Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors report the values of mean hemispheric blood-flow and cerebral arterial consumption they found in 34 neurosurgical comatous cases in acute state. In basal conditions, mean values of mean hemispheric bloodflow and oxygen consumption are lowered. There seems to be a relation between the values found and the comatous stage on one hand, the prognosis on the other hand. The cerebral response to hypercapnia (16 assays) allows to separate 2 groups, one with a noticeable improvement of cerebral bloodflow, the other with only a minimal response. There was no significant variation of cerebral oxygen consumption in both group. Cerebral response to CO2 seems to be clearly related to the stage of coma (low in the most severe cases) but pronostic incidence remained uncertain. A hypertensive test by means of Aramine (18 assays) allows to separate 3 groups : 1 group (8 cases) where the mean hemispheric bloodflow remained stable during hypertension as did the cerebral oxygen consumption -(autoregulation remained unchanged), 1 group (4 cases) where mean hemispheric bloodflow and cerebral oxygen consumption were lowered (excessive autoregulation), 1 group (6 cases) where mean hemispheric bloodflow increases clearly while under Aramine perfusion (loss of autoregulation). Those dynamic tests, either hypercapnic or hypertensive, allow, in comparing oxygen consumption variations with cerebral bloodflow variations, the distinction between : patients where metabolic autoregulation seems maintained (good prognosis) - (10 cases), patients where metabolic regulation is lost with either "luxury perfusion" (14 cases) - poor prognosis, or "insufficient perfusion" (10 cases). The authors are discussing the treatment concerning those last mentioned patients.
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PMID:[Value of cerebral metabolic exploration in post-traumatic coma states in the acute phase]. 1 86

In 34 comatose patients in the acute phase, the mean hemispheric CBF is lowered as well as the CMRO2, with a quite good relation between these values and the coma level and prognostic so. The cerebral response to a PaCO2 range indicates a quite good relation with the coma level (the lowest value in the most severe comas). The cerebral autoregulation study, using Aramine induced hypertension, can separate the cases with a present autoregulation and the cases with a loss of autoregulation (the most severe and the poorest prognosis). In dynamic conditions (variation of the PaCO2 or Aramine induced hypertension), the change in CMRO2 is interesting : rather good prognosis among the patients with a normal metabolic autoregulation - poor prognosis among those whose metabolic autoregulation is lost.
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PMID:[Value of brain metabolic studies in post-traumatic coma]. 2 88

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

Acute arterial hypertension was induced in male Wistar rats using two experimental techniques: (1) i.v. injection of Aramine and (2) infusion of physiological saline as a bolus via internal carotid artery. Horseradish peroxidase (HRP) was injected i.v. prior to both experimental procedures and subsequently localized in the brain by light and electron microscopy. In the saline infusion (pressure pulse) model, colloidal lanthanum was also applied as a diffusion tracer following fixation of the cerebral endothelium. In the Aramine model, extravsation of HRP correlated with abrupt elevation of blood pressure. In the pressure pulse model HRP extravasation was consistently visualized in the affected hemisphere. Electron microscopy showed consistent labeling of plasmalemmal vesicles by HRP in segments of cerebral endothelium. However, HRP was also clearly visualized in junctional pools suggesting focal opening of endothelial tight junctions as a pathway for extravasation of this tracer in both hypertensive models. Colloidal lanthanum not transported by plasmalemmal vesicles across endothelium after fixation of the brain also bypassed consecutive membrane appositions of endothelial tight junctions indicating existance of interendothelial pathways to macromolecules in acute arterial hypertension.
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PMID:Blood-brain barrier opening to horseradish peroxidase in acute arterial hypertension. 50 90

In order to delineate the critical blood flow pattern during the Cushing response in intracranial hypertension, regional cerebral blood flow was measured with radioactive microspheres in 12 anesthetized dogs at respiratory arrest caused either by expansion of an epidural supratentorial balloon or by cisternal infusion. Regional cerebrospinal fluid pressures were recorded and the local cerebral perfusion pressure calculated in various cerebrospinal compartments. In the 8 dogs of the balloon expansion group, the systemic arterial pressure was unmanipulated in 4, while it was kept at a constant low level (48 and 70 mm Hg) in 2 dogs and, in another 2 dogs, at a constant high level (150 and 160 mm Hg) induced by infusion of Aramine. At respiratory arrest, regional cerebral blood flow had a stereotyped pattern and was largely independent of the blood pressure level. In contrast, concomitant pressure gradients between the various cerebrospinal compartments varied markedly in the 3 animal groups, increasing with higher arterial pressure. Flow decreased by 85-100% supratentorially and by 70-100% in the upper brain stem down to the level of the upper pons, while changes in the lower brain stem were minor, on the average 25%. When intracranial pressure was raised by cisternal infusion in 4 dogs, the supratentorial blood flow pattern at respiratory arrest was approximately similar to the flow pattern in the balloon inflation group. However, blood flow decreased markedly (74-85%) also in the lower brain stem. The results constitute another argument in favour of the Cushing response in supratentorial expansion being caused by ischemia in the brain stem. The critical ischemic region seems to be located rostrally to the oblongate medulla, probably in the pons.
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PMID:Regional cerebral blood flow and CSF pressures during Cushing response induced by a supratentorial expanding mass. 402 56

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 effects of acute hypertension and respiratory stress induced by Aramine (metaraminol bitartrate) upon blood-brain barrier (BBB) permeability to horseradish peroxidase (HRP) were studied in adult inbred white rats. The BBB permeability was quantitated by slicing the brain of each animal into 500-mu thick sections, incubating the sections using the Reese-Karnovsky method, and counting all observed HRP perivascular exudates. No evidence of BBB compromise or significant elevation of blood pressure (BP) was observed in the following experimental groups: 1) control group of five animals; 2) hyperventilated group of five animals (final mean arterial blood gases; pO2, 104.2 mm Hg; pCO2, 24.8 mm Hg; pH, 7.53); 3) anoxic-stress group of five animals (final mean arterial blood gases; pO2, 31.4 mm Hg; pCO2, 58.2 mm Hg; pH 7.21). However, in a group of 15 animals subjected to anoxic stress followed by hyperventilation, in addition to extreme changes in the levels of arterial blood gases, a significant BP increase occurred (mean BP increase per second, 3.43 +/- 0.25 mm Hg; final mean BP, 163.3 +/- 3.18 mm Hg); as well as significant BBB opening (mean number of HRP exudates per animal, 12.2 +/- 0.85). Likewise, a final group of 10 animals given intravenous Aramine displayed a significant systemic BP elevation (mean BP increase per second, 6.9 +/- 0.38 mm Hg; final mean BP, 165.8 +/- 3.16 mm Hg), accompanied by BBB opening (mean number of exudates per animal, 51.5 +/- 5.95). The variable most strongly associated with the degree of barrier opening was the rate of BP rise (correlation coefficient = +0.84).
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PMID:Influence of respiratory stress and hypertension upon the blood-brain barrier. 677 41