Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal diseases have been recognized as both a cause and a consequence of hypertension. Orthostatic renal hypertension is caused by ischemia resulting from elongation, twisting and angulation of renal vessels when a hypermobile kidney is present. Recent observation of a 22-year-old woman in whom orthostatic renal hypertension was cured by nephropexy prompted this report. Clinical manifestations, diagnosis and therapy of this condition are also discussed.
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PMID:[Hypertension and nephroptosis]. 205 70

An 11-year-old boy with slowly progressive gangrene caused by vasculopathy similar to that of neurofibromatosis (NF) type 1 (NF I; von Recklinghausen disease [NFvR]) and a newborn girl with idiopathic gangrene with vascular changes resembling those of NFvR prompted the analysis of all 105 propositi with NF (NF I and NF II) evaluated between January 2, 1982, and December 31, 1986, at the genetics clinic of University of South Florida. They were analyzed for renal hypertension, symptomatic ischemia, and known vascular changes. One additional 27-month-old boy with NFvR was found to have extensive vascular changes with renal hypertension. The vasculopathy indicated asymmetric over/undergrowth of cellular and extracellular components of the vascular wall and implied dysregulation of the paracrine growth mechanism. Immunocytochemical studies of affected vessels were done only in the 11-year-old boy and showed positive neuron-specific enolase, S-100 protein, and glial fibrillary acidic protein (GFAP) reactions indicative of Schwann cell involvement. The vascular changes in children with NFvR are mostly asymptomatic; however hypertension secondary to renal artery stenosis and/or Moya-moya disease have been reported infrequently. Our patients with vasculopathies provoked thoughts in regard to the so-called vascular NF, its place in current NF nomenclature and classification, relationship to fibromuscular dysplasia (FMD), and possible role in infantile gangrene.
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PMID:"Vascular neurofibromatosis" and infantile gangrene. 251 May 17

In rats with artificial renal hypertension, the amount of erythrocytes in the blood was increased in 43% of cases within 2-3 months after surgery. Diverse changes of the blood oxygen-transport properties indicate several mechanisms of the organism adaptation to changes in oxygen regiment in response to the arterial pressure increase due to ischemia of renal tissue: an increase in the blood oxygen capacity; changes of the hemoglobin oxygen-binding properties. The parameters under study, except the arterial pressure, did not differ from the control ones in a number of experimental animals.
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PMID:[Oxygen transport properties of the blood in experimental renal hypertension in the rat]. 309 88

We have previously shown that dogs with renal hypertension and left ventricular hypertrophy have larger infarcts (per risk area size) than do control animals. A potential explanation for this is that collateral resistance is higher in these dogs. Paradoxically, previous postmortem studies in human hearts with left ventricular hypertrophy have suggested that coronary collaterals are actually increased in this condition. To test the hypothesis that left ventricular hypertrophy is associated with alterations in coronary collateral resistance, studies were performed in dogs with renal hypertension and left ventricular hypertrophy and in patients with aortic valvular disease at the time of cardiac surgery. With an isolated, adenosine-vasodilated, blood-perfused cardiac preparation, collateral and normal zone pressure-flow relationships were established by means of radioactive microspheres in nine dogs with renal hypertension and left ventricular hypertrophy and in 17 controls. Collateral resistance calculated from these pressure-flow relationships were similar in both groups (4.0 +/- 0.7 in dogs with renal hypertension and left ventricular hypertrophy and 3.9 +/- 0.4 mm Hg/ml/min/100 g in controls). In addition, normal zone resistance was not different between groups (transmural resistances 0.17 +/- 0.01 in controls and 0.18 +/- 0.02 in dogs with renal hypertension and left ventricular hypertrophy. In five patients with aortic valve disease, left ventricular hypertrophy, and normal coronary arteries and in six patients without left ventricular hypertrophy who had normal left anterior descending coronary arteries, a 7 MHz suction-mounted echo transducer was used to monitor systolic wall thickening during transient occlusions of the left anterior descending artery at the time of cardiac surgery. Because noncollateralized myocardium ceases to contract promptly after coronary occlusion, this approach provides an indirect index of collateral perfusion. Twenty seconds after the onset of coronary occlusion, systolic thickening had markedly decreased in both groups (15 +/- 10% of control values in nonhypertrophied hearts and 10 +/- 10% in hearts with left ventricular hypertrophy; p = NS between groups). Thus the severity of contraction abnormality induced during transient coronary occlusion in these two groups of patients was similar, suggesting that the degree of severity of ischemia was comparable between the two groups. We conclude that collateral resistance is not altered by hypertension and left ventricular hypertrophy and that left ventricular hypertrophy in patients is not associated with functional evidence of an enhanced collateral circulation.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The effect of cardiac hypertrophy on the coronary collateral circulation. 315 52

Over a 10-year period, positive criteria of the Howard test and the Rapoport Index have shown consistently good correlation with sustained relief or marked improvement in hypertension, in patients with main renal artery lesions. Similar correlation was obtained with ischemic criteria from histopathologic studies.Differential function studies did not reveal positive ischemic criteria in any patient operated upon for unilateral parenchymal disease. Histopathologic criteria of ischemia were also infrequent in this group. Nevertheless, marked improvement or cure of hypertension occurred in 62% of the latter. No factor can be used to predict improvement in this type of renal hypertension. Differential renal function criteria may occasionally appear to indicate renal artery ischemia in the more normal kidney in patients with unilateral parenchymal renal disease; wrong interpretation is avoided by taking differential creatinine clearance into account. Until vasopressor substances can be easily measured and accurately interpreted, aortography is indicated in selected patients.
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PMID:Differential renal function studies in the diagnosis of renal hypertension. 543 68

Systolic wall thickening abnormalities are sensitive indicators of ischemia and infarction. One purpose of this investigation was to assess the relation between coronary risk area, infarct size and wall thickening abnormalities (dyskinesia) using 2-dimensional echocardiography (2-D echo) in a closed-chest conscious dog model of acute myocardial infarction. The second purpose was to study the effects of systemic hypertension (SH) and left ventricular (LV) hypertrophy on these relations. Our hypothesis was that the infarct size and the extent of 2D echocardiographic dyskinesia would be quantitatively different in SH-LV hypertrophy, a condition in which coronary vascular reserve is diminished. Permanent circumflex coronary occlusion was performed in 15 conscious normal dogs and in 14 dogs with LV hypertrophy secondary to renal hypertension. Two-dimensional echocardiograms were obtained before, 20 minutes after and 2 days after coronary occlusion. The systolic wall thickening along 12 equidistant radii was analyzed in short-axis images. Percent dyskinesia on 2-D echo was defined as the percentage of radii showing systolic thinning. Infarct size was determined pathologically and risk area was determined angiographically. For a given risk area, coronary occlusion resulted in a larger infarction in dogs with SH-LV hypertrophy than in normal dogs (p less than 0.05). Two-dimensional echocardiographic dyskinesia correlated well with infarct size both at 20 minutes (r = 0.92) and 2 days (r = 0.94); dyskinesia modestly overestimated the infarct size and underestimated the risk area. The relations were similar in both normal and SH-LV hypertrophy groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relations between 2-dimensional echocardiographic wall thickening abnormalities, myocardial infarct size and coronary risk area in normal and hypertrophied myocardium in dogs. 622 35

The present study was carried out on male rats, using three models of experimental hypertension: cerebroischemic, single clamp bilateral and combined, induced by ischemia of the brain and one of the kidneys. The authors determined DA, NA, A in the hypothalamus and medulla oblongata as well as A, NA in plasma in view of the connection between CA (catecholamine) and cerebral and renal renin-angiotensin system (RAS). In rats with cerebral hypertension there was activation of noradrenergic neurons in the hypothalamus and medulla oblongata. There were no changes in the content of A. In rats with renal hypertension the activation of noradrenergic neurons in the hypothalamus was due to exhaustion of NA stores with normal amount of DA, but still the adrenergic neurons were activated. In rats with combined hypertension there was lowering of NA and DA in the hypothalamus, but A was not altered, e.g. the changes, observed singly and in cerebral and renal hypertension were combined. In the three forms of hypertension there were similar changes in medulla oblongata (reduced DA, increased NA and unaltered) and in plasma (A without significant changes). The changes in the level of CA in cerebral and combined hypertension could be explained by a change in the sinocarotid reflex, but in the renal-with the increased level of plasma angiotensin. The authors suggest that the connection between cerebral CA and cerebral RAS is not a direct one and RAS is not directly involved in the inverse interrelationships between cerebral and renal RAS.
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PMID:[Central and peripheral catecholamines in combined cerebral and renal hypertension]. 701 87

Primary clinical manifestations in patients with Takayasu arteritis are mostly unspecific signs of inflammation. First involved are the main brachiocephalic arteries and the aorta. Later the disease becomes symptomatic through organ ischemia. Often a renal hypertension appears due to an arteritic stenosis of the renal artery. Here we present a patient suffering from Takayasu arteritis. The disease first appeared with renal hypertension and an encephalopathy. The hypertension was induced by compression of the right renal artery which in turn was caused by an aortic aneurysm. The aneurysm had been resected and the aorta was reconstructed by aorto-aortal prosthetic interposition and implantation of the renal arteries. The postoperative course was uneventful.
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PMID:[Atypical initial manifestation of Takayasu arteritis]. 867 2

We have compared the myocardial alterations in rats made hypertensive by the chronic inhibition of nitric oxide biosynthesis with those having renal hypertension (two kidney-one clip model). Male Wistar rats were chronically administered the nitric oxide synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME) for 2, 4 and 8 weeks. Both groups initially developed a similar increase in blood pressure but only the 2K-1C rats developed myocardial hypertrophy after 2-4 weeks. L-NAME-treated animals developed a similar degree of hypertrophy following 8 weeks of treatment. As observed by light microscopy, the myocardial alterations in the latter animals consisted of extensive areas of fibrosis and myocardial necrosis, especially in regions of the subendocardium. The histological alterations induced by L-NAME were not caused by the accompanying hypertension, since the 2K-1C animals had a similar increase in arterial blood pressure without any significant alterations in the heart morphology. 2K-1C rats treated chronically with L-NAME behaved in a manner similar to the L-NAME-treated animals with regard to both the blood pressure increases and cardiac morphological alterations. Animals which received the inactive enantiomer D-NAME did not develop hypertension nor did they have any morphological abnormalities. Both the coronary flow and the contractile capacity of hearts isolated from rats treated with L-NAME for 8 weeks were impaired compared to control animals. These results indicate that the chronic inhibition of NO biosynthesis causes cardiac ischemia associated with a mechanical dysfunction that is unrelated to cardiac hypertrophy which is similar to those seen in some patients suffering from chronic arterial hypertension.
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PMID:Chronic nitric oxide inhibition as a model of hypertensive heart muscle disease. 883 44

Angiotensin converting enzyme inhibitors (ACEIs) not only reduce angiotensin II synthesis but also potentiate endogenous kinins. In addition to their antihypertensive actions, accumulated evidence has demonstrated an improvement by ACEIs of cardiac function, cardiac structural and metabolic status, and myocardial blood flow in conditions such as cardiac ischemia, left ventricular hypertrophy, and myocardial infarction. The mechanisms underlying the antihypertensive and cardioprotective actions of ACEIs are under intensive investigation. A reduction of angiotensin II synthesis is undoubtedly responsible for a major part of the antihypertensive effects of ACEIs. However, in experimental renal hypertension but not in genetic hypertension, bradykinin potentiation has been shown to partially mediate the acute and chronic antihypertensive actions of these drugs. In addition, experimental observations suggest that bradykinin potentiation plays a pivotal role in the cardioprotective effects of ACEIs.
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PMID:Role of bradykinin in the antihypertensive and cardioprotective actions of converting enzyme inhibitors. 884 16


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