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

Eleven freshly removed brains and 20 lenticulostriate arteries (collected at emergency surgery for intracerebral hemorrhage) were examined by electron microscopy in a search for the mechanism of arterial rupture in hypertensive intracerebral hemorrhage. Forty-six of 48 ruptured arteries examined showed severe arteriosclerosis including degenerative changes of the media at or near bifurcations. Atrophy and fragmentation of smooth muscle cells gave them a moth-eaten appearance. Material resembling basement membrane and cell debris was also present in the arterial walls. The above findings were restricted to the middle and distal portions of the perforating arteries. Rupture from a miliary aneurysm was observed in only 2 of the 48 specimens examined. These resembled saccular aneurysms, ultrastructurally. They seemingly formed at a cavity which we strongly felt may have been formed by complete or incomplete subclinical hemorrhages; reabsorption of the hemorrhage from the dissection resulted in the aneurysms seen. Degeneration of smooth muscle cells may be the result of prolonged tension or spasm of the arterial wall as a result of longstanding hypertension.
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PMID:Electron microscopic studies of ruptured arteries in hypertensive intracerebral hemorrhage. 682 83

1. Late cerebral arterial spasm was induced by repeated injections of autologous blood in a total amount of 14-33 ml into the basal cisterns of baboons to mimick subarachnoid hemorrhage (SAH). Regional cerebral blood flow (CBF), sagittal sinus pressure, cerebral arterial caliber from angiograms, and cerebral metabolic rate of oxygen (CMRO2) were measured before and after the experimental SAH to determine responses to hypercapnia and induced hypertension. The effect of the calcium antagonist, Nimodipine, on CBF autoregulation pre- and post-SAH was tested. 2. One week after the blood injections were started there was about 10-20% reduction, depending on territory measured, in the arterial diameter of the carotid and vertebral systems. This was associated with an 18% reduction in CBF and 9% decrease in the brain metabolism. 3. During hypercapnia before and after experimental SAH the flow increased with a mean of 3.7 and 1.8 ml, respectively, for each mm Hg elevation of PaCO2. In control animals, graded angiotensin-induced hypertension did not overtly affect CBF. Following SAH, the CBF autoregulation was impaired in 5 of 6 animals tested. 4. I.v. infusion of Nimodipine markedly curtailed the CBF autoregulation in pre-SAH animals and, to a somewhat slighter extent, also in post-SAH animals.
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PMID:Late cerebral arterial spasm: the cerebrovascular response to hypercapnia, induced hypertension and the effect of nimodipine on blood flow autoregulation in experimental subarachnoid hemorrhage in primates. 682 30

Approximately 6 per cent of placentae of babies admitted to a special care paediatric unit show evidence of peripheral villous stem branch oedema. In more than half of these cases there is evidence of fibrinous vasculosis (FV) in truncal veins. The affected placentae are generally thick and of small diameter, often of extrachorialis type, very congested and often cyanosed. The aetiology of the lesions is discussed with reference to abnormal fetal vascular patterns, poor perfusion, anoxia, oedema and spasm and the effect such factors may have on vessels with an irregularly distributed muscle coat and tendency to a spiral course. A small heterogeneous group with FV lesions unassociated with stem branch oedema was also identified. Chorionic vessels were more commonly involved in this group, and it would seem that, in addition to the other factors mentioned above, pressure variations may have some aetiological significance. Lesions of FV occurred mainly in mature placentae. The mothers showed a high incidence of pregnancy-induced hypertension and other complications. Fetal distress and asphyxia at birth were common. Where chorionic vessels were involved there was a high risk of intrauterine death (40 per cent) and coagulopathy among survivors (46.7 per cent). FV lesions affecting truncal vessels carried no greater risk than truncal arterial thrombotic lesions, which have been assessed in the past. In both these groups the hypoxia and intrauterine growth retardation which the babies showed are probably the most important factors, though one could postulate that their clotting mechanism was already triggered.
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PMID:Fibrinous vasculosis in the human placenta. 685 90

All contributory factors to the unusual occurrence of stroke in young people were evaluated in patients under age 40 admitted to the Stroke Unit of the Austin Hospital in Melbourne, Australia. Over the August 1977 to December 1980 period there were 700 admissions. Of these 14 patients were under the age of 40. There were 7 males and 7 females whose ages ranged from 17-38 years. Each patient was screened for factors which might contribute to premature vascular disease including hypertension, diabetes, smoking, obesity, and hyperlipidemia. In addition, the following tests were performed to exclude an arteritic process: full blood examination; ESR; protein electrophoresis; syphilis serology; and the presence of antinuclear factor. Each of the 14 patients suffered cerebral infarction. A summary of each case is presented in a table. In 9 patients, infarction occurred in the carotid territory of supply. Large cortical infarcts with or without subcortical involvement occurred in cases 1-8, of whom 5 had major vessel occlusion demonstrated angiographically and another had stenosing and ulcerative atheromatous disease at the extracranial carotid bifurcation. In a further 4 patients, infarction occurred within the vertebrobasilar territory and was either confined to the brain stem, the occiptal cortex, or involved both. Angiograms were performed in 2 of these patients and showed irregular narrowing of the vertebral artery which was interpreted as spasm and segmentally narrowing of the basilar artery. The final patient had several ischemic events which included right sided amaurosis fugax, and left frontal, right parieto-occipital and left occipital infarctions. Angiography was normal. All patients survived the stroke and were able to go home. There may be an interrelationship between the pathological findings of Irey et al. (1978) and the effect oral contraceptives (OCs) has on migraine. This is relevant to Case 13. Sustained exposure to OCs may produce the pathological changes described (visible as segmental narrowing angiographically). In 2 patients cerebral infarction was caused by atheromatous or hypertensive occlusive vascular disease. In Case 3 an embolus occluded the middle cerebral artery. Infarction complicating migraine was diagnosed confidently in 4 patients on the basis of typical migrainous symptomatology in the past and accompanying the stroke. Of the 12 patients fully evaluated, there were no cases of polycythemia or thrombocytosis. There were no abnormalities of the clotting factors. Almost every patient had some form of emotional upset, and there were 7 who had significant psychiatric illness and emotional problems of extreme magnitide.
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PMID:Stroke syndromes in young people. 692 82

As we age, our arteries elongate and our brains "sag." As a consequence of these processes, redundant arterial loops and bridging or intrinsic hindbrain veins may cause cross-compression of cranial nerve root entry zones in the cerebellopontine angle. This pulsatile compression can be seen to produce hyperactive dysfunction of the cranial nerve. Symptoms of trigeminal or glossopharyngeal neuralgia (somatic sensory), hemifacial spasm (somatic motor), tinnitus and vertigo (special sensory) and some cases of "essential" hypertension are caused by these vessels compressing cranial nerves V, IX--X, VII, VIII, and left X and medulla oblongata. Using microsurgical techniques, the symptoms may be relieved by vascular decompression, findings and results in 695 paients are briefly reviewed and correlated. A chronic primate model of "essential" hypertension is briefly described.
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PMID:Neurovascular compression in cranial nerve and systemic disease. 696 43

Rupture of a cerebral aneurysm during angiography, with confirmation by computed tomography (CT), is described. A review of 30 additional reported cases demonstrates no unusual profiles, with the exception of the predominance of female patients (71%), and the presence of pre-angiographic arterial hypertension. Experimental and clinical evidence increasingly suggests that intravascular pressures are transiently elevated during cerebral angiography. These changes may be enhanced by increased flow rates of contrast media, smaller diameters of the catheters, and the presence of intracranial arterial spasm, the latter presenting as a very prominent feature in intra-angiographic arterial rupture. However, direct evidence of elevation of the intra-aneurysmal pressure has not been documented, and may have occurred in only a portion of the cases.
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PMID:Cerebral aneurysmal rupture during angiography with confirmation by computed tomography: a review of intra-angiographic aneurysmal rupture. 698 59

The calcium channel blocking agents have multiple hemodynamic effects that make them potentially valuable in treating many cardiovascular disorders. They are potent dilators of coronary and peripheral arteries and in isolated tissue preparations exert potent negative inotropic, chronotropic, and dromotropic effects. In intact animals the peripheral arterial vasodilatation induces reflex-mediated adrenergic activity, which opposes the direct negative inotropic, chronotropic, dromotropic, and hypotensive effects. The individual calcium channel blockers have different relative potencies on various cardiovascular functions. The net hemodynamic and electrophysiologic effect of each agent, therefore, results from a complex interplay of direct and reflex phenomena. The clinical efficacy of these agents in classic angina pectoris relates to their ability to decrease afterload, myocardial contractility, and heart rate and increase coronary blood flow. The agents have been used to prevent coronary spasm in Prinzmetal's variant angina. The negative inotropic effects of verapamil are valuable in improving the symptoms and hemodynamic disturbances of hypertrophic cardiomyopathy. The role of these agents in treating arterial hypertension, unstable angina pectoris, acute myocardial infarction, and ischemia during cardiopulmonary bypass needs to be determined.
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PMID:Calcium channel blocking agents in the treatment of cardiovascular disorders. Part II: Hemodynamic effects and clinical applications. 700 93

Vascular spasm has been considered to be an important component of the eclamptic state. If this abnormal vascular reactivity affects the coronary arteries in eclampsia, one might expect to find areas of myocardial contraction band necrosis, a lesion secondary to coronary reflow after periods of no flow. We reviewed the cardiac findings in the 34 patients with fatal eclampsia (hypertension, edema, proteinuria, and convulsions without evident cause) autopsied at The Johns Hopkins Hospital since 1899, and compared each with the next pregnant or puerperal nontoxemic autopsied patient. The eclamptic patients were 15-45 years old (average 27 years). Convulsions began antepartum in 21 patients, intrapartum in eight, and postpartum in five. The hearts weighed 200-407 g (average 312 g). One heart had rheumatic valvular disease and one had myocarditis. Histologic study of heart sections showed the presence of contraction band necrosis in 12 cases (35%). The control cases included two patients with rheumatic valvular disease, two with endocarditis, two with myocarditis, two with pericarditis, and one with leukemic infiltration. Only one control patient (3%) had contraction band necrosis (p less than 0.001). The frequent occurrence of myocardial contraction band necrosis suggests that coronary artery spasm may be common in patients who die with eclampsia.
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PMID:Morphologic evidence for coronary artery spasm in eclampsia. 719 18

The postoperative intracranial pressure (ICP) in 36 patients operated on for cerebral aneurysm following subarachnoid hemorrhage was studied. Not only was the baseline ICP significantly lower in patients whose outcome was assessed as "good" as compared with those patients with a worse outcome at 1 month after surgery, but also the height of the plateau waves and B-waves was significantly less in the patients who did well. The baseline ICP and the height of the B-wave formation were unrelated to the position of the aneurysm. Plateau waves were marginally significantly higher in aneurysms of the anterior communicating artery complex. Neither preoperative hypertension nor the use of antifibrinolytic agents made any difference to postoperative ICP. In patients with cerebral arterial vasospasm found preoperatively on the angiograms, the ICP tended to be lower in the postoperative period than in those without spasm.
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PMID:Postoperative intracranial pressure in patients operated on for cerebral aneurysms following subarachnoid hemorrhage. 724 Nov 81

Recently it has been recognized that coronary vasospasm plays a significant role in precipitating myocardial ischemic pain in a significant minority of individuals with coronary atherosclerosis (approximately 27-35% of patients with angina pectoris at rest). In these individuals normal physiological vasoconstrictor stimuli appear to trigger a spasm of the large epicardial coronary vessels; evidence suggests that it may be caused by the release of increased amounts of calcium from augmented sarcolemmal storage sites. The calcium entry blockers are remarkably effective in preventing coronary spasm by reducing intracellular calcium, but by different mechanisms. Verapamil appears to reduce intracellular and, more specifically, sarcolemmal calcium stores directly. Diltiazem appears to reduce intracellular calcium by stimulating the sarcolemmal sodium-potassium pump and reducing intracellular sodium, and by this mechanism. potentiating passive sodium-calcium exchange. The effects of the calcium entry blockers on myocardial contractility, cardiac pacemaker and conduction tissue, and regional vascular smooth muscle are also different. This makes some of these agents more suitable than others for therapy of other clinical problems such as chronic stable angina pectoris, supraventricular tachycardia, hypertension, hypertropic cardiomyopathy, and protection of the ischemic myocardium during cardiac surgery.
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PMID:Clinical use of calcium entry blockers. 730 98


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