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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Superior sagittal sinus pressure, intracranial pressure and arterial pressure were recorded in an experimental series on 10 cats. During drug-induced, severe, acute arterial hypertension and parallel hypercapnia, venous pressure could exceed intracranial pressure in both the supra- and infratentorial compartment. From these data it is concluded that cerebral venous pressure during acute arterial hypertension may contribute to protein extravasation at the postcapillary-venular level.
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PMID:Cerebral venous pressure during actively induced hypertension and hypercapnia in cats. 736 47

Exposure of the vascularly isolated carotid sinuses of 8 conscious dogs to static pressures between 50 and 240 mmHg caused significantly smaller increases [23 +/- 5(SE) mmHg] than decreases (37 +/- 4 mmHg) in arterial pressure frossure and heart rate and shifted the stimulus-response curve upward. Bilateral cervical vagotomy in conscious dogs caused sustained (3 h) increases in arterial pressure (40 +/- 5 mmHg), significantly larger than after atropinization (7 +/- 2 mmHg). In anesthetized, but not in conscious dogs, high sinus pressure reversed the hypertension caused by vagotomy. After vagotomy, low sinus pressure resulted in arterial pressures greater than 200 -mHg. In conscious dogs the carotid baroreflex can widely vary arterial pressure and heart rate despite buffering by extracarotid baroreceptors with vagal afferents, but cannot fully compensate for the acute loss of the latter. Extracarotid baroreceptors actively participate with carotid baroreceptors in the regulation of arterial pressure and better buffer carotid baroreflex-induced increases than decreases in arterial pressure.
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PMID:Reflexes from isolated carotid sinuses of intact and vagotomized conscious dogs. 738 40

A rat model was developed to determine the role of sinus thrombosis and elevated sinus pressures in the pathogenesis of dural arteriovenous malformations (AVMs). Five protocols were tested to compare various sinus pressures and thrombosis of a sinus: 1) Control I, sham operation (five animals); 2) Control II, occlusion of the right common carotid artery, the right external jugular vein, and the vein draining the left transverse sinus, as well as thrombosis of the sagittal sinus (10 animals); 3) arteriovenous fistula (AVF) I, anastomosis of the right common carotid artery to the external jugular vein causing retrograde flow through the transverse sinus (10 animals); 4) AVF II, anastomosis (as described in AVF I) and thrombosis of the sagittal sinus (12 animals); 5) AVF III, anastomosis (as described in AVF I) as well as thrombosis of the sagittal sinus and occlusion of the vein draining the transverse sinus on the left (12 animals). Mean arterial and sagittal sinus pressures were monitored and cerebral angiograms were obtained intraoperatively and again 90 days later. Afterward, the animals were sacrificed and their brains and dura were examined histologically. Formation of a fistula resulted in a significant (p < 0.05) threefold increase in sagittal sinus pressure in the AVF II group and a significant (p < 0.05) sixfold increase in the AVF III group. Seven dural AVMs (three in the AVF II group and four in the AVF III group) were demonstrated angiographically and histologically. The seven malformations were located adjacent to a thrombosed sagittal sinus. All lesions were within the dura and sinus wall with direct thrombus-sinus wall connections demonstrated in four of the malformations. The other three lesions displayed arteriovenous connections within the sinus wall and dura. These data suggest the importance of not only sinus thrombosis but also sinus hypertension in the development of a dural AVM.
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PMID:Genesis of a dural arteriovenous malformation in a rat model. 766 34

A case of unruptured arteriovenous malformations (AVMs) presenting benign intracranial hypertension is reported. A 14-year-old male suffered from headache and papilledema. Intracranial pressure was 260 mmH2O. Unenhanced CT demonstrated no evidence of hemorrhage or hydrocephalus. Angiogram demonstrated a large AVM in the left temporal lobe supplied by the left posterior cerebral artery and left middle cerebral artery. It drained into the transverse sinus. Surgical excision of the AVM eliminated the headache and papilledema. AVM causes hemorrhage in 50% of cases, seizure in 30%, and other focal neurological deficits in 20%. Benign intracranial hypertension is an uncommon effect of unruptured AVMs. Only 13 cases have been reported in the literature. Benign intracranial hypertension associated with unruptured AVMs occurs in young patients with high flow AVMs that drain into the major sinus. The mechanism of intracranial hypertension associated with unruptured AVM is unknown. However, there are several possible mechanisms of intracranial hypertension associated with unruptured AVMs. The arterial blood shunting into a major sinus impedes venous return from the surrounding brain. That causes the increase of cerebral blood volume and the elevation of sinus pressure. This mechanism would reduce CSF absorption and would increase intracranial pressure. Pharmacological therapy is ineffective in controlling intracranial hypertension. Surgical excision of AVM effectively reduced intracranial hypertension. Thus, surgical excision of AVMs, if it can be done with low risk, is the treatment of choice to decrease intracranial hypertension in patients with unruptured cerebral AVMs.
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PMID:[A case of intracranial arteriovenous malformation presenting with intracranial hypertension]. 819 38

1. The hindlimb vasoconstrictor effects of distension of the urinary bladder were studied at different levels of input from the carotid sinus baroreceptors in the dog anaesthetized with a mixture of chloralose and urethane. 2. The vascularly isolated hindlimb was perfused at constant blood flow through its femoral artery, so that a change in pressure gradient (mean femoral arterial perfusion pressure minus mean inferior vena caval pressure) indicated a similar directional change in vascular resistance. The vascularly isolated carotid sinus regions were perfused with blood at a constant pulsatile flow. 3. Raising the carotid sinus mean perfusion pressure in randomly selected steps of 30 mmHg from 60 to 210 mmHg had little effect on heart rate unless the blood pressure was controlled, when a progressive bradycardia occurred, but caused a progressive reduction in arterial blood pressure and vasodilatation in the perfused hindlimb. Distension of the bladder at each level of carotid sinus pressure resulted in tachycardia, hypertension and hindlimb vasoconstriction. 4. The cardiac responses to bladder distension were the same at all carotid sinus pressures. When the blood pressure was controlled, however, the response was reduced at high and low sinus pressures. 5. The relationship between the carotid sinus perfusion pressure and hindlimb perfusion pressure (i.e. vascular resistance) was affected by distension of the bladder in two ways. In the one, hindlimb perfusion pressure increased by approximately the same amount at all levels of carotid sinus pressure indicating resetting of the carotid sinus baroreceptor reflex control of hindlimb vascular resistance towards vasoconstriction without change in gain of the reflex. In the other, the pressure increases were diminished at the higher levels of carotid sinus pressure indicating both resetting and an increase in gain of the reflex. 6. Both types of response occurred in the spontaneously breathing animal, in animals artificially ventilated, while pacing the heart, with the arterial blood pressure maintained constant at about 100 mmHg, and after division of the cervical vagosympathetic nerves. The frequency of occurrence of each type of response, however, varied under the different conditions. 7. The possible reasons for the two types of vascular response are discussed.
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PMID:Effects of distension of the urinary bladder on the cardiovascular reflexes from the carotid baroreceptors in the dog. 824 97

The ability of the carotid sinus baroreflex to elicit reflex changes in vascular capacity was studied in chronically hypertensive (one-kidney, one-clip) and sham-operated normotensive dogs under pentobarbital sodium anesthesia. Vascular compliances and reflex-induced changes in external reservoir volume were measured in response to changes in isolated carotid sinus pressure (CSP). The mean arterial pressure-CSP reflex characteristic curve was shifted to a higher arterial pressure with hypertension with no change in maximum reflex gains. Arterial compliance in both groups increased significantly (P < 0.01) when CSP was increased from 50 to 200 mmHg. Total, arterial, and venous vascular compliances were not different in normotensive and hypertensive groups. Changes in CSP caused no significant changes in either total systemic vascular or calculated venous compliances. A decrease in CSP from 250 to 50 mmHg resulted in an increase in external reservoir volume of 8.02 +/- 1.03 and 7.44 +/- 1.33 ml/kg in normotensive and hypertensive groups, respectively, with changes in venous volume of 11.99 +/- 1.39 and 12.58 +/- 1.52 ml/kg (NS). We conclude that despite the increase in arterial resistance, Goldblatt hypertensive dogs retain the ability to make short-term reflex adjustments in both arterial pressure and venous blood volume.
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PMID:Baroreflex control of arterial and venous compliances and vascular capacity in hypertensive dogs. 834 71

We examined whether partial coronary sinus obstruction affects the latency of the early ventricular fibrillation (VF) of acute ischemia. During baseline trials 15 of 19 open-chest dogs fibrillated repeatedly and predictably within 2 to 5 minutes (251.6 +/- 64 seconds) after reversible, double coronary artery occlusion without developing profound hemodynamic deterioration. The effect of partial coronary sinus obstruction sufficient to increase coronary sinus pressure to 40 mm Hg could be adequately tested in 11 dogs. Coronary sinus obstruction consistently prevented VF in five dogs, significantly prolonged the VF latency in three (p < 0.01 to p < 0.001), and had no clear effect in another three. The overall effect was significant at the p < 0.01 level. VF latency prolongation/prevention was also positively correlated to the residual coronary sinus pressure at the time of VF (r = 0.76; p < 0.008), as well as the baseline VF latency (r = 0.75; (p < 0.008). The protective effect of coronary venous hypertension most likely reflects preservation of adequate extracellular fluid in the ischemic region after the perfusion arrest. This extracellular fluid may constitute a key component in the prevention of early ischemic arrhythmias by preserving interstitial hydraulic continuity and tissue homogeneity through enhanced dilution and diffusion of solutes.
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PMID:Protective effect of coronary sinus obstruction from primary ischemia-induced ventricular fibrillation in the dog. 846 71

The purpose of this study was to determine whether baroreflex control of respiratory responses is diminished in hypertension. Ten dogs were made chronically hypertensive with use of a bilateral renal wrap technique. Eight sham-operated dogs served as normotensive controls. After the development of experimental hypertension, carotid baroreflex control of arterial pressure, heart rate, respiratory frequency, tidal volume, and ventilation was acutely assessed. Under pentobarbital anesthesia and with bilateral vagotomy, the carotid sinuses were isolated and perfused at controlled pressures. Before the carotid sinus region was manipulated, the mean arterial pressure was significantly higher (P < 0.005) in the hypertensive group (146.4 +/- 2.3 mmHg) than in the normotensive group (124.7 +/- 2.6 mmHg). The mean arterial pressures and heart rates measured at every level of carotid sinus pressure were significantly higher in the hypertensive group. Reflex gain of heart rate, but not mean arterial pressure, was significantly reduced in the hypertensive group. Respiratory frequency, tidal volume, and ventilatory responses to changes in carotid sinus pressure were significant and resulted in an approximately 40% reflex change in ventilation. These responses were not diminished in the hypertensive group. We conclude that respiratory baroreflex responses are preserved in experimental hypertension.
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PMID:Hemodynamic and respiratory responses to carotid sinus pressure alteration in experimental hypertension. 848 67

It has been shown that alcohol administration causes baroreceptor reflex inhibition. The site of action of alcohol could reside anywhere within the baroreceptor reflex arc. Therefore, the goal of this study was to determine the effects of acute administration of alcohol on carotid sinus baroreceptor discharge characteristics. In pentobarbital-anesthetized dogs, the carotid sinus was isolated and perfused. Single unit baroreceptor discharge was recorded from the carotid sinus nerve along with carotid sinus diameter using sonomicrometry. Carotid sinus pressure-baroreceptor discharge and carotid sinus pressure-diameter curves were constructed. Perfusion of the carotid sinus with alcohol (100 mmol/L) significantly decreased the pressure threshold from 91.1 +/- 2.8 to 86.4 +/- 2.9 mm Hg (p < 0.05) and increased the peak discharge rate from 45.8 +/- 3.4 to 52.8 +/- 3.6 spikes per second (p < 0.01). The same phenomenon was seen during perfusion of the carotid sinus with acetaldehyde (2.5 mmol/L) but was not seen during perfusion with acetate (2.5 mmol/L). During perfusion of the carotid sinus with alcohol, the carotid sinus pressure-carotid sinus diameter relation did not change. The baroreceptor sensitization induced by alcohol is not an endothelium-dependent mechanism, because endothelial denudation did not block this alcohol-induced effect. Measurement of the duration of postexcitatory depression of carotid sinus baroreceptors, which is related to Na+,K(+)-ATPase activity, showed that perfusion of the carotid sinus with alcohol or acetaldehyde significantly reduced the duration of postexcitatory depression, indicating that the alcohol- and acetaldehyde-induced effect on baroreceptor discharge is most likely mediated by an inhibition of Na+,K(+)-ATPase.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1993 May
PMID:Acute alcohol administration stimulates baroreceptor discharge in the dog. 849 3

This study evaluated acute resetting of carotid baroreflex control of arterial blood pressure and renal or thoracic sympathetic nerve activity in thiopental-anesthetized mongrel dogs with the use of a vascularly isolated carotid sinus preparation, the experimental model used previously to characterize acute resetting in carotid baroreceptor afferent fibers. Carotid baroreceptors were conditioned with a pulsatile pressure for 20 minutes at three pressure ranges: low (50 to 75 mm Hg), mid (100 to 125), or high (150 to 175). Blood pressure and nerve activity were recorded in response to slow ramp increases in sinus pressure; nonlinear regression and best-fit analyses were used for determination of curve fit parameters of the blood pressure and nerve activity versus sinus pressure response curves. Carotid sinus pressure thresholds for blood pressure and renal nerve activity responses at all conditioning pressures were significantly different; however, only the pressure threshold for thoracic nerve activity at the low conditioning pressure was significantly different from the responses at other conditioning pressures. Average renal activity resetting (0.506 +/- 0.072) was significantly greater than blood pressure resetting (0.335 +/- 0.046) in the same dogs, and thoracic activity (0.200 +/- 0.057) was not different from blood pressure resetting (0.194 +/- 0.031) in the same dogs. In a previous investigation, our laboratory had demonstrated that type 1 carotid baroreceptors acutely reset at a value of about 0.15. These results indicate that (1) renal and thoracic nerve activities and blood pressure acutely reset to a greater degree than type 1 carotid baroreceptors and that (2) renal activity acutely resets to a greater degree than blood pressure and thoracic nerve activity.
Hypertension 1996 Mar
PMID:Acute baroreflex resetting: differential control of pressure and nerve activity. 869 51


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