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

A case of salt-losing congenital adrenal hyperplasia with severe hyponatremic dehydration is presented. Clinical signs and symptoms of cerebral edema with elevated intracranial pressure were present. Conventional treatment was started, and after initial concern regarding future head growth and development, there was a good outcome with normal development at 1 year of age. This course is suggestive of benign intracranial hypertension. Possible mechanisms are discussed with a review of the relevant literature.
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PMID:Benign intracranial hypertension following severe hyponatremic dehydration in congenital adrenal hyperplasia. 405 82

The antidiuretic hormone, arginine-vasopressin (AVP), may participate in the regulation of blood pressure (BP) through its vasoconstrictor effects. In anesthetized rats, exogenous AVP induced stronger vasoconstriction in the mesenteric than in the renal vascular bed. Conversely, mesenteric but not renal vascular resistance was reduced by a vascular antagonist of AVP, d(CH2)5 VDAVP, in rats with increased endogenous AVP after anesthesia, dehydration, or injection of glycerol. Another vascular AVP-antagonist, d(CH2)5 Tyr (Me) AVP, induced a transient fall in BP in conscious primates (marmosets) after diuretic-induced volume depletion. In conscious rats with established deoxycorticosterone acetate (DOCA)/salt hypertension, d(CH2)5 Tyr (Me) AVP decreased systolic BP after acute administration. After chronic administration of this antagonist during 6 weeks after the beginning of DOCA/salt treatment, the severity of hypertension was reduced. When another, AVP-antagonist, d(CH2)5-D-Tyr (Et) VAVP, which blocks vascular and renal tubular AVP-receptors, was administered chronically, the development of DOCA/salt hypertension was prevented at the expense of severe and persistent hypernatremia. These results demonstrate that under certain conditions the vascular effects of AVP may contribute to the maintenance of BP, AVP appears to participate in the pathogenesis of DOCA/salt hypertension through both its vasoconstrictor and its antidiuretic effects.
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PMID:The significance of vasopressin as a pressor agent. 620 52

Vasopressin has been shown to elicit vasoconstriction in unanaesthetized animals at plasma concentrations similar to those associated with its renal antidiuretic effect. The vasconstrictor effects of vasopressin do not normally translate into pressor responses until relatively high plasma concentrations are reached. This appears to be related to very effective buffering by the baroreceptor reflex. In the absence of afferent signals from the baroreceptors (surgical denervation, but more importantly, low arterial pressure), the vasoconstriction elicited by vasopressin represents a significant part of the mechanisms that determine blood pressure. Vasopressin is clearly involved in the short-term control of blood pressure in situations such as haemorrhage, other volume-depleted states and dehydration. However, it is only one of several short-acting mechanisms which complement each other in the defence against hypotensive stresses. Under different conditions, the cardiovascular effects of vasopressin seem to have a component related to the central nervous system control of the circulation. Whether or not circulating vasopressin interacts with the newly described network of extrahypothalamic projections from the paraventricular nucleus is yet conjectural. However, the presence in the brain of vasopressin-containing pathways and of various types of receptors to vasopressin, as well as the existence of cardiovascular effects elicited by central administration of antidiuretic hormone, suggests a role for cerebral vasopressin in the control of autonomic function. Slightly elevated levels of vasopressin have been found in various forms of hypertension. Yet, the role of vasopressin, when present, may be more related to its antidiuretic than to its vasoconstrictor properties.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vasopressin in cardiovascular control: role of circulating vasopressin. 623 29

Renal venous thrombosis, a clotting process that originates in the venous radicles and progresses into the main renal vein and vena cava, predominantly affects newborn infants. It may be manifest in one or both kidneys and follow maternal diabetes, diarrhea and dehydration, congenital heart disease, acute blood loss, sepsis, asphyxia, and shock. The most common signs include gross hematuria, enlarged palpable kidneys, and thrombocytopenia. Evaluation should include ultrasonography of the kidneys (demonstrating renal enlargement with disruption of the normal echo pattern), computed tomography, and renal isotope scanning. The initial treatment is supportive. Surgical intervention is not indicated in the acute phase except in the rare instance of bilateral disease. Anticoagulant therapy is still controversial. Late sequelae include impairment of renal function, shrunken hypoplastic kidney, arterial hypertension, and tubular defects.
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PMID:Renal venous thrombosis in children: changes in management. 635 1

In 19 children with acute infantile hemiplegia an ischemic cerebral infarct was found clinically and by serial computertomography. In 11 patients an angiography has been performed in addition. 9 of the children had chronic diseases which are known as predisposing factors for cerebrovascular disease (congenital heart disease in 7 and chronic renal failure with hypertension in 2). One child had a severe hypernatremic dehydration due to infantile diarrhea and in 1 child thrombosis of the internal carotid artery occurred 3 days after a perforating trauma of the soft palate. No obvious reason for the ischemic stroke could be evaluated in 8 children. The onset of symptoms was either acute or slowly progressive. An altered state of consciousness was present in 11 children. Hemiparesis was found in 18 patients (13 right, 5 left) accompanied by facial palsy in 12 and aphasia in 6. Seizures occurred in 6 patients. One patient with incomplete occlusion of a vertebral artery showed acute cerebellar ataxia. In children without predisposing factors the prevalence of girls was higher (2 : 6) and there was a history of a preceding acute febrile illness in 5 of 8 patients. Laboratory investigations showed polycythemia in 4 children with cyanotic heart disease and additional hypochromia in two. Blood sedimentation rate was increased in 6 out of 8 patients without a known predisposing factor. Cerebrospinal fluid (CSF) showed a slight increase of erythrocytes (36-88/cmm) in 4 children, in two others purulent CSF was obtained after the infarct had developed into a brain abscess. The etiology of ischemic stroke in childhood and the possibility of an inflammatory vascular disease are discussed.
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PMID:Acute infantile hemiplegia caused by cerebral ischemic infarction. Etiology, clinical features and investigations. 647 69

A case of acute intestinal vascular necrosis in a 19-year-old user of oral contraceptives (OCs) is described, and hypotheses explaining the digestive complications of synthetic estrogens are reviewed. The patient had originally presented with a violent gastric pain that subsequently spread to the entire abdomen. An abrupt worsening of her condition involved cardiovascular collapse associated with a peritoneal syndrome, vomiting and dehydration, and hyperleukocytosis. Emergency opening of the peritoneum was followed by evacuation of a large quantity of fetid gas and alimentary debris, and observation of a completely necrosed stomach. A careful lavage of the entire intestinal cavity led to temporary improvement, but it became clear during an attempt at gastrectomy that further treatment would be unavailing and the patient died shortly thereafter. Estrogens were believed to be responsible for the digestive necrosis because it occurred in a young woman who had used an estrogen-rich OC for 3 years and who smoked; a hapatic biopsy confirmed the diagnosis. No traces of other risk factors such as hypertension, hyperlipidemia, diabetes, neoplasia, or obesity were observed. Recent publications indicate that OCs are responsible for a certain number of digestive problems, which may include acceleration of intestinal transit, severe diarrhea, rectorrhagia, ischemic or ulcerative colitis, intestinal infarct which is usually localized, and hepatocellular problems ranging from moderate hepatic insufficiency to malignant tumor and Budd-Chiari syndrome. OCs do not modify hemodynamic regimes, but they may cause elevation of fibrinogen and thrombin, diminution of antithrombin III acitivty, increased platelet adhesivity, and decreased fibrinolysis leading to hypercoagulability. These modifications in hemostasis occur in all OC users and are not statistically correlated with occurence of thrombotic accidents. OCs are probably responsible for parietal vascular lesions; experimental injection of synthetic estrogens is associated with both arterial and venous lesions. The most characteristic anomaly is at the level of the intima, with proliferation of smooth muscle cells and increased conjunctive tissue fibers associated with proliferation of the media or the endothelium. The absence of lipid deposits, the simultaneous appearance of arterial and venous lesions, and other evidence argues against and atheromatous origin of parietal lesions. A significant correlation has been found between high levels of anti-synthetic ethinyl estradiol antibodies and the presence of vascular lesions. It is hypothesized that these circulating immune complexes penetrate the vascular walls of OC users and produce lesions, which may depend on factors such as smoking.
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PMID:[Digestive complications of oral contraceptives: a case of extensive digestive necrosis in a young woman]. 647 54

The effect of weight loss produced by gastric exclusion on the metabolism of previously morbidly obese persons was examined. A standardized gastric exclusion procedure was performed in 150 morbidly obese patients during a 6 year period. These patients were followed for from 6 to 60 months (mean 27.8 months). The mean excess weight loss was 75 percent and was maintained from 2 to 5 years. A small but significant decrease was noted during the first 3 to 6 postoperative months in the parameters of protein metabolism examined. Although this may reflect mild depletion in protein stores, of greater importance was the demonstration that these parameters spontaneously corrected themselves by 12 months. Mild abnormalities in serum electrolyte concentrations were noted in the postoperative period. They appeared to be related to dehydration, were not clinically significant, and also resolved spontaneously. Clinically significant abnormalities in divalent ions were absent. Significant and sustained reductions in blood pressure, fasting glucose concentration, serum triglyceride values, and uric acid and hepatic enzyme concentrations were demonstrated in the entire population. A small and non-sustained decrease in cholesterol was seen. Hypertension was eliminated in 96 percent of the affected subpopulation, diabetes in 100 percent, gout in 100 percent, hyperlipidemia in 92 percent, and improved hepatic function was found in 95 percent. These changes should reduce the overall morbidity and mortality of the patient population in the future.
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PMID:Prospective metabolic evaluation of 150 consecutive patients who underwent gastric exclusion. 671 48

In rabbits subjected to bicuculline (BC)- or pentylenetetrazole (PTZ)-seizures of 3 or 20 min duration or to adrenaline-induced hypertension, specific gravity (SG) was measured bilaterally in 15 regional brain areas in order to detect possible associations between the regionally limited blood-brain barrier openings due to these insults (see Nitsch and Klatzo 1983) and the presence of brain edema. In controls, a large variation between regional SG levels became evident: between 1.0467 in cerebellum and 1.0417 in preoptic area. A seizure duration of only 3 min was not sufficient to change SG significantly. After 20 min of seizures independent from the inducing agent, SG increased in all brain areas. The degree of increase seemed to be unrelated to presence or absence of a blood-brain barrier opening. In an attempt to avoid the influence of blood impregnation on the SG value, blood was replaced by saline before measurement. In controls, saline perfusion decreased SG only in the two areas with the highest original levels, thus documenting the partial dependency of the regional SG on the hematisation of the tissue. After 20 min of PTZ-induced seizures, SG in saline-perfused rabbits increased, but no longer significantly in all brain areas. This suggests that a part of the seizure-induced SG increase can be attributed to the hyperemia of the brain during the convulsions. On the other hand, an increase in flow volume due to hypertension did not change SG with the exception of the septum, preoptic area and hypothalamus. The direct measurement of water content with the classical wet/dry method in 4 gross brain areas showed that early seizure periods are in fact associated with a dehydration of the brain. This phenomenon could be explained by a glucose- and lactate-induced rise in blood osmolarity which in turn might cause a dehydration of the brain tissue.
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PMID:Specific gravity increases and brain water content decreases during short epileptiform seizures in discrete rabbit brain areas. 674 60

Contrast nephropathy is an adverse alteration in renal function induced by intravascular contrast media. Most cases involve transient asymptomatic episodes; yet a significant number involve oliguria and/or permanent renal damage. The incidence of contrast nephropathy in the general hospitalized population is about 5%, and is associated with preexisting renal insufficiency and diabetes mellitus. The incidence in patients with normal renal function is significantly lower - 0.6% following IVP and 2% following angiography. Angiography carries risks inherent to the technical problems of the procedure itself. Preexisting renal insufficiency is the most significant predisposing condition of contrast nephrotoxicity. As many as two-thirds of patients with chronic renal failure may experience an acute deterioration in renal function following exposure. Most of these episodes are transient and benign. Diabetic patients with preexisting renal insufficiency are at an even greater risk; about 75% of such patients will experience renal complications. The risk is even higher in JODM patients with severe renal disease; there is an over 90% incidence of nephrotoxicity with as many as half sustaining permanent renal damage. Adequate hydration does not appear to reduce the incidence of contrast nephropathy in susceptible patients, but it may reduce the likelihood of oliguria and permanent damage. In multiple myeloma the risk of contrast-induced renal failure is low, and probably involves a different pathogenesis than seen in other cases of contrast nephropathy. The incidence in myeloma patients is probably increased in the presence of dehydration and renal insufficiency. Peripheral vascular disease, hypertension, old age and large and repeated doses of contrast may increase the risk in susceptible patients. Prevention of contrast nephropathy must start with identification of patients at risk. In patients with preexisting renal insufficiency, and especially diabetic patients with preexisting renal insufficiency, the anticipated benefit should outweigh the potential risk of exposure to contrast media.
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PMID:Contrast nephropathy. 675 74

Increased intracranial pressure due to brain oedema was produced in albino rabbits by combining a cryogenic lesion in the left hemisphere with the intraperitoneal administration of 6-aminonicotinamide (cytotoxic agent). The most effective reduction in ICP (74%) was achieved when furosemide and mannitol were used in combination. When either mannitol or furosemide was employed alone, the average ICP reduction was approximately 53%. Peak ICP reduction occurred at 45 minutes with furosemide, 30 minutes with mannitol and furosemide combined, and at 60 minutes with a combination of mannitol and acetazolamide. Also studied simultaneously in these animals were investigated elastance (Em), brain water content, hemispheric water volume content, electrolytes, EEG, and gross pathology. Following therapy there was a statistically significance reduction of water content in the left hemisphere (cryogenic lesion) by all therapeutic modalities except with furosemide alone. In the right hemisphere the water content was reduced by furosemide and the furosemide-mannitol combination but not by the association of mannitol with acetazolamide. A significant decrease of brain sodium was noted only for the combination of mannitol and furosemide. This study indicates that effective reduction of cytotoxic-cryogenic brain oedema and intracranial hypertension can be obtained with a variety of diuretic agents. From the standpoint of tissue dehydration, restoration of tissue electrolyte balance, and rate of ICP reduction, the combination of furosemide-mannitol appears to offer advantages over furosemide alone, or acetazolamide-mannitol.
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PMID:Intracranial hypertension and brain oedema in albino rabbits. Part 2: Effects of acute therapy with diuretics. 679 66


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