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

Interrelationship between the breakdown of the blood-brain barrier (BBB) to Evans blue and elevations in the regional cerebral blood flow (rCBF) was studied in rabbits subjected to adrenaline- or metaraminol-induced systemic hypertension and also in bicuculline-induced seizures. The rCBF was assessed in small samples from various regions of the brain with the use of [3H]nicotine, and the permeability of the BBB was evaluated with an Evans blue tracer. In acute hypertension, Evans blue extravasations were observed in the occipital cortex and sometimes in the superior colliculus, i.e., the regions which also showed the highest elevations in rCBF. The breakdown of the BBB in acute hypertension was clearly related to the rate of mean arterial blood pressure rise, being much less pronounced in the metaraminol group, which showed a much slower blood pressure elevation rate. In bicuculline-induced seizures, there was no evident correlation between the amplitude of rCBF elevations and Evans blue extravasations. Preservation of BBB integrity was observed in areas showing high elevations in the rCBF.
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PMID:Regional changes in cerebral blood flow and blood-brain barrier permeability during epileptiform seizures and in acute hypertension in rabbits. 669 17

Acute hypertension, produced by i.v. Aramine injection, opened the blood-brain and blood-cerebrospinal fluid (CSF) barriers to Evans blue-albumin. In rabbits the threshold for blood-brain barrier (B-BB) opening was approximately 160 mm Hg and for blood--CSF barrier opening 150 mm Hg. The blood-brain and blood-CSF barriers were not opened by blood pressure elevations less than 80 mm Hg. Multiple blue spots (1- to 10-mm diameter) which show Evans blue-albumin extravasation, were seen throughout the cerebral cortex, occasionally in the medulla-pons, and cerebellum. Diffuse extravasation was not seen and the extravasation was nearly symmetrical in the two hemispheres. The barrier permeability was increased when systemic blood pressure was elevated rapidly rather than gradually to the threshold level. Endothelial or epithelial cell destruction was never observed in light and electron microscopic studies. Arterial blood and CSF PCO2, PO2 and pH remained constant, which is indicative of the lack of significant metabolic effect caused by hypertension. Barrier opening in acute hypertension is postulated to be due primarily to the direct mechanical effect of increased intraluminal pressure in cerebral vessels, which may cause widening of the tight junctions between endothelial cells.
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PMID:Pathophysiology of the opening of the blood-brain and blood-cerebrospinal fluid barriers in acute hypertension. 670 83

The reversibility of blood-brain barrier (BBB) dysfunction was examined in rats after acute experimental hypertension. A short-lasting (less than or equal to 4 min) acute hypertension was produced by intravenous injection of 20 micrograms/kg angiotensin. Evans blue, the barrier tracer, was administered intravenously either prior to or at intervals of 3, 10, 20, 30, and 60 min after the angiotensin injection. It was observed that the BBB dysfunction showed a peak 30 min after the angiotensin injection. Three of six animals that received Evans blue 60 min after angiotensin administration showed extravasation of the tracer on gross inspection. We concluded that BBB dysfunction may remain even 60 min after an acute hypertensive episode of short duration.
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PMID:Reversibility of blood-brain barrier dysfunction in acute hypertension induced by angiotensin. 672 87

Alternative hypotheses concerning the pathogenesis of hypertensive encephalopathy are that vasospasm produces cerebral ischemia and cerebral edema, or that passive dilation of cerebral vessels during severe hypertension produces disruption of the blood-brain barrier and cerebral edema. Stroke-prone spontaneously hypertensive rats (SHRSP) were studied when they developed signs of neurological dysfunction. We measured regional cerebral blood flow (rCBF) with 14C-iodoantipyrine, and permeability of the blood-brain barrier with Evans blue dye. Twelve rats had focal disruption of the barrier without histological evidence of ischemic infarction or cerebral hemorrhage: areas with disruption of the barrier had severe focal edema in seven rats and minimal edema in five rats. In areas with disruption of the barrier and marked focal edema, rCBF was decreased to 38 +/- 8 (mean +/- SE) ml/min/100 g vs 102 +/- 13 (p less than 0.05) in other areas of the ipsilateral hemisphere, and 86 +/- 16 in the homologous area of the contralateral hemisphere (p less than 0.05). In contrast, in areas with disruption of the blood-brain barrier with only minimal edema, rCBF was normal or increased: rCBF was 100 +/- 11 ml/min/100 g vs 85 +/- 12 in other areas of the ipsilateral hemisphere (p greater than 0.05) and 64 +/- 8 in the homologous area contralaterally (p less than 0.05). The findings indicate that edema precedes reduction in rCBF in SHRSP and suggest that the initiating event in hypertensive encephalopathy is disruption of the blood-brain barrier, and not vasospasm.
Hypertension
PMID:Evidence that disruption of the blood-brain barrier precedes reduction in cerebral blood flow in hypertensive encephalopathy. 672 73

Acute hypertension impairs the function of biological barriers, e.g. that of blood-brain barrier. We tested the hypothesis that chronic hypertension might influence the penetration of compounds through blood-brain and blood-testis barriers. With this in mind, the penetration of relatively small radioactive compounds (14C-2-methyl-4-chlorophenoxyacetic acid = 14C-MPA, 14C-sucrose and 14C-antipyrine, 5 microCi/kg intravenously) into the brain, liquor space and testis was compared in male normotensive (Wistar and chronically hypertensive SH rats (11-22 months old). In chronic hypertension after 14C-MCPA and 14C-sucrose administration the penetration of radioactivity into the brain, cerebrospinal fluid and testis had significantly decreased or showed evidence of decrease, while after 14C-antipyrine administration the penetration remained unchanged. Penetration of Evans blue-albumin complex into the brain was studied by giving intravenous injection of Evans blue (5% solution) which is firmly bound to serum albumin. Extravasation of dye-protein complex into the brain showed no difference between Wistar and SH rats. The results suggest that chronic hypertension does not increase the penetration of compounds into the brain and testis but rather, reduces it.
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PMID:Penetration of some compounds through blood-brain and blood-testis barriers in chronically hypertensive rats. 674 74

The effect of unilateral, electrical stimulation of the cervical sympathetic chain in rabbits anesthetized with pentobarbital sodium and vasodilated by hypercapnia, acetazolamide, papaverine or PGI2 was investigated to determine to what extent the sympathetic nerves to the brain and the eye cause vasoconstriction and prevent overperfusion in previously vasodilated animals. Evans blue was given as a tracer for protein leakage. Blood flow determinations were made with the labelled microsphere method during normotension and acute arterial hypertension. Hypertension was induced by ligation of the thoracic aorta and in some animals metaraminol or angiotensin was also used. Acetazolamide caused a two to threefold increase in cerebral blood flow (CBF) and hypercapnia resulted in a fivefold increase. CBF was not markedly affected by papaverine or PGI2. In the choroid plexus, the ciliary body and choroid, papaverine and hypercapnia caused significant blood flow increases on the control side. Sympathetic stimulation induced a 12% blood flow reduction in the brain in normotensive, hypercapnic animals. Marked effects of sympathetic stimulation at normotension were obtained under all conditions in the eye. In the hypertensive state the CBF reduction during sympathetic stimulation was moderate, but highly significant in hypercapnic or papaverine-treated animals as well as in controls. Leakage of Evans blue was more frequently seen on the nonstimulated side of the brain. In the eye there was leakage only on the control side except in PGI2-treated animals where 2 rabbits had bilateral leakage. The effect of sympathetic stimulation on the blood flow in the cerebrum and cerebellum in vasodilated animals seems to be small or absent if the blood pressure is normal. In the eye pronounced vasoconstriction occurs under these conditions. In acute arterial hypertension sympathetic stimulation protects both the cerebral and ocular barriers even under conditions of marked vasodilation.
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PMID:Effects of sympathetic stimulation on cerebral and ocular blood flow. Modification by hypertension, hypercapnia, acetazolamide, PGI2 and papaverine. 675 90

1. Vasopressin deficient homozygous Brattleboro rats develop malignant renal hypertension following complete aortic-ligature between the renal arteries. 2. This form of hypertension is associated with high plasma renin activity (PRA) and plasma angiotensin II (AII) levels and a high incidence of the specific vascular lesions of fibrinoid necrosis in both Brattleboro and Long-Evans rats. 3. The levels of PRA and AII in the malignant hypertensive Brattleboro rats were not different from those in Long-Evans rats with malignant hypertension. 4. No compensation by the renin-angiotensin system therefore could be demonstrated for the lack of vasopressin in malignant hypertensive Brattleboro rats. 5. Vasopressin does not appear to be essential as a pressor hormone in the development of malignant renal hypertension and fibrinoid can occur in the absence of vasopressin.
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PMID:Vascular lesions and angiotensin in malignant hypertension in the absence of vasopressin. 675 78

1. The effects of isolation on systolic blood pressure, heart rate and fluid and electrolyte balances were studied in rats with a congenital inability to synthesize vasopressin (Brattleboro strain) and in the normal parent strain (Long Evans). 2. There was no significant difference between the systolic blood pressures of Brattleboro rats and Long Evans rats while the animals were housed in groups, although the heart rates of the Brattleboro rats were significantly higher. 3. After 5 days of isolation in metabolism cages, systolic blood pressure was significantly increased in the Long Evans rats, but not in the Brattleboro rats. 4. Since there were no significant differences between the fluid and electrolyte balances of the two groups after 5 days of isolation, it is unlikely that the hypertension in the Long Evans rats was attributable to a renal action of vasopressin. 5. It is possible that vasopressin was involved in the development of isolation-induced hypertension by virtue of its pressor effects. Alternatively, the failure of Brattleboro rats to develop hypertension may have been due to some abnormality in these animals other than the lack of vasopressin.
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PMID:The cardiovascular and renal responses to short-term isolation in Brattleboro rats. 682 8

In three groups of cats, the authors studied the effect of subarachnoid hemorrhage (SAH) on the permeability of the blood-brain barrier (BBB) to the penetration of Evans blue-protein complex. One group received arterial hypertension alone, one group SAH alone, and one group SAH followed by arterial hypertension. Animals subjected to arterial hypertension alone showed areas of BBB breakdown. However, when cats were rendered hypertensive after SAH, there were no demonstrable BBB lesions. The SAH was produced by intracisternal injection of whole blood and hypertension by the intravenous injection of metaraminol. The preservation of the BBB after SAH is discussed. Vasospasm is considered as a possible hemodynamic variable responsible for the protection of the BBB from hypertensive damage. The need for a new model is proposed to further investigate the state of the BBB after SAH.
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PMID:The blood-brain barrier following experimental subarachnoid hemorrhage. Part 1: Response to insult caused by arterial hypertension. 682 18

Erectile impotence is a commonly reported undesired side effect in patients treated for hypertension with alpha-methyldopa. However, the mechanism of that dysfunction has not been determined. In this study we report the effect of 12 days of daily intraperitoneal injections, 300 mg./kg., of alpha-methyldopa on adult male, Long-Evans rats and their age-matched saline controls. The effect of the drug upon copulation, penile reflexes and tissue catecholamines was measured. The results showed significant differences between control and experimental animals in all parameters studied. Tests of copulatory ability showed significant decreases in mounts from 5.8 +/- 1.6 (mean +/- standard error) to 3.1 +/- 1.3; penile intromissions from 27.0 +/- 3.8 to 4.8 +/- 1.9; and ejaculations from 2.1 +/- 0.3 to 1.1 +/- 0.6 per 30 minute test period. Penile reflexes measured as erection and cup formation showed similar significant reductions. The norepinephrine content of the penile corpora in the controls was 0.460 +/- 0.084 ng./mg. wet weight and 0.112 +/- 0.022 ng./mg. wet weight in the experimental group. There were similar significant reductions of norepinephrine content in the vas deferens of these animals 32.95 +/- 4.31 ng./mg. and 0.25 +/- 0.1 ng./mg. wet weight in the control and experimental groups respectively.
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PMID:The effect of chronic alpha-methyldopa upon sexual function in the adult male rat. 683 69


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