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

Changes in auditory brain-stem responses (BER's) and somatosensory evoked responses (SER's) were investigated to correlate mass volume, intracranial pressure, and neurological dysfunction in mass-induced intracranial hypertension in cats. As the intracranial pressure was raised by expansion of a supratentorial balloon, the late components of the SER's were suppressed first, followed by the early components of the SER's, then Wave V and Wave IV of the BER's, in that order. This suggests that the nonspecific reticular projections are most vulnerable to compression ischemia, and the specific somatosensory pathways are the next most vulnerable. Neural activity of the auditory pathways in the upper brain stem was also gradually suppressed, but less so than that of the somatosensory pathways. After complete transtentorial herniation, in spite of immediate mass evacuation, the function of the somatosensory pathways was greatly impaired, often irreversibly. The neural activity of the auditory pathways in the upper brain stem revealed progressive recovery during a 3-hour period. The measurements of BER Wave V is thought to be useful in predicting transtentorial herniation.
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PMID:Acute intracranial hypertension and auditory brain-stem responses. Part 1: Changes in the aduitory brain-stem and somatosensory evoked responses in intracranial hypertension in cats. 50 7

Eighteen patients with idiopathic optic neuropathy lacked symptoms and signs of cardiovascular and cerebrovascular disease, especially when compared to three groups of patients with sudden visual loss caused by retinal infarction, transient ischemia, and cerebral infarction. Many patients in the latter groups had hypertension, carotid bruits, heart disease, transient ischemic attack, and stroke. But among the patients with ischemic optic neuropathy, hypertension was the only evidence of cardiovascular disease, affecting 44% of the patients. We argue that, in many cases, ischemic optic neuropathy represents a direct and early complication of hypertension arterial disease affecting small arterioles supplying the anterior part of the optic nerve. The pathologic process may thus be similar or identical to lacunar infarction of the brain.
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PMID:Ischemic optic neuropathy as a possible early complication of vascular hypertension. 51 8

Dahl 'S' rats become hypertensive when fed a high NaCl diet but remain normotensive on a low NaCl diet. Dahl 'R' rats are normotensive on either diet. For a given perfusion pressure, isolated 'S' kidneys excrete 50% less Na than 'R' kidneys. Therefore, we searched for a Na-retaining hormone in 'S' rats. Kidneys were isolated without ischemia from normal rats and were continuously perfused at 125 mm Hg with blood from Dahl 'S' and 'R' rats, all on low NaCl diets. Kidneys and adrenals had been extirpated from the perfusing rats. During 15 min of perfusion, the isolated 'normal' kidneys excreted a mean of 164 micronEq of Na/min/100 g during 26 perfusion experiments with blood from 'R' rats. The 'normal' kidneys excreted a mean of 84 micronEq Na during 24 perfusions with blood from 'S' rats. Thus, the normal kidneys excreted half as much Na when perfused with 'S' blood compared with 'R' blood (p less than 0.02). Seemingly, a Na-retaining humoral agent is present in the blood of 'S' rats on a low Na diet in the absence of renal and adrenal tissue. Moreover, in these normal kidneys, perfusion with 'S' blood induced a 16% higher renal vascular resistance than perfusion with 'R' blood (p less than 0.01), indicating vasoconstricting agents in 'S' blood. However, the Na-retaining humoral effect in 'S' blood could lead to Na retention by 'S' kidneys in vivo, which could partially account for the susceptibility of 'S' rats to NaCl hypertension. Hypertension in Dahl 'S' rats can be almost completely prevented by concomitant treatment with thiazide diuretics which act mainly on the kidney to facilitate Na excretion. This result is in agreement with the hypothesis that a shift in the pressure natriuresis curve, reducing Na excretion for a given arterial pressure, is partially responsible for the great sensitivity to NaCl hypertension in the 'S' rat. The Na-retaining hormone may contribute to this shift.
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PMID:Evidence for Na-retaining humoral agents and vasoconstrictor humoral agents in hypertension-prone Dahl 'S' rats. Prevention of NaCl-induced hypertension in Dahl 'S' rats with thiazide. 53 85

Subcortical arteriosclerotic encephalopathy, a chronic vascular dementia with hydrocephalus, was characterized pathologically in five patients by severe thickening of small vessels and by diffuse regions of white matter loss with gliosis. Lacunar infarcts were also present. The clinical picture in 11 patients was characterized by: (1) persistent hypertension and systemic vascular disease; (2) acute strokes; (3) subacute accumulation of focal neurologic symptoms and signs over weeks to months; (4) long plateau periods; (5) lengthy clinical course; (6) dementia; (7) prominent motor signs and pseudobulbar palsy and; (8) hydrocephalus. The pathogenesis of subcortical arteriosclerotic encephalopathy is unknown; possible mechanisms include diffuse ischemia and fluid transudation with subsequent gliosis related to subacute hypertensive encephalopathy.
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PMID:Clinical features of subcortical arteriosclerotic encephalopathy (Binswanger disease). 56 79

Ischemic cardiopathies in Eastern Africans at Djibouti are frequent: 2.9 % of the in patients and 73 % of the cardiac diseases. Male prevalence is marked. Coronary insufficiency is most often demonstrated by the usual symptomatology. Three groups of electrocardiopathic manifestations have been individualised: ischemia proving angor (288 cases), anginose syndromes revealing a myocardic infarct (81 cases), acute myocardic infarcts (62 cases). The patients come for the most part from Djibouti and belong to any social class. The part played by a food mainly constituted of complex glucids, refined sugar and lipids is pointed out. Arterial hypertension, diabetes, essential hypercholesterolemia and tobacco intoxication are the most frequent risk factors. This coronary pathology is closer the one met with in the Near East than ischemic cardiopathies observed in tropical Africa which begin to emerge.
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PMID:[Ischemic cardiopathies in Africans in Djibouti. Study of 431 cases in 5 years]. 58 Sep 20

We present clinical and electrophysiological data on 9 patients with paroxysmal reciprocating sinus tachycardia (PRST) of whom only 6 described palpitations. Sinus node disease was present in 5 and cardiac ischemia and/or hypertension in another 3; the remaining case had apparently coincidental Wolff-Parkinson-White (WPW) syndrome. PRST could be initiated in all cases, and terminated in the 4 in whom it was sustained, by suitably timed atrial premature beats over a zone that was dependent on the effective atrial extrastimulus coupling interval (A1-A2) in the high right atrium (HRA). The sequence of atrial depolarization during PRST was similar to that of sinus beats although minor changes in both the P wave and the configuration of the HRA electrogram were observed in half the cases. During paroxysms, cycle length variation and sensitivity to alterations in vagal tone were common. In 6, paroxysms could be initiated by moderately rapid atrial pacing. Repetitive attacks were usually initiated by increases in the sinus rate and not be an antecedent premature atrial extrasystole. Verapamil suppressed sinus node reentry in 5 patients while small doses of atropine favored initiation in 3. PRST was seen in association with AV reentry tachycardias in the patient who had the WPW syndrome.
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PMID:Paroxysmal reciprocating sinus tachycardia. 59 Feb 95

Severe renin-mediated hypertension was noted in 2 children as a result of selective renal damage from vesicoureteral reflux during the early years of life. In each case the reflux had been corrected successfully long before hypertension developed. In 1 case the late damage involved only 1 kidney and nephrectomy resulted in immediate relief of the hypertension. In the second case, even though both kidneys showed segmental scarring from calicectasis and chronic pyelonephritis, removal of the atrophied lower pole of 1 kidney made hypertension amenable to medical treatment and reduced excessive renin output to a fraction of the original high levels. The mechanism of renin-mediated hypertension in kidneys with segmental scars of chronic pyelonephritis is believed to be ischemia of the relatively normal renal cortex in proximity to areas of interstitial fibrosis, within which are tortuous interlobular and smaller arterioles with severe intimal thickening. Hypertrophy of normal renal segment occurs in young patients with segmental chronic pyelonephritis. To accommodate this enlargement the original calix develops an extension or elongation readily distinguishable from other dilated calices.
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PMID:Malignant hypertension in children secondary to chronic pyelonephritis: laboratory and radiologic indications for partial or total nephrectomy. 61 6

This report describes a case of bilateral post-traumatic carotid-carotid-cavernous fistulae (CCF), of both typical and atypical types, with delayed clinical deterioration. Unusual neuropathological lesions, distinctive from those due to direct cerebral trauma, are related to combined arterial ischemia and venous hypertension. Atypical CCF is not necessarily a benign disorder. Radiological monitoring is essential to detect spontaneous progressive intracranial shunting, to predict areas that are at risk from venous hypertension, and to identify remote sites of circulatory vulnerability.
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PMID:Bilateral carotid-cavernous fistulae of mixed types with unusual radiological and neuropathological findings. 61 11

Although many patients with coronary artery disease (CAD) have a positive exercise test without pain, the frequency and significance of this "silent" ischemia is unclear. Therefore, we studied 122 consecutive clinically stable patients with angiographically defined CAD (greater than 75 per cent luminal stenosis) and a positive exercise test. Seventy-eight patients had pain or anginal equivalent during or after a positive exercise test; 44 did not, including 32 (26 per cent) with no symptoms at all. Patients were evaluated as to age, sex, prior myocardial infarction, congestive failure, hypertension, diabetes mellitus, and digoxin or propranolol therapy--in addition to anginal symptoms before, during, or after the exercise itself. Extent of CAD, presence of collaterals, and left ventricular ejection fraction were also determined. All exercise tests were evaluated for evidence of ST-T abnormalities or prior infarction on the control ECG as well as peak heart rate during exercise and post-exercise degree of ST segment depression. There were no significant differences between patients with and without exercise-induced pain in regard to any of the clinical and angiographic features noted above, demonstrating that "silent" myocardial ischemia during or after exercise testing is not uncommon and is not readily attributable to any obvious clinical or catheterization findings. Further studies are necessary to determine if patients with evidence of "silent" myocardial ischemia are especially prone to sudden death.
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PMID:"Silent" myocardial ischemia during and after exercise testing in patients with coronary artery disease. 63 80

The left ventricular dysfunction following acute pulmowary hypertension remains unexplained. We wondered if acute pulmonary hypertension could alter the transmural flow distribution within the left ventricular myocardium, independent of coronary flow and perfusion pressure. We used a canine preparation in which the left coronary system was perfused at constant flow and induced a two- to three-fold increase in pulmonary artery pressure by banding the pulmonary artery. Regional myocardial blood flow of the left coronary system was measured using radioactive microspheres, injected into the left coronary system before and after 10-30 min of banding of the pulmonary artery. The left ventricular subendocardial:epicardial ratio fell by 12 and 31% (p less than 0.05) of control value, 10 and 30 min, respectively, after banding of the pulmonary artery, the total flow to the left coronary system being kept constant. Left atrial mean pressure increased from 2.9 +/- 2.4 to 3.6 +/- 1.9 and 6.0 +/- 2.1 (p less than 0.05) following banding. The mechanism of the redistribution of coronary flow may relate to inappropriate vasodilation of the right septal myocardium with consequent relative left ventricular subendocardial hypoperfusion which might aggravate left ventricular ischemia in the presence of hypotension and hypoxia.
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PMID:Redistribution in left ventricular regional flow following acute right ventricular pressure overload. 63 69


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