Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of hydrochlorothiazide and atenolol on serum lipoproteins was investigated in a randomized, prospective study on 68 men with essential hypertension. Cholesterol, high density lipoprotein (HDL) cholesterol, low density lipoprotein (LDH) cholesterol, triglycerides, and the apolipoproteins AI and B were followed up to 42 months after starting therapy. Following atenolol serum (HDL) cholesterol decreased and serum triglycerides increased significantly (p less than 0.01) from 6 to 42 months. After hydrochlorothiazide serum triglycerides, LDL cholesterol and total cholesterol all increased significantly (p less than 0.01) from 12 to 42 months. The changes were more pronounced under higher doses with beta blockade, but not with diuretics. Thus, both atenolol and hydrochlorothiazide have adverse but different effects on serum lipoproteins after long-term administration. Continuing investigation is necessary to determine whether these side effects decrease the benefit of blood pressure reduction in patients with hypertension.
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PMID:Serum lipoproteins during antihypertensive therapy with beta blockers and diuretics: a controlled long-term comparative trial. 354 79

Burkitt's lymphoma was first reported by Burkitt in 1958 as a sarcoma involving the jaw in African children with characteristic symptoms. Forty three Japanese cases have been reported since the first description by Oboshi et al. in 1969. We report a case of Burkitt's lymphoma with left total ophthalmoplegia. A 73-year-old Japanese female was admitted in Sadamoto Hospital on July 11, 1983 with a two-week history of headache, ptosis and double vision. The patient was exposed to the atomic bomb in Hiroshima and had ten-year history of hypertension. On admission, physical examination showed hypertension and neurological examination revealed only left total ophthalmoplegia (such as left ptosis, external ophthalmoplegia, mydriasis and deficit of light reflex). Plain X-ray film and enhanced CT scan showed no remarkable abnormalities. Laboratory examinations revealed high serum levels of GOT(51 K.U.) and LDH (1300 U.). Left carotid and right retrograde branchial angiograms showed no remarkable abnormal findings. While the patient was treated only conservatively, left abducent and trochleal nerve palsy appeared on August 5, 1983. On plain and enhanced CT scans at the time, abnormal density mass with bone destruction of the left sphenoidal sinus was demonstrated. Biopsy specimen from the left sphenoidal sinus showed lymphosarcomatous cells. Peripheral blood and bone marrow smears showed lymphoma cells which are compatible with L3-Burkitt's type according to FAB leukemia classification. The patient was diagnosed as leukemic transformation of Burkitt's lymphoma and treated with CHOP; Cyclophosphamide (C), Hydroxydaunorubicin(H), Vincristine (O), and Prednisolone (P).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of Burkitt's lymphoma with total ophthalmoplegia]. 408 40

Three different pressure groups of rats, stroke-prone spontaneously hypertensive rats (SHRSP, 200-270 mmHg), stroke-resistant SHR (SHRSR, 160-240 mmHg), and Wistar rats (WR, 120-160 mmHg) were used to investigate the effect of prior existing hypertension on the severity of brain damage induced by ischemia. The cerebral ischemia was induced by bilateral common carotid artery ligation (BLCL) and the survival rate, cerebral blood flow, cerebral energy metabolites (ATP, lactate c-AMP) and water content were measured. Colloidal carbon perfusion was also performed. Sixteen-week-old male rats were used. The survival rate was observed until 24 hours after BLCL. Cerebral blood flow was measured in parietal cortex by hydrogen clearance method. ATP was measured by luciferin-luciferase method, and lactate by enzymatic method using LDH. c-AMP was measured by radioimmunoassay. Brain water content was measured by freeze-dry method. These measurements were done for animals surviving 6 hours of BLCL. Colloidal carbon perfusion was done according to Ames' Method. The survival rate was lower in the hypertension group. The survival of SHRSP and SHRSR were 20% compared to 71% in WR after 24 hours of BLCL. The cerebral circulation of SHRSP fell abruptly and was near to zero after one hour of BLCL. In SHRSR this fall of cerebral blood flow was prominent in the rats of higher blood pressure. On the other hand there was no apparent fall of cerebral blood flow in WR after BLCL. The cerebral energy metabolites. ATP and c-AMP showed the lowest level in SHRSP which had the negative correlation to blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Experimental cerebral ischemia after bilateral common carotid artery ligation in SHRSP, SHRSR and Wistar rats: correlation between blood pressure and degree of ischemia]. 609 92

The effects on the neonate of severe maternal hypertension originating before the thirty-sixth week of gestation were determined by comparing data obtained on 28 preterm infants born of hypertensive mothers with data from 28 gestational age-matched controls. All hypertensive mothers had diastolic blood pressure greater than or equal to 110 mm Hg, proteinuria, and systemic symptoms of their disease; over half had thrombocytopenia and significant elevations of LDH and SGOT. All hypertensive mothers had been treated intravenously with magnesium sulfate, and 79% received other antihypertensive agents. When compared to control infants, the infants of hypertensive mothers had a significantly higher incidence of somatic growth retardation, microcephaly, thrombocytopenia, leukopenia, neutropenia, low Apgar scores, delayed adaptation, patent ductus arteriosus, hypotonia, and gastrointestinal hypomotility. Apgar scores, platelet count, WBC count, neutrophil count, and weight percentile correlated with the severity of maternal platelet and enzyme abnormalities. The occurrence of gastrointestinal hypomotility, hypotonia, and patent ductus arteriosus may be related to transplacental passage of maternally administered drugs.
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PMID:Neonatal manifestations of severe maternal hypertension occurring before the thirty-sixth week of pregnancy. 705 37

Myometrial lactate dehydrogenase isoenzymes were investigated in 32 pregnant women and in 21 women during labor. During pregnancy and labor the H-type LDH isoenzymes were found to preponderate in contrast to M-type LDH isoenzymes. Both H-LDH and M-LDH isoenzyme activities showed a tendency to increase in normal pregnancy. In severe pre-eclampsia and in chronic hypertension, the uterine M-LDH level decreased. In normal labor, M-LDH activity declined in both the uterine and the rectus abdominis muscles.
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PMID:Lactate dehydrogenase isoenzymes in human myometrium during pregnancy and labor. 709 Jul 48

LDH and CK isoenzyme patterns are determined electrophoretically (Beckman) from various aortic regions and layers and in atherosclerotic plaques as compared to control areas. Throughout consecutive layers of human aorta LDH isoenzymes show a continuous cathodic shift from both surfaces towards the center with a maximum between the inner and middle third. CK shows a heterogenous pattern with maxima at CK MM and CK BB and less CK MB. Most of the CK MM is located in the intima, the media contains more of CK BB. Regional analysis shows an anodic shift of CK from proximal to distal thoracic aorta. In experimental short term hypertension a definite anodic CK isoenzyme shift is observed with increased relative CK BB activity.
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PMID:Topochemical variation of LDH and CK isoenzyme patterns in aorta. 721 42

Male and female, spontaneously hypertensive rats (SHR) with blood pressures ranging from 190-210 mmHg were subjected unilateral or bilateral carotid artery ligation. Representative numbers of animals were killed 2, 4, 6, 8, 10, 12, 24 and 48 hours later. Severe cerebral ischemia caused a significant and protracted increase in the pre-existent high blood pressure, the enzymes CPK, SGOT and LDH triglycerides, free fatty acids, glucose, and corticosterone. Despite these marked pathophysiologic changes, the brains of these animals were free of real damage except for cerebral edema and scattered petechiae. Some of the animals developed massive atrial thrombi and myocardial infarcts. It is suggested that severe cerebral ischemia precipitated the myocardial infarcts through the aegis of the hypothalamic-pituitary-adrenal stress response.
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PMID:Comparative effects of unilateral and bilateral carotid artery ligation in the spontaneously hypertensive rat. 735 34

A genetic variant of the spontaneously hypertensive rat (SHR) has been produced which becomes markedly obese as well as hypertensive, i.e. Obese/SHR weigh 800 g as against 300 g for non-obese cohorts. Serum enzymes (CPK, SGOT, SGPT and LDH) are frequently abnormally elevated, concomitantly with a high incidence of myocardial necrosis. Obese/SHR are hyperlipidaemic with severe fatty infiltration of the liver; they are hyperglycaemic with enormous islets of Langerhans and extensive beta-cell degranulation; despite elevated blood urea nitrogen (BUN) levels, they manifest little or no renal damage. Measurement of corticosterone, deoxycorticosterone (DOC) and aldosterone in Obese/SHR demonstrate marked hyper-responsiveness to moderate stress. Circulating prolactin levels are lower in Obese and non-obese/SHR compared to SHR, but Obese/SHR manifest unusually high increases incirculating prolactin levels in response to stress. Obese/SHR are hyperinsulinaemic and have subnormal growth-hormone levels. Desite mild hypertension, hyperglycaemia and hyperlipidaemia, Obese/SHR show no evidence of atheromatous change but do develop early polyarteritis nodosa. It is believed that the genetically programmed hypertension and hyperglycaemia is mediated by increased DOC, aldosterone and corticosterone production respectively, and that the obesity, hypertension, and diabetes in Obese/SHR may be likened to human Cushing's disease.
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PMID:Pathophysiological differences between obese and non-obese spontaneously hypertensive rats. 742 76

A twenty-one-year-old male was admitted to our hospital because of hypertension and proteinuria. He had felt general fatigue and low grade fever for one month. Blood pressure was 180/120 mmHg on admission. Laboratory findings showed 3+ proteinuria and 1+ occult blood in urinalysis; an accelerated erythrocyte sedimentation rate (ESR) of 39 mm/hr; elevation of LDH to 755 IU/l. Antinuclear antibody was positive with a titer of 1: 160, with a speckled pattern. Plasma renin activity and serum aldosterone were markedly elevated to 25.8 ng/ml/hr and 585.3 pg/ml, respectively. Renal function had declined mildly; endogenous creatinine clearance was 60 ml/min. Renal arteriogram demonstrated multiple intrarenal aneurysms in the bilateral kidneys. Aneurysms, 5-8 mm in diameter were located in the arteries from the interlobar to interlobular region. He was diagnosed as having polyarteritis nodosa (PN) and was then treated with 20 mg/day of prednisolone and monthly pulse therapy of cyclophosphamide. After steroid, cyclophosphamide and anti-hypertensive therapy, he became well and had normal blood pressure. The patient was considered a rare case of PN with multiple intrarenal aneurysms and accelerated hypertension. We discuss aneurysms in PN and accelerated or malignant hypertension documented in the literature.
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PMID:[A case of polyarteritis nodosa presenting with multiple intrarenal aneurysms and accelerated hypertension]. 769 55

A 78-year-old man was hospitalized because of muscular weakness and acute renal failure. He had been taking glycyrrhizin (280 mg/day) for the last 7 years. Hypertension was noted in his history. Serum potassium was 1.9 mEq/l with metabolic alkalosis. There was hyporeninemic hypoaldosteronism. Serum enzymes, including GOT, LDH and CPK were markedly elevated. In addition, serum myoglobin was as high as 46 micrograms/ml with massive myoglobinuria. Oliguria occurred and blood urea nitrogen and serum creatinine rapidly elevated from 20.9 to 87 mg/dl and from 1.3 to 6.7 mg/dl, respectively. Profound calcium deposition was found in the damaged skeletal muscles, including the quadriceps femoris, axillar, neck, and cardiac muscles. These results indicate that licorice-induced pseudoaldosteronism produces hypokalemic rhabdomyolysis, resulting in acute renal failure and profound deposition of calcium into the damaged skeletal and cardiac muscles.
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PMID:An autopsy case of licorice-induced hypokalemic rhabdomyolysis associated with acute renal failure: special reference to profound calcium deposition in skeletal and cardiac muscle. 785 65


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