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

This study was performed to evaluate the direct and indirect effects of acute coronary sinus hypertension (CSH) on systolic and diastolic left ventricular (LV) function. Coronary sinus pressure was elevated to 25 mmHg for 3 h in eight pentobarbital-anesthetized dogs and then relieved. LV contractility was assessed by preload recruitable stroke work (PRSW) and end-systolic elastance (Ees). Diastolic function was assessed by the time constant of isovolumic relaxation (tau) and the end-diastolic pressure volume relationship (EDPVR). PRSW and Ees decreased progressively, and tau and the slope of the EDPVR increased progressively with CSH. These changes persisted after relief of CSH. beta-Adrenergic and cholinergic receptor blockade, performed in six dogs, did not alter the effects of CSH on systolic or diastolic function. The LV wet-to-dry weight ratios of the groups with CSH were significantly greater than those of a control group without CSH. We conclude that CSH results in changes in the left ventricle that depress contractility, prolong active relaxation, and increase diastolic stiffness. The dysfunction was not the direct effect of CSH or autonomic reflex activation, but may have been induced by fluid accumulation within the interstitium.
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PMID:Acute transient coronary sinus hypertension impairs left ventricular function and induces myocardial edema. 885 15

Systemic arterial blood pressure (BP)-heart rate (HR) relationship (the pressor test) is often used as an index of baroreflex. We evaluated this index by simultaneously comparing BP-HR, right carotid sinus pressure (CSP)-nerve action potentials (NAP), and NAP-HR relationship in dogs anesthetized with pentobarbital. BP was increased or decreased stepwise by intravenous (IV) infusions of phenylephrine or sodium nitroprusside, respectively. In nine dogs BP-HR and CSP-NAP relationships were measured and NAP-HR relationship was constructed before and after sequential and stepwise sectioning of the left aortic depressor nerve (LADN), the right aortic depressor nerve (RADN), and blockade of the left carotid sinus nerve (BLK) with 1% lidocaine. We found that HR was a negative sigmoidal function of BP in intact dogs. Linear slope of this relationship was significantly reduced after sectioning of LADN and RADN, but returned toward baseline after BLK. NAP was a positive sigmoidal function of CSP in intact dogs. Linear slope of this relationship was significantly depressed after sectioning of LADN and RADN. However, after BLK, the slope surpassed control, suggesting the existence of a central communication between the two carotid sinuses. HR was a negative function of NAP in intact dogs. However, as the other baroreflex feedback loops were eliminated, the slope of the NAP-HR relationship approached zero indicating that a closed integrated parallel feedback system is required for reflex regulation of HR. Our findings suggest that under normal conditions the pressor test is a valid index for baroreceptor function, but its use may not be warranted in chronic pathological states, such as atherosclerosis and hypertension. However, in contrast to the present acute experimental model, chronic pathological processes may not develop in sequence, and baroreceptor function on the affected site may not be completely eliminated from the baroreceptor loop such as performed in this study.
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PMID:Pressure-heart rate relationship in intact and after stepwise elimination of three major baroreflex loops in dogs. 889 70

It has been shown that nitric oxide in the brain stem plays an important role in the control of sympathetic nerve activity. We examined the role of endogenous nitric oxide in the brain stem in the rapid central adaptation of baroreflex control of sympathetic nerve activity in anesthetized rabbits. Bilateral carotid sinuses were isolated, and a stepwise increase in pressure of 25 or 50 mm Hg for 50 to 60 seconds was applied to the carotid sinuses while the arterial pressure and renal sympathetic nerve activity were recorded. The renal sympathetic nerve activity was inhibited by the stepwise increase in carotid sinus pressure, but thereafter it gradually returned toward the baseline level despite the fact that carotid sinus pressure was kept constant. This procedure was performed after intracisternal injection of N(omega)-nitro-L-arginine methyl ester (L-NAME, 8 micromol), N(omega)-nitro-D-arginine methyl ester (D-NAME, 8 micromol), L-arginine (40 micromol), or the vehicle solution. The magnitude of the immediate and maximal inhibition of renal sympathetic nerve activity caused by a stepwise increase in carotid sinus pressure was similar between the vehicle and L-NAME treatment, but the rate of recovery of the renal sympathetic nerve activity after immediate inhibition was faster after L-NAME than after vehicle. L-Arginine reversed the effects of L-NAME. However, D-NAME or L-arginine alone had no such effects on the rate of recovery of the nerve activity. These results thus suggest that endogenous nitric oxide in the brain stem attenuates rapid adaptation of the arterial baroreflex control of the sympathetic nerve activity in rabbits.
Hypertension 1998 Jan
PMID:Role of endogenous nitric oxide in the brain stem on the rapid adaptation of baroreflex. 944 86

Coronary venous hypertension induced by partial coronary sinus obstruction (CSO) in the dog, prevents or delays the predictable ventricular fibrillation (VF) of the early phase of acute ischemia. Also, CSO acting presumably through enhanced myocardial hydration, normalizes the inhomogenous extracellular potassium ([K+]o) accumulation, a major factor in producing the electrophysiological disparities, characteristic of arrhythmogenic substrate. To further clarify the mechanism of early ischemic VF prevention in dogs, radioactive microspheres were used to evaluate regional perfusion changes, resulting from CSO sufficient to raise the coronary sinus pressure to 40 mmHg, before and during ischemia induced by double coronary artery occlusion (CAO) (n=5). Also, global or regional unipolar electrogram mapping was used to assess changes of epicardial ventricular activation times (AT) and sequence and activation recovery intervals (ARI) during CSO, CAO and combined CSO and CAO, induced in random order (n=8). CSO did not affect regional perfusion nor improved collateral blood flow during ischemia. With CSO, AT shortened modestly over time (0.41+/-1.1 ms/min, r=0.85, P<0. 05) and ARI transiently decreased by up to 5.5%. With CAO, AT became variably delayed and isochrone map distortions were indicative of localized conduction delays or blocks, consistent with elevated [K+]o. In contrast, when CAO was preceded by CSO, AT delays were homogenous and normal activation sequence was preserved. Also, whereas with CAO, ARI shortened unequally over the ischemic region by as much as 43% at individual sites (average of 38.3+/-6.8 ms, P<0. 001), with combined CSO and CAO, ARI shortening was less pronounced and more homogenous (26.1+/-5.6 ms, P<0.05), not exceeding 29% at any site. Thus, in accordance with previous findings of enhanced [K+]o homogeneity, coronary venous hypertension reduces the disparities of activation and refractoriness of ischemia attributable, at least in part, to disparate [K+]o accumulation. Since no collateral blood flow improvement could be identified, the salutary electrophysiological effects of CSO may reflect a more homogenous extracellular environment, due to preservation of normal microvascular pressure (Pmv) and sustained filtration and lymph flow.
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PMID:Coronary venous hypertension prevents the formation of the electrophysiological arrhythmogenic substrate of acute ischemia in the dog: salutary effects of preserved myocardial hydration. 951 2

Arterial baroreceptors reset rapidly within minutes during acute hypertension; baroreceptor pressure threshold (Pth) is increased and the pressure-baroreceptor activity relation is shifted to the right. The purpose of the present study was to determine if prostacyclin (PGI2) or other prostanoids, released during acute hypertension modulate the magnitude of baroreceptor resetting. Baroreceptor activity was recorded from the vascularly-isolated carotid sinus during distension of the sinus with slow pressure ramp in rabbits anesthetized with chloralose. Pressure-activity curves were generated after holding carotid sinus pressure for 10-15 min from 30 to 100 mmHg. In control, the elevation of holding pressure increased Pth from 44+/- to 65+/-5 mmHg (p < 0.05, n = 12). In the presence of PGI2 (20 microM), Pth averaged 43+/-4 and 45+/-3 mmHg (n = 12) after holding pressure at 30 and 100 mmHg, respectively. In the control group before exposing the carotid sinus to indomethacin, an elevation of holding pressure increased Pth from 49+/-2 to 71+/-3 mmHg (p < 0.05, n = 12). After inhibition of the endogenous formation of prostanoids with indomethacin (20 microM), Pth increased by a significantly greater extent from 61+/-2 to 90+/-3 mmHg (p < 0.05, n = 12) with the increase in holding pressure. The slope of the pressure-activity curve (baroreceptor gain) was not influenced by the change in holding pressure. It was increased significantly by PGI2, while decreased by indomethacin. Neither the change in holding pressure nor PGI2 affected the circumferential wall strain of carotid sinus over a wide range of pressure alteration. The results suggest that PGI2 or other prostanoids released during acute hypertension sensitizes baroreceptors and provides a negative feedback mechanism that opposes and limits the magnitude of rapid baroreceptor resetting.
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PMID:Opposition of rapid baroreceptor resetting by prostanoids in rabbits. 1085 64

Spontaneous contractions of the urinary bladder (SBCs) and experimental elevations of carotid sinus pressure (CSP) have been shown to result in respiratory inhibition with preferential reduction in hypoglossal (HG) nerve activity as compared with that of phrenic nerve discharge. We assessed the interaction between these respiratory inhibitory stimuli in decerebrate, vagotomized, paralyzed and artificially ventilated cats. We denervated the right carotid sinus and pressurized the isolated left carotid sinus region within the linear range of the baroreflex, while maintaining systemic arterial pressure at approximately 100 mmHg. We monitored the HG and phrenic nerve responses to SBCs, to elevations in CSP between SBCs, and to elevations in CSP during SBCs. Our results show that superimposing these stimuli results in respiratory inhibition, especially of HG activity, that exceeds that resultant from either stimulus alone. We speculate that the combined presence of SBCs and episodic hypertension may contribute to the development of periodic breathing or obstructive apnea, particularly during sleep.
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PMID:Respiratory response to baroreceptor stimulation and spontaneous contractions of the urinary bladder. 1117 72

Carotid sinus hypersensitivity (CSH) is a well-described cause of syncope, resulting in bradycardia and/or hypotension in response to neck pressure. The authors hypothesized that (CSH) represents an inappropriate response of the baroreflex system to a nonphysiologic stimulus, rather than a truly hypersensitive carotid sinus (ie, excessive vagotonia and sympathoinhibition in response to arterial hypertension). To test their hypothesis, the authors used a neck chamber to deliver stepped, R-wave-triggered changes in transmural carotid sinus pressure, from +40 to -60 mm Hg, during a single held expiration. The authors studied 7 men (age 69 +/- 8y; mean age +/- SD) with carotid sinus syndrome and 10 age- and sex-matched controls. Seven repetitions of pressure changes were averaged, and the carotid sinus response described by changes in the R-R interval. There was no statistical difference in carotid-cardiac baroreflex gain (R-R interval/pressure change; mean gain +/- SD, 3.0 +/- 2.1 msec/mm Hg and 2.2 +/- 3.0 msec/mm Hg, respectively) or other markers of carotid baroreflex responses between the subjects and controls. These preliminary results suggest that (CSH) may not be a "hypersensitive" reflex, but rather an inappropriate response, or "irritability," of the baroreflex system to nonphysiologic deformation of the carotid sinus and/or surrounding tissues.
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PMID:Carotid sinus "irritability" rather than hypersensitivity: a new name for an old syndrome? 1157 May 99

We developed a new model to examine the role of arterial baroreceptors in the long-term control of mean arterial pressure (MAP) in dogs. Baroreceptors in the aortic arch and one carotid sinus were denervated, and catheters were implanted in the descending aorta and common carotid arteries. MAP and carotid sinus pressure (CSP) averaged 104 +/- 2 and 102 +/- 2 mmHg (means +/- 1 SE), respectively, during a 5-day control period. Baroreceptor unloading was induced by ligation of the common carotid artery proximal to the innervated sinus (n = 6 dogs). MAP and CSP averaged 127 +/- 7 and 100 +/- 3 mmHg, respectively, during the 7-day period of baroreceptor unloading. MAP was significantly elevated (P < 0.01) compared to control, but CSP was unchanged. Heart rate and plasma renin activity increased significantly in response to baroreceptor unloading. Removal of the ligature to restore normal flow through the carotid resulted in normalization of all variables. Ligation of the carotid below a denervated sinus (n = 4) caused a significant decrease in CSP but no systemic hypertension. These results indicate that chronic unloading of carotid baroreceptors can produce neurogenic hypertension and provide strong evidence that arterial baroreceptors are involved in the long-term control of blood pressure.
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PMID:Unloading arterial baroreceptors causes neurogenic hypertension. 1189 8

Cerebral venous hypertension (VH) is a pathological condition associated with arteriovenous malformation, and is an important determinant factor for clinical symptom and outcome. Using a rat whole brain VH model created by a carotid-jugular fistula and contralateral jugular vein ligation we measured superior sagittal sinus pressure (SSSP) and cerebral blood flow (CBF) by the 14C-iodoamphetamine (IMP) indicator fractionation technique under isoflurane anesthesia with controlled ventilation. SSSP was significantly elevated in the fistula group (15 +/- 1 mmHg) (mean +/- SEM) compared to the vessel occlusion (5 +/- 1) and sham operated groups (5 +/- 1) (P < 0.05). Mean absolute CBF in the fistula (103 +/- 3 ml/ min/100 g) and vessel occlusion (90 +/- 4) groups were elevated compared to the sham group (77 +/- 3) (P < 0.05). Physiological parameters (mean blood pressure, heart rate, and blood gas analysis) before measurement were not different. In this VH model we found increases in SSSP and IMP uptake in the brain. We assume the mechanism of IMP uptake increase in VH animal may be slow circulation with a possible change of first pass extraction of IMP.
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PMID:Iodoamphetamine (IMP) uptake in the brain is increased after experimental cerebral venous hypertension in the rat. 1475 37

Pseudotumor cerebri (PTC) is a syndrome of increased intracranial pressure without hydrocephalus or mass lesion and with normal cerebrospinal fluid (CSF) composition. Although often considered to be "idiopathic," detailed investigation has revealed a high incidence of venous outflow abnormalities in PTC syndrome patients. The thought that elevated intracranial venous sinus pressure is a "universal mechanism" for PTC syndrome of varying etiologies has been called into question by a study indicating that the increased venous pressure in idiopathic PTC patients is caused by the elevated intracranial pressure and not the reverse, suggesting that "the chicken is the CSF pressure elevation and the egg is the venous sinus pressure elevation." Vitamin A toxicity may play a role in the pathogenesis of idiopathic PTC. The treatment of PTC has two major goals: the alleviation of symptoms and preservation of visual function. When medical therapy fails or when visual dysfunction deteriorates, surgical therapies for PTC should be considered. The two main procedures performed include lumboperitoneal shunt and optic nerve sheath fenestration. Because of the association of PTC with venous sinus hypertension, some authors are considering venous sinus stenting for refractory cases of PTC. It is still unclear if primary treatment of the observed venous stenosis benefits patients with idiopathic PTC. This should be no surprise, as it is not certain whether the stenoses are the cause or the result of idiopathic PTC.
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PMID:Pseudotumor cerebri. 1498 82


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