO) in which carotid sinus pressure was reduced to 41 +/- 2 mm Hg (mean +/- SEM). Arterial baroreflex sensitivity, which was assessed by determining the change in heart interval (i.e., change in RR) per unit change in systolic AP (delta RR/delta AP), was significantly lower during the hypertensive challenge in the trained dogs compared to the untrained dogs (2.2 +/- 0.3 vs 6.8 +/- 1.5 ms.mm Hg-1, respectively). Similarly, the delta RR/delta AP was substantially lower during the hypotensive challenge in trained dogs vs the untrained dogs (1.2 +/- 0.3 vs 1.8 +/- 0.4 ms.mm Hg-1, respectively). In addition, the HR response to the BCO was significantly less in trained dogs (22 +/- 2 bpm) vs untrained dogs (32 +/- 5 bpm). The open-loop gain (Go), which was used to quantitate the effectiveness of the carotid baroreflex to increase mean systemic AP during BCO, was similar in both untrained and trained dogs (2.9 +/- 0.6 and 2.4 +/- 0.5, respectively). These data indicate that, while endurance training significantly reduces the HR component of the arterial baroreflex, the arterial pressure response apparently is not altered.
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PMID:Endurance training alters arterial baroreflex function in dogs. 235 17

Arterial baroreceptors in the carotid sinus and aortic arch regions reflexly regulate heart rate and peripheral vascular responses during changes in arterial pressure. The relative influence of these two arterial baroreflex pathways on the control of these autonomic responses is debatable. Recent studies in our laboratory demonstrate that the aortic baroreflex produces substantial and sustained inhibition of efferent sympathetic nerve activity to muscle (MSNA) during increases in arterial pressure. The regulation of MSNA by these two baroreflexes in humans during hypotension, and particularly the role of the aortic baroreflex, remains undefined. We therefore performed a new series of studies to assess the relative influence of the aortic and carotid baroreflexes on MSNA responses during sustained decreases in arterial pressure. In eight normal male subjects, aged 23 +/- 1 years (mean +/- SEM), we directly measured mean arterial pressure, heart rate, central venous pressure, and MSNA (microneurography) during hypotension (combined aortic and carotid baroreceptor deactivation) produced by intravenous infusion of sodium nitroprusside and during nitroprusside infusion with superimposed application of external neck suction. Neck suction was applied at levels sufficient to maintain transmural carotid sinus pressure above control levels (carotid baroreceptor activation) while the aortic baroreflexes remained deactivated. Central venous pressure was maintained constant with volume infusion. We also studied responses of these same subjects to direct carotid baroreceptor deactivation with the application of external neck pressure. During neck pressure alone, there was a reflex increase in mean arterial pressure; thus, during this portion of the protocol, we achieved carotid baroreceptor deactivation with some aortic baroreceptor activation. Nitroprusside infusion (combined aortic and carotid deactivation) decreased mean arterial pressure from 90.8 +/- 3.1 to 77.8 +/- 1.1 mm Hg (p less than 0.01) with concomitant increases in heart rate from 62.6 +/- 3.0 to 89.7 +/- 6.1 beats/min (p less than 0.001) and in MSNA from 273.8 +/- 43.0 to 950.6 +/- 133.5 units (p less than 0.001). During continued nitroprusside infusion with superimposed neck suction (aortic baroreceptor deactivation and carotid baroreceptor activation), mean arterial pressure decreased to 70.3 +/- 1.9 mm Hg (p less than 0.001 vs. control), heart rate decreased to 82.5 +/- 6.5 beats/min (p less than 0.01 vs. control or vs. nitroprusside alone), but MSNA remained markedly increased at 889.7 +/- 105.1 units (p less than 0.001 vs. control; p = NS vs. nitroprusside alone).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Importance of aortic baroreflex in regulation of sympathetic responses during hypotension. Evidence from direct sympathetic nerve recordings in humans. 291 May 47

The purpose of this study was to contrast the effects of static and pulsatile pressure on carotid baroreceptor activity over a wide range of mean arterial pressure. Static and pulsatile pressure were applied to the isolated carotid sinus of dogs anesthetized with chloralose. Recordings were obtained from single baroreceptor units as well as from the whole sinus nerve or a large strand of the nerve. Three observations are reported. First, in single units the pulsatile pressure threshold, which averaged 48 +/- 8 (SEM) mm Hg, was far below the static pressure threshold, which averaged 79 +/- 8 mm Hg (p less than 0.05, n = 15). Thus, pulsatility decreased the threshold by an average of 31 mm Hg in contrast to the minimal or lack of decrease in threshold reported by others in aortic baroreceptors. Second, at moderate arterial pressures a shift from static to pulsatile pressure caused a decrease in single and multiple unit activities. In single units, the decrease approximated 15% (from 42.0 +/- 2.1 to 35.5 +/- 1.9 spikes/sec, p less than 0.05, n = 25). In all units, there was no diastolic nerve activity ("silence") when diastolic pressure was 1 to 10 mm Hg above static pressure threshold; 80% of the units exhibited "diastolic silence" when diastolic pressure was 20-30 mm Hg above threshold and 40% of the units showed silence at diastolic pressures 40-50 mm Hg above threshold. In whole nerve recordings, pulsatility increased activity from 57 +/- 15 to 142 +/- 29 spikes/sec (p less than 0.05) at low mean arterial pressures (50 and 75 mm Hg), as expected from the reduction in pressure threshold noted in single units, and decreased activity by approximately 15% (from 373 +/- 69 to 320 +/- 55 spikes/sec, p less than 0.05, n = 9) at mean arterial pressures of 125 and 150 mm Hg. This decrease in activity with a shift from static to pulsatile pressure at moderate arterial pressures has not been reported previously. Third, the static pressure-activity curve was sigmoid, and its gain peaked sharply at 75-100 mm Hg; in contrast, the pulsatile pressure-activity curve was linear between 25 and 150 mm Hg, and its maximum gain was half the maximum gain during static pressure. These differences between the static pressure-activity curve and the pulsatile pressure-activity curve were noted during both increases and decreases in carotid sinus pressure; both curves exhibited some hysteresis during the decreases in pressure.
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PMID:Contrasting effects of static and pulsatile pressure on carotid baroreceptor activity in dogs. 366 74

Cerebrovascular volume and transmural pressure loads accompanying acute increases in cerebral blood flow are implicated in the pathogenesis of periventricular-intraventricular hemorrhage in preterm infants. An acute increase in cerebral blood flow would be expected during acute recovery from asphyxia. Therefore, cerebrovascular hemodynamics, including flow (microspheres), were studied during and after acute recovery from asphyxia in seven newborn dogs in order to study the determinants of these volume and pressure loads. During the acute recovery phase, cerebral hemispheric blood flow was 69.6 +/- 10 ml/100 g/min (mean +/- SEM) representing a 250% increase from baseline values of 19.9 +/- 1.8 ml/100 g/min (p less than 0.005), while combined cerebellar-brainstem flow was 204.3 +/- 19.3 ml/100 g/min representing a 536% increase from baseline values of 32.0 +/- 1.5 ml/100 g/min (p less than 0.005). Blood flow to both areas had returned to baseline levels 20 min after the onset of recovery. Associated with this cerebral hyperemia was an acute increase in mean arterial pressure from 21.3 +/- 4.5 mm Hg at end asphyxia to 69.5 +/- 6.0 mm Hg at peak recovery (p less than 0.01), and parallel acute increases in sagittal sinus pressure (from 4.0 +/- 0.4 to 14.6 +/- 1.9 mm Hg, p less than 0.01) and cerebrospinal fluid pressure (from 3.8 +/- 0.4 to 14.3 +/- 1.9 mm Hg, p less than 0.01). Central venous pressure fell from 4.3 +/- 0.6 mm Hg at end asphyxia to 1.6 +/- 0.5 mm Hg, and thus is not a determinant of the elevation in sagittal sinus pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cerebrovascular hemodynamics during and after recovery from acute asphyxia in the newborn dog. 383 77

The authors studied the effects of positive end-expiratory pressure (10 cmH2O PEEP), abdominal compression, and neck compression on dural venous sinus pressure (VSP) in seated dogs. Abdominal compression increased the central venous pressure (CVP) as well as both the systemic arterial pressure and the cardiac output and thus may offer a useful substitute for an antigravity suit. Except when CVP was greater than 8 mmHg, there was little or no correlation between CVP and VSP. Moreover, each method increased VSP, but this effect was closely related to VSP prior to application of the method (pre-VSP). On comparing the VSP changes in relation to the pre-VSP levels when they were either above or below -1.0 mmHg, significant differences were noted in VSP increases, i.e., -0.4 +/- 1.3 (mean +/- SEM) and 4.3 +/- 1.2 mmHg by PEEP, 1.9 +/- 0.3 and 6.4 +/- 0.4 mmHg by abdominal compression, and 10.2 +/- 1.3 and 1.5 +/- 0.5 mmHg by neck compression, respectively. This indicates that PEEP and abdominal compression were more effective in increasing relatively highly negative pre-VSP (less than -1.0 mmHg), while neck compression greatly increased pre-VSP when it was at or above a slightly negative pressure (-1.0 mmHg). The authors conclude that a single application of any one of these three methods during sitting-position surgery may not be effective in increasing cerebral dural sinus pressure.
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PMID:Cerebral venous sinus pressure in seated dogs: impact of PEEP, cervical venous compression, and abdominal compression. 389 29

We studied the contribution of carotid vs. extracarotid baroreceptors in control of heart rate in normal humans. We measured heart interval (HI) and arterial pressure during steady-state infusion of phenylephrine (PE). PE increased mean arterial pressure (MAP) by 13 +/- 2 mmHg (mean +/- SEM; n = 10) and thus stimulated both carotid and aortic baroreceptors. Neck pressure (NP) was applied during PE infusion to counter the increase in transmural carotid sinus pressure, thus leaving only aortic baroreceptors stimulated by the increase in arterial pressure. PE infusion alone prolonged HI by 230 +/- 24 ms (P less than 0.05). Application of NP attenuated the HI response to 65 +/- 22 ms above control (P less than 0.05 vs. PE alone). During these steady-state increases in arterial pressure, elimination of the carotid baroreflex contribution reduced the HI prolongation by 41-70% in five subjects and by greater than 93% in five subjects. We also measured the HI response to dynamic ramp elevation of systolic arterial pressure (SAP) using bolus administrations of PE. Baroreflex control was calculated from the slope of the regression correlating SAP to succeeding HI for PE alone (carotid and aortic baroreceptor activation) and for PE plus superimposed dynamic NP at levels equal to the increases in SAP (aortic baroreceptor activation). During PE alone, the baroreflex slope was 20.2 +/- 2.9 ms/mmHg (n = 10). During PE plus NP, the baroreflex slope was reduced by 30% to 14.1 +/- 2.8 ms/mmHg (P less than 0.02 vs. during PE alone). Thus, during dynamic increases in arterial pressure, eliminating the carotid baroreflex contribution reduced the HI response by 30%. These studies indicate that extracarotid (presumably aortic) and carotid baroreflexes both participate in control of heart rate in humans. Extracarotid (aortic) baroreflexes appear to have the greater role in control of heart rate during dynamic increases in arterial pressure.
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PMID:Relative contribution of aortic and carotid baroreflexes to heart rate control in man during steady state and dynamic increases in arterial pressure. 407 78

The confluent sinus pressure was measured in eight mongrel dogs in the head-up position to compare the effectiveness of positive end-expiratory pressure (PEEP) and jugular venous compression in increasing cerebral venous pressure. When the head was elevated 30 cm above the heart, confluent sinus pressure decreased from 9.6 +/- 1.8 (mean +/- SEM) to -5.3 +/- 0.5 mmHg. At constant arterial carbon dioxide tension (PaCO2 = 28 +/- 2 mmHg), PEEP (20 cmH2O) did not increase cerebral venous pressure. However, when the jugular veins were compressed with a neck tourniquet with pressures of 20-140 mmHg, cerebral venous pressure increased rapidly. When neck tourniquet pressure was maintained at 40 mmHg, confluent sinus pressure in all dogs was increased and sustained at 2.4 +/- 0.8 mmHg. Carotid artery pressure measured distal to the tourniquet was not altered. The efficacy of extrathoracic venous pressure elevation (neck tourniquet) is greater than intrathoracic (PEEP), and this may relate to the Starling resistor effects of neck veins and the presence of jugular venous valves. We conclude that prophylactic use of PEEP in the prevention of air embolism during the sitting position may not be as effective as jugular venous compression.
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PMID:Comparison of the effects of positive end-expiratory pressure and jugular venous compression on canine cerebral venous pressure. 638 Mar 44


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