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

Cardiac rupture occurs in 10 per cent of patients who die with acute myocardial infarction, but the pathogenesis remains unclear. Twenty randomly selected patients with cardiac rupture were reviewed retrospectively at autopsy, and the findings were compared with those of 20 age- and sex-matched control subjects who had died of acute transmural myocardial infarction without rupture. The times from the onset of chest pain to death were similar in the two groups (5.7 +/- 5.8 days for patients with rupture versus 4.2 +/- 4.9 days for control subjects), and there were no differences in the incidences of systemic hypertension, diabetes mellitus, hypercholesterolemia, history of myocardial infarction, or angina pectoris. The severity of coronary atherosclerosis was different in the two groups, with 55 per cent of the patients with cardiac rupture having single-vessel disease and 70 per cent of the patients without cardiac rupture having disease in three vessels. Additionally, the incidence of thrombosis was greater in patients with cardiac rupture than in those without. The inflammatory cell response in each patient was quantitated microscopically (number and type of leukocytes) in ten high-power fields. The inflammatory response was greater in patients with cardiac rupture. The number of eosinophils in the inflammatory response was significantly (P less than 0.01) greater in hearts associated with cardiac rupture (29.5 +/- 4 per cent) than in control hearts (11.7 +/- 3.1 per cent). It is postulated that eosinophils rich in arylsulfatase B, peroxidase, glucuronidase, beta-glycerophosphatase, major basic protein, and eosinophilic cationic protein may further weaken the necrotic myocardium and, in part, determine whether acute myocardial infarction will eventually result in cardiac rupture.
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PMID:Association of eosinophils with cardiac rupture. 399 34

The site of action and the distribution of angiotensin II have been studied in the mouse. A comparison of the ratios of angiotensin-(14)C and inulin-(3)H at the time of the pressor effect reveals an extracellular pattern of distribution. Morphological studies were made using angiotensin coupled to exogenous enzymes which can be demonstrated histochemically. Coupling of angiotensin to horseradish peroxidase or cytochrome c, with glutaraldehyde or difluorodinitrodiphenylsulfone (FNPS) as the coupling agent, does not alter the pattern of its vasopressor response or that of its inactivation; nor are differences present between angiotensin and the angiotensin-enzyme complexes in the stimulation of in vitro tissue preparations. Dissociation of the complexes was shown not to occur in vitro, but the possibility of a serum factor splitting the complexes immediately after intravenous injection cannot be excluded. Since these complexes are localized on the endothelium and not on the smooth muscle at the time of maximum hypertension, the endothelium is proposed as the site of action for angiotensin.
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PMID:The cellular site of action of angiotensin. 432 16

The ultrastructure of retinal arterial vessels from rats with severe renal hypertension has been studied. The permeability of retinal vessels has also been examined by means of vascular labeling technics utilizing horseradish peroxidase and microperoxidase as tracer substances. Small retinal arteries and arterioles exhibit foci of smooth muscle necrosis characterized initially by fragmentation of medial smooth muscle cells, and subsequently by loss of myofilaments and release of free vesicles, vacuoles and other cytoplasmic organelles extracellularly. Evidence for increased permeability is observed occasionally in retinal capillaries and less frequently in arteries and arterioles. The enzymatic tracers penetrate the tight junctions of the endothelial cells and are found in the basement membranes adjacent to endothelial and smooth muscle cells, as well as in expanded extracellular spaces around the capillaries. The alterations in the ultrastructure and permeability of retinal vessels in experimental hypertension have been compared with that of visceral and cerebral cortical vessels.
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PMID:The cellular pathology of experimental hypertension. VI. Alterations in retinal vasculature. 508 Jul

The effect of acute hypertension, induced in rats by intravenous injection of methoxamine chloride (Mexan), on the stria vascularis and spiral ligament was studied electronmicroscopically with the tracer method of horseradish peroxidase (HRP). Considerable extravasation of HRP occurred in the stria vascularis, due to the increased vesicular transport. The leaked HRP spread into intercellular spaces, but was prevented from spreading towards the endolymph by zonulae occludentes between marginal cells and towards the perilymph by zonulae occludentes between basal cells. The reaction product was occasionally found between basal cells. No leakage of HRP from capillaries was observed in the spiral ligament, although some labelled micropinocytotic vesicles were present in the endothelium. It is suggested that, under acute hypertensive conditions, areas of zonulae occludentes bordering the stria vascularis play an important role as a barrier to HRP, whereas capillaries in the spiral ligament themselves act as a barrier to it.
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PMID:Ultrastructural study of the effect of acute hypertension on the stria vascularis and spiral ligament. 619 34

Acute hypotension was produced in rats by using two experimental techniques: intravenous infusion of a ganglion-blocking agent (Arfonad), and venesection of a femoral vein. Horseradish peroxidase (HRP) was injected intravenously after each procedure, and subsequently observed in the inner ear by light and electron microscopy. In both experimental models, a large amount of tracer spread into the intercellular spaces, but it was halted by tight junctions bordering the stria vascularis. The endothelium exhibited a high distribution density of labelled vesicles, which suggested increased vesicular transport. There was no extravasation of HRP from capillaries in the spiral ligament in spite of the presence of some labelled pinocytotic vesicles. The present study was concerned with the discovery of enhanced capillary permeability of the stria vascularis under acute hypotension, as in the case of acute hypertension (Sakagami et al., 1984).
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PMID:Increased capillary permeability of the stria vascularis to HRP, induced by experimental acute hypotension in rats. 646 26

Anionic groups on cerebral arteriolar endothelium were localized using cationized ferritin (CF), and alterations in the distribution of these groups were documented in arterioles with increased permeability to horseradish peroxidase (HRP) in angiotensin-induced acute hypertension. Normotensive animals showed a uniform distribution of anionic groups on the endothelial luminal plasma membrane when fixed or live vessels were reacted with CF. Anionic groups were localized at the mouth of pinocytotic vesicles in both preparations; however, only live cells demonstrated CF particles within vesicles, and the possibility that these represent pinocytosed CF particles cannot be ruled out. Cationized ferritin particles were not observed on the plasma membranes within interendothelial spaces in either of the preparations. Sixty percent of hypertensive animals with pressures over 200 mmHg showed increased arteriolar permeability to HRP. At 2.5 min, permeable arteriolar segments with active vesicular transport of HRP showed marked reduction or loss of CF binding. Capillaries and venules in the adjacent cortex and nonpermeable arterioles demonstrated linear endothelial CF binding similar to controls. Most permeable vessels of animals killed 6-20 min after onset of acute hypertension when the blood-brain barrier is usually closed showed CF binding on endothelium indicating that there is rapid restoration of the net negative charge. These studies demonstrate that increased arteriolar permeability in acute hypertension is associated with a transient alteration of surface charge. The mechanism by which charge is altered remains to be determined.
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PMID:Cerebral endothelial surface charge in hypertension. 647 87

The effects of acute hyper- and hypotension on the stria vascularis and spiral ligament of the rat were studied electron microscopically with the horseradish peroxidase (HRP) tracer method. Acute hypertension was induced by i.v. infusion of methoxamine chloride (Mexan), and acute hypotension by i.v. infusion of a ganglion-blocker (Arfonad) and by venesection. In both acute hyper- and hypotensive experiments, a large amount of leaked HRP spread into the intercellular spaces until it was stopped by tight junctions bordering the stria vascularis. The stria capillary endothelium displayed a dense distribution of labelled vesicles, which suggests increased vesicular transport. There was no extravasation of HRP from capillaries in the spiral ligament, despite the presence of some labelled pinocytotic vesicles. The present paper deals with the discovery of enhanced capillary permeability of the stria vascularis under acute hyper- and hypotension, and makes comparison between acute hyper- and hypotension in order to define the function of the stria vascularis.
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PMID:Ultrastructural study of the effect of acute hyper- and hypotension on the stria vascularis and spiral ligament. 659 6

Evidence for the brain renin-angiotensin system being involved in the hypertension of the spontaneously hypertensive rat (SHR) includes central administration of angiotensin II (AII) antagonists and converting enzyme inhibitors that lower blood pressure in SHR. Using the unlabeled antibody enzyme method, we have found a significant difference in the distribution of brain angiotensin in SHR and Wistar-Kyoto controls (WKY). Six rats of each group were perfused with buffered picric acid-paraformaldehyde, and their brains sectioned at 50 and 100 mu. The sections were reacted with a 1:1000 dilution of AII antiserum for 36 hours followed by goat antirabbit immunoglobulin G and rabbit peroxidase antiperoxidase. For controls, preabsorption with AII, arginine vasopressin or preimmune serum were evaluated. The results showed over twice as many cells and fibers staining for AII-like immunoreactivity in SHR. The AII immunoreactive cell bodies were localized, in the order of their relative preponderance, in supraoptic and paraventricular nuclei of the hypothalamus, hippocampus, and cortex. The most prominent demonstration of AII-like immunoreactivity was observed in fiber profiles containing densely stained varicosities, which were present in many neuroanatomical subdivisions of the brain and brain stem including anterior and middle hypothalamus, basal ganglia, thalamus, locus coeruleus, nucleus of the solitary tract, limbic structures, and reticular formation. The increased fiber staining in the SHR was particularly evident in the frontal hypothalamic region, medial preoptic, and stria terminalis. We conclude that the results support the hypothesis of brain AII involvement in hypertension.
Hypertension
PMID:Angiotensin-like immunoreactivity in the brain of the spontaneously hypertensive rat. 675 94

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

Three models of hypertension were induced in Wistar rats: (1) aortic ligature between renal arteries, (2) uninephrectomy and Na-rich diet, (3) uninephrectomy, 0.9 per cent NaCl as drinking fluid and subcutaneous administration of desoxicorticosterone acetate (DOCA). We studied the aortic endothelium during the early (7 to 10 days) and late (40 days) phases of these models and quantified: (1) thymidine index and cell density using autoradiography on en face preparations, and (2) internal aortic circumference by planimetry. We also examined by means of scanning electron microscopy the surface morphology of the aorta in rats with aortic ligature. Thymidine index was constantly increased in the early phases of all models; it reverted to normal levels in the late phases. Endothelial cell density was slightly but significantly increased in the early and late phases after aortic ligature and in the early phase after Na-rich diet; it increased strikingly in the early and late phases after DOCA. There were no significant correlations between the variations of the internal aortic circumference and blood pressure, thymidine index, or cell density. Scanning electron microscopy showed no discontinuity of the endothelial cell layer either in the early or late phases after aortic ligature; bulging of endothelial cells into the lumen and appearance of cell clusters with numerous surface projections were seen during the early phase after aortic ligature. These changes produce a remodeling of the aortic endothelial layer which is maximal in the early phase after aortic ligature and in the early and late phases after DOCA and correlates with the previously reported increase of endothelial permeability to horseradish peroxidase in the same hypertensive situations.
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PMID:Remodeling of the rat aortic endothelial layer during experimental hypertension. Changes in replication rate, cell density, and surface morphology. 682 89


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