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

The present studies were performed in order to determine whether "filtration edema" will develop as a consequence of cerebral vasoparalysis, vasoparalysis in combination with arterial hypertension or arterial hypertension alone. A series of dogs, anaesthetised with i.v. Chloralose-Urethane were exposed 1) to cerebral vasoparalysis, produced by hypercapnia (PaCO2 about 150 mm Hg) and hypoxaemia (PaO2 40-60 mm Hg); 2) to arterial hypertension and 3) to a combination of cerebral vasoparalysis and arterial hypertension. Following cerebral vasoparalysis and arterial hypertension, a significant decrease of total cerebrovascular resistance and moderate increase of venous resistance was observed. Regional cerebral blood flow (133Xe), intracranial pressure, as well as the pressure in postcapillary venous outflow (sinus sagittalis wedge pressure and confluence sinuum pressure) were increased. Neither normotonic vasoparalysis nor vasoparalysis in combination with slight arterial hypertension (MABP more than 90 min above 180 mm Hg) resulted in cerebral edema. In contrast, cerebral vasoparalysis in combination with severe arterial hypertension (MABP more than 90 min above 220 mm Hg) resulted in a statistically significant increase in the water content in the white matter without evidence of protein extravasation. Multiple small foci of Evans blue extravasates, however, were found in the cortex following arterial hypertension in combination with vasodilation, indicating a damage of the blood brain barrier. In these blue stained cortical areas the water content was significantly in creased. The following conclusions were drawn from the results. Vasoparalysis during normotension does not produce brain edema despite the slightly elevated hydrostatic pressure gradient between intravasal and extracellular space. Only considerable increase of this hydrostatic pressure gradient caused by a combination of vasoparalysis with severe arterial hypertension is able to produce brain edema in the white matter. In addition, acute hypertension may cause minor multifocal damage of the blood brain barrier in the cerebral cortex. It is concluded that so-called brain swelling, which has been described by several authors in states of cerebral vasoparalysis, is not predominantly caused by brain edema but by vascular congestion. The clinical aspects of the result are discussed.
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PMID:[Cerebral vasoparalysis, arterial hypertension and brain edema (author's transl)]. 5 29

Experiments have been done on rats, rabbits and baboons to elucidate the role of the cranial sympathetic nerves originating in the superior cervical ganglia in the regulation of local cerebral blood flow, including its autoregulation, and in blood-brain barrier functions. Flow was measured by the [14C] ethanol technique, thermoclearance, and xenon-133 clearance. Blood-brain barrier functions were studied by the extravasation of an Evan's blue-albumin complex and by calculation of brain uptake index for two compounds (noradrenaline and inulin). Electrical stimulation of the sympathetic nerves reduces regional flow to a degree that is related to the amount of local perivascular innervation. The breakthrough of autoregulation during induced systemic hypertension is prevented by bilateral stimulation of the superior cervical ganglia. Acute sympathectomy markedly enhances the vascular penetration both at normotension (tested by brain uptake index for noradrenaline and inulin) and rapidly induced hypertension (evidenced by extravasation of Evans' blue). This extravasation of Evans' blud during acute hypertension can be counteracted by sympathetic nerve stimulation. The results give further support for the view that the cranial sympathetic nerves afford an efficient control of the cerebrovascular bed.
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PMID:Influence of the cerebrovascular sympathetic innervation on regional flow, autoregulation, and blood-brain barrier function. 9 65

The blood-brain barrier to intravascular Evans blue-albumin was opened in monkeys and rabbits by infusing isotonic saline for 15 s into the common carotid artery, when the external carotid was clamped temporarily and the lingual was catheterized for measuring pressure. Barrier opening correlated better with infusion pressure than with infusion rate, and occurred at carotid artery pressures above 170 mmHg. Systemic hypertension induced by Aramine increased barrier vulnerability by causing a higher net carotid artery pressure to be attained at a given infusion rate.
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PMID:Blood-brain barrier opening by isotonic saline infusion in normotensive and hypertensive animals. 10 49

The influence of stimulation of the cervical sympathetic chain on the response of cerebral blood flow to hypertension induced by the intravenous infusion of angiotensin was studied in anaesthetised baboons. Cerebral blood flow was measured by the intracarotid 133Xenon injection technique. Possible lesions of the blood-brain barrier were studied by injecting Evans blue towards the end of the experiment and ischaemic brain damage was assessed following perfusion fixation. In a control group of five baboons blood flow increased by 53 +/- 9% (mean +/- S.E.) from the base line values in the arterial pressure range 130-159 mm Hg. In four baboons subjected to unilateral sympathetic stimulation flow increased by 16 +/- 4% in the same pressure range. In three baboons subjected to bilateral sympathetic stimulation there were no significant increases in flow until the arterial pressure had increased above 159 mm Hg. Disruption of the blood-brain barrier in the parietooccipital regions was only seen in the control animals but not in the stimulated baboons. Ischaemic brain damage was not observed with the exception of one small lesion in a single stimulated baboon. These findings provide strong support for the observations of Bill and Linder (1976) that activation of the cervical sympathetic can modify the level at which breakthrough of cerebral blood flow occurs in association with systemic hypertension.
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PMID:Effects of increasing arterial pressure on cerebral blood flow in the baboon: influence of the sympathetic nervous system. 10 11

Venous distensibility in essential hypertension has been reported to be unchanged or decreased; its pathophysiologic role is uncertain. In 27 male hypertensive patients and 21 normotensive control subjects, forearm venous distensibility and capillary filtration rate at 30 cm of H2O distending pressure were measured by strain gauge plethysmography. Plasma renin activity (PRA), plasma volume (PV) by the Evans blue dye dilution technique, mean arterial pressure (MAP) by cuff, and cardiac output (CO) by the CO2 rebreathing method were also measured. Compared to values in normotensive control subjects, forearm venous distensibility in hypertensive subjects was decreased (P less than 0.05); the forearm venous pressure-volume curves (deflation phase) were shifted in the direction of the pressure axis (P less than 0.02); and the capillary filtration rate was increased (P less than 0.05). Venous distensibility changes in hypertensive subjects were unrelated to PRA, MAP, PV, CO, stroke volume, and total peripheral resistance. These findings confirm previous reports of decreased venous distensibility in hypertension and provide direct evidence for increased capillary filtration rate. In view of the lack of significant correlation between venous distensibility and the measured hemodynamic parameters, a patho-physiologic role for venous distensibility in hypertension could not be established.
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PMID:Decreased venous distensibility in essential hypertension: lack of systemic hemodynamic correlates. 37 15

In 64 patients with ischemic strokes that occurred on the background of atherosclerosis (33) and a combination of atherosclerosis with arterial hypertension (31) using the dilution method of Evans's blue the authors studied indices of general hemodynamics compared to rheoencephalographic data. Twenty similar patients without signs of brain circulation disturbances and 20 healthy persons were taken as control groups. In 69% of the patients with ischemic strokes deep disturbances of general hemodynamics were observed. An increase of tonus, a decrease of elasticity of cerebral vessels and deficit of pulse blood repletion were determined rheoencephalographically. Insufficiency of general hemodynamics in conditions of changed autoregulation of brain circulation promotes development of ischemic disorders of brain circulation and unfavourably influences the course and outcome of the stroke.
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PMID:[State of general and cerebral hemodynamics in patients with ischemic strokes]. 42 64

Acute arterial hypertension was produced in male Wistar rats by pressure pulse through the right internal carotid artery. The pressure pulse was induced by infusion of physiological saline as a bolus, at a rate of 0.63 ml per second by syringe pump. Evans blue (Eb) was used to visualize the areas of blood-brain barrier opening. Intravenously injected horseradish peroxidase (HRP) was used to study the ultrastructural basis of permeability changes in cerebral endothelium. Eb outlined circumscribed areas of blood-brain barrier opening. HRP extravasation was found mainly around small arteries. The capillary network was affected to a much lesser extent. Electron microscopy showed that HRP crossed the endothelial cell layer by intercellular routes. Glutaraldehyde fixed brain samples permeated with colloidal lanthanum supported these observations.
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PMID:Opening of tight junctions in cerebral endothelium. II. Effect of pressure-pulse induced acute arterial hypertension. 43 71

Acute experimental hypertension induces protein leakage in the brain. The protein is thought to be, at least to a great extent, transported through the endothelial cells by pinocytosis. An anion transport inhibitor, 4 acetamido-4-isothiocyano-stilbene-2,2'-disulfonic acid, markedly reduced adrenaline or bicuculline-induced leakage of 125IHSA and Evans blue-albumin in all areas of the rat brain. The preventive effect of dexamethasone was less pronounced and no effect was seen of haloperidol.
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PMID:Prevention of protein extravasation in the brain by an anion transport inhibitor in acute experimental hypertension in rats. 45 24

1. The Carworth Long-Evans rat has been reported to develop adrenal-regeneration hypertension but not deoxycorticosterone acetate (DOCA) hypertension. Deficiency of a hypothalamic receptor for deoxycorticosterone which mediates saline polydipsia has been postulated to underlie this resistance. Since a mineralocorticoid etiology for adrenal-regeneration hypertension has been postulated and all mineralocorticoids are thought to act on common receptors, these previous reports are difficult to reconcile. 2. To determine if an absolute or relative resistance to mineralocorticoids is present, Charles River Long-Evans and Sprague-Dawley rats were given 40 mg (107 micromol) of DOCA pellets/rat or 250 microgrms (0.65 micromol) of 2 alpha-methyl-9-alpha-fluorocortisol/day subcutaneously. 3. Saline polydipsia occurred with both steroids with both rat strains, though significantly less with the Long-Evans rats. Both types of rats became hypertensive and developed cardiac and renal enlargement with both steroids. Hypertension developed more rapidly with 2 alpha-methyl-9 alpha-fluorocortisol. 4. Thus mineralocorticoid hypertension can be produced in the Charles River Long-Evans rat, and the development of adrenal-regeneration hypertension in this rat strain is not incompatible with a mineralocorticoid etiology for adrenal-regeneration hypertension.
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PMID:Hypertension with mineralocorticoid administration to the Long-Evans rat. 47 92

In our laboratory, chronically feeding cadmium to groups of rats has been reproducibly associated with average increases of 15 to 20 mm Hg in systolic pressure. A total of 497 female Long-Evans rats were continuously provided with drinking water fortified with five essential elements and containing from 0.01 to 50 ppm cadmium, as the acetate, from weaning for as long as 30 months. These rats, plus 311 matched control animals which received fortified water without added cadmium, were fed a special low-cadmium diet. All 808 rats were weighed at least monthly as a screen for cadmium toxicity, and their systolic pressures were measured every 3 or 6 months. The two lowest concentrations of cadmium tested (0.01 and 0.03 ppm) were not pressor; the three highest concentrations (10, 25, and 50 ppm) ultimately proved to be toxic. All indirect systolic pressures (each measured in triplicate) of all rats which received 0.1 to 5 ppm cadmium (i.e., nontoxic pressor doses) averaged 15.0 mm Hg more than simultaneously measured pressures of control rats. This average increase over the control pressure is extremely significant statistically, even though it seems relatively small in absolute terms. Occasionally, however, some rats had much larger than average increases in pressure; thus, 10 of 60 rats receiving from 0.1 to 0.5 ppm cadmium for 18 months had systolic pressures that were more than 50 mm Hg above the average pressure of the control rats. Cadmium-induced hypertension is not limited to females or to a particular strain. Although we have usually used one strain of female Long-Evans rat from a single source, males of the same strain and female Sprague-Dawley rats have also developed comparable hypertension. All subgroup II elements can apparently induce similar increases in systolic pressure averaging 15 to 20 mm Hg, but cadmium is pressor in much smaller amounts than mercury or zinc. Thus, to induce a demonstrable increase in pressure requires more than ten times as much divalent mercuric ion as cadmium and more than 1000 times as much zinc as cadmium. Exposure to another metal along with cadmium can markedly alter the ability of cadmium to induce hypertension. Selenium protects against the hypertension induced by twice as much cadmium. Large excesses of both zinc and copper have also inhibited the induction of hypertension by cadmium. In contrast, lead, which like cadmium, can also induce hypertension, augments rather than inhibits cadmium-induced hypertension; thus, lead and cadmium together can induce an average increase in systolic pressure in excess of 40 mm Hg, at least twice as large as is usually induced by either metal alone.
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PMID:Increase in the systolic pressure of rats chronically fed cadmium. 48 39


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