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

Although indapamide has been used for many years as a first-line treatment of hypertension, it is only recently that some of its activities on the changes of the cardiovascular system, brought on by age and high blood pressure, have been studied. Indapamide appears to reduce blood pressure by a combined diuretic and direct vascular activity reducing vascular reactivity and total peripheral resistance. In addition, it has discrete effects on a number of interrelated systems that may protect the cardiovascular system. Indapamide reduces intracellular calcium levels, maintains magnesium ions, but reduces phosphate ions that may be involved in arterial rigidity. Circulating catecholamines remain unchanged but there is a reduction in normetanephrine, suggesting a reduction in sympathetic tone. It stimulates prostacyclin synthesis, increases levels of circulating prostacyclin, reduces platelet aggregation and stimulates the vasodilation elicited by endothelium-derived relaxing factor in the presence of bradykinin. In addition, it inhibits the formation of the vasoconstrictor prostanoid, thromboxane A2. The free radical scavenging activity of indapamide could also protect the vascular smooth muscle from the reperfusion injury of cerebral and myocardial ischemia. Indapamide induces a reduction in cerebral ischemia after carotid ligation. Unlike some other antihypertensives, it does not upset the high-density/low-density lipoprotein-cholesterol balance, reducing the possible risk of atherosclerosis. Moreover, the combination of binding to elastin and reduction in uptake of calcium and phosphate into the smooth muscle could be a mechanism for reducing arterial rigidity seen in the elderly and hypertensive patient. In hypertensive patients, these properties induce an improvement in arterial compliance, and in the long term a reduction in left ventricular hypertrophy. These pharmacologic and clinical results, together with a good antihypertensive efficacy and acceptability, suggest that indapamide may be a preferential agent in the long-term cardiovascular protection of the hypertensive patient.
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PMID:Cardiovascular protective properties of indapamide. 218 50

There can be no doubt about the relevance of various established risk factors of stroke, which therefore will not be discussed. When trying to manipulate factors as hypertension, hyperlipoproteinemia and smoking, in most cases an improvement of the flow properties of blood can be observed. This makes flow properties at least very likely to trigger cerebral ischaemia and stroke. Furthermore there is increasing evidence, that single factors, contributing to a deterioration of blood rheology (i.e. haematocrit, fibrinogen, plasma viscosity, red cell rigidity) may be considered risk factors of apoplexie depending on the quality of interaction. There seem to exist positive correlations to the extent of atherosclerotic alterations of the vessel system. Blood viscositiy and red cell aggregation can be interpreted as the respective state of different pathologic profiles of blood rheology and thus might reach pathologic levels already before it is notified by single factors. In conclusion there is a good chance for blood viscosity and red cell aggregation to play an independent role as risk factors of apoplexie derived from cerebral ischaemia.
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PMID:[Rheologic risk factors of apoplexy]. 220 40

Global cerebral ischemia (four vessel model) was induced in renovascular hypertensive rats (two kidney, one clip model) chronically treated with intraperitoneal administration of angiotensin I converting enzyme inhibitors, either captopril (100 mg/kg per day) or Wy-44,655 (10 mg/kg per day). Mortality following cerebral ischemia was higher in renovascular hypertensive rats than in normotensive controls. Reduction of blood pressure with captopril or Wy-44,655, lowered mortality. In surviving renovascular hypertensive and normotensive rats cerebral ischemia induced hyperactivity and lesions of the CA1 area of the hippocampus. Prolonged treatment with captopril--but not with Wy-44,655--reduced hyperactivity and the extent of the CA1 lesions. In conclusion, hypertension increases mortality following cerebral ischemia but does not affect the extent of brain injury in survivors. Prior treatment with converting enzyme inhibitors lowers mortality. Treatment with captopril attenuates brain injury in survivors.
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PMID:The angiotensin I converting enzyme inhibitors, captopril and Wy-44,655 attenuate the consequences of cerebral ischemia in renovascular hypertensive rats. 220 71

Between 1984 and 1989, orthotopic cardiac transplantations were done in 90 patients from 10 to 65 years of age for end-stage, refractory congestive cardiomyopathy. Two patients had had ischemic strokes 5 months and 18 years, respectively, before transplantation. Six patients (7%) suffered acute neurologic events perioperatively. Three patients suffered cerebral infarctions. In 1 case this occurred 10 days before transplantation--probably as a result of systemic hypoperfusion--with the placement of ventricular assist devices. Two others suffered infarctions 5 and 21 days, respectively, after transplantation, each of probable embolic origin. Two patients had an acute intracerebral hemorrhage 21 and 36 days, respectively, after transplantation; both were located within the basal ganglia and subcortical regions. Both patients had moderate to severe hypertension, and in 1, renal failure and a coagulopathy developed before hemorrhage. Tremor, seizures, and an altered level of consciousness developed in 1 patient as an apparent toxic reaction to cyclosporine treatment. Only 1 patient died as a result of the neurologic complication--of an acute intracerebral hemorrhage. Three patients recovered fully, 2 partially. Only the case of drug toxicity could be directly attributed to the transplantation procedure itself. We conclude that the risk of an acute neurologic insult with orthotopic cardiac transplantation is low but may result from drug toxicity, cerebral ischemia, or hemorrhagic mechanisms.
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PMID:Neurologic complications of cardiac transplantation. 221 70

Several mechanisms impair cerebral vasodilatation during chronic hypertension. First, the external diameter of cerebral arterioles is reduced during chronic hypertension by structural 'remodeling'. Thus, both vascular hypertrophy and remodeling result in encroachment on the lumen. Second, endothelium-dependent dilatation of cerebral vessels is impaired during chronic hypertension. Third, blood flow through cerebral collaterals is impaired by chronic hypertension, so that an important compensatory mechanism is compromised. Impaired vasodilator responses, together with limitation of increases in collateral blood flow, may predispose to cerebral ischemia and stroke during chronic hypertension.
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PMID:Impaired dilatation of cerebral arterioles in chronic hypertension. 224 46

Five hundred thirty-nine patients with no symptoms of cerebral ischemia undergoing coronary artery bypass were preoperatively evaluated for presence of carotid stenosis by noninvasive methods (duplex scanning and ocular pneumoplethysmography-Gee). Overall prevalence of carotid stenosis greater than 75% was higher (8.7%) than that generally reported. Age greater than 60 years was significantly related to presence of carotid stenosis greater than 75% (11.3% vs 3.8%, p = 0.003). Risk factors such as hypercholesterolemia, hypertension, diabetes mellitus, and smoking were not predictive for carotid stenosis, postoperative stroke, or death. Carotid stenosis greater than 75% (odds ratio 9.87, p less than 0.005) and coronary artery bypass redo (odds ratio 5.26, p less than 0.05) were both independent predictors of stroke risk. Patients were divided into four groups: group 1, minimal or mild degree of carotid stenosis (less than 50%), not submitted to prophylactic carotid endarterectomy (432 patients, 80.1%); group 2, moderate degree of stenosis (50% to 75%), no prophylactic carotid endarterectomy (60 patients, 11.2%); group 3, severe carotid stenosis; (greater than 75%), submitted to prophylactic carotid endarterectomy (19 patients, 3.5%), group 4, severe carotid stenosis (greater than 75%) no prophylactic carotid endarterectomy (28 patients, 5.2%). Patients in group 4 had significantly higher stroke rate (14.3%) compared to the other three groups (1.1%) (p = 0.0019). The finding of carotid stenosis greater than 75% in patients over 60 years of age was associated with occurrence of stroke in 15% of cases. Carotid screening is helpful to determine patients at increased risk of stroke and should be performed in patients greater than 60 years.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of carotid screening before coronary artery bypass. 224 8

Color-flow Doppler is a new development of duplex sonography of the peripheral vessels. In this study 844 consecutive patients were evaluated (a) to assess the comparative value of these two methods, (b) to see if there is a correlation between the degree of stenosis and the incidence of neurological symptoms and (c) to find a possible relationship between the plaque structure and the incidence of neurological deficits. (a) In 89%, the color-flow assessment was in complete agreement with the duplex assessment. In the remaining 11%, important additional results were discovered in the color flow examination. (b) Non-stenotic plaques were seen more often (43%) in the wide carotic bulb, stenotic plaques and occlusion were found more often (66 and 82%) in the internal carotic artery. Vessel occlusion was found most often in patients with cerebral ischemia. Color-flow Doppler demonstrated a higher incidence of hemodynamic stenosis in patients with peripheral vascular disease, hypertension and bruits. (c) Patients with heterogeneous plaques demonstrated a significantly higher risk of neurological deficits than those with homogeneous plaques. The great advantage of color-flow Doppler is that it enables sonomorphological (plaques, stenoses, occlusion) and functional parameters (turbulences, flow enhancement) to be studied during the same procedure.
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PMID:[Color-coded Doppler sonography in the diagnosis of carotid artery diseases]. 226 37

We used positron emission tomography to examine retrospectively the effects of blood pressure on regional cerebral blood flow and oxygen metabolism in seven normotensive and eight hypertensive patients with a history of transient neurologic deficits. In the hypertensive patients, a decrease in regional cerebral blood flow was closely related to blood pressure; these changes were most pronounced in the supratentorial structures, especially the striatum and thalamus. In contrast, the regional cerebral metabolic rate for oxygen was less related to blood pressure. Consequently, the regional oxygen extraction fraction was increased in the hypertensive patients, while regional cerebral blood volume and the regional cerebral blood flow volume ratio were unchanged. Multivariate regression analysis confirmed that hypertension was an independent factor affecting regional cerebral blood flow. The analysis also disclosed that age, sex, hematocrit, smoking, and PaCO2 affected regional cerebral blood flow. These findings suggest that the hemodynamic reserve in hypertensive individuals is reduced, which may predispose them to cerebral ischemia and perhaps stroke, even during small decreases in cerebral perfusion pressure.
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PMID:Cerebral blood flow and metabolism in normotensive and hypertensive patients with transient neurologic deficits. 230 5

The relationship between systemic arterial pressure (SAP) and neocortical microcirculatory blood-flow (CBF) in areas of focal cerebral ischemia was studied in 15 spontaneously hypertensive rats (SHRs) anesthetized with halothane (0.5%). Ischemia was induced by ipsilateral middle cerebral artery/common carotid artery occlusion and CBF was monitored continuously in the ischemic territory using laser-Doppler flowmetry during manipulation of SAP with I-norepinephrine (hypertension) or nitroprusside (hypotension). In eight SHRs not subjected to focal ischemia, we demonstrated that 0.5% halothane and the surgical manipulations did not impair autoregulation. Autoregulation was partly preserved in ischemic brain tissue with a CBF of greater than 30% of preocclusion values. In areas where ischemic CBF was less than 30% of preocclusion values, autoregulation was completely lost. Changes in SAP had a greater influence on CBF in tissue areas where CBF ranged from 15 to 30% of baseline (9% change in CBF with each 10% change in SAP) than in areas where CBF was less than 15% of baseline (6% change in CBF with each 10% change in SAP). These findings demonstrate that the relationship between CBF and SAP in areas of focal ischemia is highly dependent on the severity of ischemia. Autoregulation is lost in a gradual manner until CBF falls below 30% of normal. In areas without autoregulation, the slope of the CBF/SAP relationship is inversely related to the degree of ischemia.
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PMID:Autoregulation of cerebral blood flow in experimental focal brain ischemia. 232 21

To evaluate the safety and possible efficacy of high-dose naloxone for the treatment of acute cerebral ischemia, 38 patients received a loading dose of 160 mg/m2 over 15 minutes followed by a 24-hour infusion at the rate of 80 mg/m2/hr. Nausea and/or vomiting were common side effects. Naloxone was discontinued in seven patients (because of hypotension in one, bradycardia and hypotension in two, myoclonus in one, focal seizures in two, and hypertension in one); all seven patients responded to treatment and no permanent sequelae to naloxone were noted. Twelve of the 38 patients showed early neurologic improvement (by completion of the naloxone loading dose). However, there was no correlation between such a loading dose response and clinical outcome at 3 months. Our experience suggests that naloxone is safe at the dose used, but data for efficacy are inconclusive.
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PMID:High-dose intravenous naloxone for the treatment of acute ischemic stroke. 233 51


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