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

Data from humans and experimental animals indicate that hypertensive diseases triggered by extracellular fluid volume expansion are characterized, in their chronic phases, by relatively normal blood volume (BV) and heightened pressure-volume relationship may be viewed as corresponding to a condition of "virtual hypervolemia," where BV is inappropriately "high" relative to blood pressure. The limited data available on the phasic relationship between these variables indicate that the BV expansion appears to be a prerequisite to alterations in vascular ion metabolism, that both of these changes precede the rise in blood pressure, and that structures within the central nervous system may be a critical link between the body fluid volumes and vascular functional changes. In contrast, hypertensive diseases triggered by secretion of pressor agents or their precursors appear to be characterized in their chronic phases by low BV. These relationships and the associated alterations in plasma aldosterone and renin levels are summarized for a variety of clinical syndromes, including essential hypertension and pregnancy-induced hypertension. Direct or indirect evidence of a primary or secondary defect in renal function is apparent as an underlying event in many of these diseases.
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PMID:Sodium chloride, extracellular fluid volume, and blood pressure regulation. 353 23

Profound clinical and radiographic arterial vasospasm in all major intracerebral vessels was identified in a patient with an intraparenchymal hemorrhage that extended into the lateral, 3rd, and 4th ventricles. By computed tomographic criteria and on early cerebrospinal fluid examination, no subarachnoid blood was detected. The temporal appearance of vasospasm was consistent with that typically seen in subarachnoid hemorrhage. Despite hypervolemia and iatrogenic hypertension, cerebral infarction occurred contralateral to the hemorrhage. We conclude that patients without significant subarachnoid hemorrhage (as determined by computed tomographic scanning) may still be at risk for developing vasospasm.
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PMID:Profound cerebral vasospasm without radiological evidence of subarachnoid hemorrhage: case report. 371 18

Delayed ischemic deficits from vasospasm after subarachnoid hemorrhage remain a major source of death and disability to patients surviving subarachnoid hemorrhage. Ideal treatment for this condition would prevent or reverse spasm in major subarachnoid vessels. This goal remains elusive. Considerable success has been obtained with augmentation of flow in ischemic regions by induced hypertension and hypervolemia. Some patients are not good candidates for this therapy because of underlying cardiovascular disease or the presence of unsecured aneurysms. A total of 11 patients have recently undergone extracranial-intracranial bypass for the treatment of symptomatic vasospasm. Bypass was performed in 4 patients due to failure of medical management and in 7 patients due to our reluctance to induce hypertension in the setting of unsecured aneurysms. Eight of the 11 patients responded neurologically to the bypass procedure within 24 hours. In 6 cases, neurological deficits either improved or resolved. After operation, all 8 patients maintained their preoperative neurological status with lower mean arterial blood pressures than before bypass. Noncomatose patients with focal middle cerebral ischemic deficits and secured aneurysms in whom medical management has failed or in whom these measures are contraindicated may indeed benefit from extracranial-intracranial bypass. Patients with unsecured aneurysms remote from an ischemic middle cerebral territory should probably be revascularized if cautious hypertension fails to improve their conditions.
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PMID:Use of extracranial-intracranial bypass in the management of symptomatic vasospasm. 374 51

Necropsy findings of hepatobiliary system from 78 patients with end-stage renal disease maintained on hemodialysis are reported. Ninety percent of the patients exhibited some abnormalities. Multiple abnormalities often coexisted in each patient. Hepatomegaly was found in 50% of the patients and could be attributed to a discernible cause in all but two of the affected patients who had isolated hepatomegaly. Hepatic congestion was also prevalent and was complicated by fibrosis, cardiac cirrhosis, and centrilobular necrosis and hemorrhage in some patients. This was associated with chronic fluid overload, hypertension, and/or cardiovascular disease in the affected patients indicating the importance of adequate control of these factors. Mild periportal hepatic fibrosis, fatty metamorphosis, triaditis, hemosiderosis, and cystic changes were also seen with some frequency--the latter were associated with polycystic kidney disease and were complicated by massive intracystic hemorrhage and abscess formation, each in one patient. Chronic active hepatitis was found in three patients and was associated with chronic HBs antigenemia in one patient and presumed non-A, non-B infection in two. Nearly 22% of the patients showed either cholelithiasis at autopsy or before cholecystectomy due to complications. Significant negative findings included lack of acute viral hepatitis, silicone hepatosis, and recently described focal anoxic lesions associated with erythrocyte sludging. In conclusion, the present study has demonstrated the spectrum of hepatobiliary pathology in a large group of patients with end-stage renal disease maintained on hemodialysis.
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PMID:Hepatobiliary pathology in hemodialysis patients: an autopsy study of 78 cases. 375 41

The prognosis of hemolytic uremic syndrome was studied in 37 children hospitalized between January 1980 and January 1985. 75% of affected children were less than 3 years of age. Twenty-two (60%) presented with anuria or oliguria (mean duration of anuria: 10.7 days). In this last group, severe extrarenal manifestations occurred: 12 cases of neurological involvement (6 involving hypervolemia), gastrointestinal involvement in 5 cases, including a case of ileal necrosis; pancreatic involvement in another. Three children died during the first month of the disease (overall death-rate: 8%). Thirty-two children were followed with a mean 24 months follow-up (6 months to 60 months). Six (19%) presented with sequellae, of which 3 were severe: one severe arterial hypertension and two with chronic renal failure of which one terminal with severe neurologic sequellae. The existence of extrarenal manifestations implies a poor prognosis. Among the 22 children with anuria or oliguria, 8 had no extra-renal manifestations. All of these recovered. Three of 11 children with one extrarenal manifestation had an unfavorable outcome. The course was unfavorable in the 3 cases with multiple extrarenal involvement.
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PMID:[Prognosis of hemolytic uremic syndrome in children. Importance of extrarenal involvement]. 376 86

The authors reviewed 22 cases of intracranial aneurysm of the anterior part of the circle of Willis. All patients presented with the signs and symptoms of subarachnoid hemorrhage (SAH) and were in good neurological condition on admission. In all cases, early operation was performed to obliterate aneurysm. Subarachnoid blood clots were extensively removed and cisternal drainage was done. With topical application of povidone-iodine and intravenous administration of antibiotics, cisternal drainage continued for 14 days or more after the onset of SAH in 21 cases. Five patients developed symptomatic vasospasm, which was treated with hypervolemia and hypertension, and three received shunts later for chronic hydrocephalus. The overall result demonstrated that 21 patients were independent and had returned to their previous social lives. Therefore, it was strongly recommended that patients is good neurological condition after SAH secondary to ruptured intracranial aneurysm be treated with early operation, removal of subarachnoid clots, and long term application of cisternal drainage.
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PMID:Cisternal drainage after early operation of ruptured intracranial aneurysm. 380 82

A generalised vasoconstriction, for almost a century believed to be the basis of all types of human hypertension, was disproved by recent haemodynamic studies. In our investigation of hypertension in chronic parenchymatous non-uraemic, non-anaemic renal disease, we have established that the earliest haemodynamic abnormality in subjects, of whom over 90% later develop high blood pressure, has actually started while their blood pressure is still normal. This consists of hypervolaemia and a high cardiac output (hyperkinesis) with tissue hyperperfusion. Hypervolaemia is due to a failure of these still normotensive patients to excrete isotonic saline as readily as subjects with completely normal kidneys.The chronic hypervolaemia in these subjects leads to a release of the natriuretic factor which depresses the Na(+)-K(+)-ATPase in the cell membranes and which is responsible for an increase in sodium (and calcium) content of the vascular smooth muscle cells, diminishing their compliance and thus raising the vascular resistance together with the thickening of the vascular wall of the originally hyperperfused vessels. With the disappearance of the vascular adjustment to the increased cardiac output, the blood pressure rises and the 'pressure diuresis' restores the circulating blood volume (and the renal homeostatic efficiency) to normal. With a further rise of the peripheral vascular resistance the cardiac output falls. At this late stage of renal hypertension renin may play a contributory role.Thus, the primary abnormality in the chain of events leading eventually to hypertension is a renal inability to maintain a proper balance between sodium intake and output. This suggested pathophysiological mechanism is probably valid in every kind of human hypertension where a reason for such a disturbance is present.
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PMID:Volume homeostasis, renal function and hypertension. 390 80

Urinary sodium excretion, central hemodynamics, and mean arterial pressure (MAP) were studied in 7 normal subjects and 19 hypertensive patients during both central hypervolemia by water immersion to the neck (NI) and extracellular volume expansion by i.v. saline infusion. During 2-hour NI, 12 out of the 19 hypertensives exhibited a significant fall in MAP (p less than 0.001). Exaggerated natriuresis did not occur in these patients (ns). In the remaining 7 hypertensive patients in whom, during NI, MAP was unchanged, exaggerated natriuresis was found (p less than 0.001). During saline infusion, MAP was either unchanged or increased and exaggerated natriuresis was found in all hypertensive patients (p less than 0.001) previously submitted to NI. Our findings suggest that a high MAP is a major determinant of exaggerated natriuresis in arterial hypertension.
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PMID:Low-pressure receptor activity and exaggerated natriuresis in essential hypertension. 401 Aug 45

A total of 117 adult patients with atrioseptal defect were studied by routine X-ray method and cardiac catheterization. The X-ray indices of pulmonary blood circulation and heart were juxtaposed that reflect the hypervolemia and hypertension with oxyhemometric volumetric percentage of the shunt, the sytolic pressure in pulmonary artery and the extent of the defect established at operation. A correlation was established between the X-ray determined stage of the pulmonary changes (from the stage of isolated hypervolemia to anatomic-fixed hypertension) and the pressure. A proportionalily was established in the degree of the shunt with the dimension of the heart with X-ray big hearts. With the small hearts, the shunt is unpredictable. There was a considerable difference depending on he size of right auricle, on the extent of the defect and the shunt mainly in the big auricles. With small auricles, the defect and shunt could be of different extent. The risk not to perform catheterization because of a small shunt in auricles with a length of 55 mm is acceptable. At the same time a hemodynamically insignificant shunt could be expected with right pulmonary artery to 17 mm. The right ventricular chanjes could be due mainly to volumetric loading.
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PMID:[Roentgeno-clinical comparisons in atrial septal defects in adults]. 409 Apr 55

The effects of dextran overload, norepinephrine drip and positive pressure ventilation upon right atrial, pulmonary wedge, left atrial and systemic arterial pressures were studied in 15 dogs. Rapid intravenous infusion of Dextran 70 invariably produced a marked and statistically significant (p < .001) rise in right atrial, pulmonary wedge and left atrial pressures. The rise in left atrial pressure invariably exceeded the rise in right atrial pressure, and the difference in maximum pressures averaged 10.8 mm Hg (p < .001). Thus acute fluid overload and pulmonary edema can be produced by rapid infusion of colloid solution in the absence of a marked rise in right atrial pressure, a point of considerable clinical importance. The rapid infusion of dextran produced a rise in systemic arterial blood pressure in all dogs so studied, though this rise was mild in some animals. This finding may explain in part the hypertension exhibited by patients in the recovery room who may have been overtransfused. A norepinephrine drip usually produced an increase in right atrial, wedge, left atrial and systemic arterial blood pressure (p < .01). When there was a significant rise in right atrial pressure and left atrial pressure, the maximum increase in left atrial pressure was always greater than the maximum increase in right atrial pressure (p < .005). This finding again emphasizes the fact that blood transfusion requirements cannot always be accurately assessed on the basis of right and left atrial pressure measurements when a vasopressor agent is being administered. Positive pressure ventilation increased both right and left atrial pressures, as expected. It was again confirmed that pulmonary wedge pressure, as measured with the Swan-Ganz catheter, is approximately equal to left atrial pressure over a wide range of induced variations. The Swan-Ganz catheter, introduced at the bedside in the intensive care unit when necessary, can provide highly useful information regarding left atrial pressure and left ventricular end-diastolic pressure.
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PMID:Fluid replacement monitoring: effect of dextran overload, norepinephrine drip, and positive pressure ventilation on systemic arterial, right atrial pulmonary wedge, and left atrial pressures in dogs. 460 83


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