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)

Many Koreans, in addition to Japanese, were killed or injured by the atomic bombs detonated over Hiroshima and Nagasaki, Japan, in 1945. Our study examined noncancer diseases of Korean A-bomb survivors in residence at Hapcheon, Republic of Korea and evaluated whether they had significantly higher prevalence of noncancer diseases than non-exposed people. We evaluated a number of tests, including anthropometric measurements, blood pressure, blood chemistry, hepatitis B surface antigen, and urinalysis, of survivors (n=223) and controls (n=372). Univariate analysis revealed significantly lower fasting glucose and creatinine, and higher diastolic blood pressure, aspartate aminotransferase, alanine aminotransferase, and blood urea nitrogen levels in the survivors than in the controls. The calculation of crude prevalence ratios (PRs) revealed that A-bomb survivors had a significantly higher prevalence of hypertension (PR, 1.16; 95% CI, 1.00-1.35) and chronic liver disease (2.20; 1.59-3.06) than controls. After adjusting for covariates (age, sex, body mass index, marital status, education, alcohol consumption, and smoking), A-bomb survivors had a significantly higher prevalence of hypertension (1.24; 1.06-1.44), chronic liver disease (2.07; 1.51-2.84), and hypercholesterolemia (1.79; 1.11-2.90) than controls. This study suggests that A-bomb exposure is associated with a higher prevalence of non-cancer diseases in Korean survivors.
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PMID:Non-cancer diseases of Korean atomic bomb survivors in residence at Hapcheon, Republic of Korea. 1677 77

N(G)-Nitro-L-arginine methyl ester hydrochloride (L-NAME) is a non-specific nitric oxide (NO) inhibitor and it has been used to eliminate the role of NO in many studies like animal models for hypertension. In this study, we aimed to investigate whether lisinopril treatment has any biochemical and/or histopathological effect on rat liver tissue in a L-NAME-induced hypertension model. Forty-eight 6-weeks-old male Spraque-Dawley rats were used in the study. The animals used in the study were randomly divided into four equal groups. To induce hypertension, L-NAME was added to drinking water at a concentration of 600 mg/l and each rat was given 75 mg/kg/day of L-NAME for 6 weeks. Tail cuff systolic blood pressure (SBP) was measured at first, third, and sixth weeks. There was a significant difference between the experiment groups and controls. In only lisinopril given and L-NAME plus lisinopril administered groups, each rat was given 10 mg/kg of lisinopril for 6 weeks. At the end of the study, the animals were sacrificed. Blood and tissue samples were collected for biochemical and histopathological analysis. It has been observed that mean NO level was significantly decreased in L-NAME given group (p<0.05). Mean ALT levels were significantly increased in lisinopril and L-NAME plus lisinopril given groups, when compared with the control group (p<0.05). AST levels were in normal range in all groups (p>0.05). Hepatocyte degeneration was prominent in lisinopril given group, whereas mononuclear cell infiltration was significant in L-NAME given groups. Although the beneficial effects in L-NAME-induced hypertension treatment, lisinopril can lead to some unexpected results like hepatocyte degeneration, serum enzyme level elevation, and slight mononuclear cell infiltration.
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PMID:Effect of lisinopril on rat liver tissues in L-NAME induced hypertension model. 1698 88

The annual incidence rate of primary intracerebral hemorrhage (ICH) in Izumo City, Japan, appears to be the highest rate among those reported. Despite improvement of management and surgical therapy, the overall morbidity and mortality after ICH are still high. The author investigated the risk factors for ICH in patients in Izumo. A case-control study of 242 patients (137 men and 105 women with ages ranging from 34 to 97 years) with primary ICH was conducted in Izumo between 1991 and 1998. Hypertension, diabetes mellitus, heart disease, liver disease, alcohol consumption, cigarette smoking, and serum levels of total cholesterol, aspartate aminotransferase, and alanine aminotransferase were assessed as possible risk factors for ICH by using conditional logistic regression. The prevalence of hypertension among ICH patients was 77% and the odds ratio (OR) for hypertension was 17.07 (95% CI: 8.30-35.09), which are much higher than figures reported from Western countries. The OR for hypertension was higher in individuals < or = 69 years of age than in those > or = 70 years of age and lower for lobar hemorrhage than for hemorrhages at other sites. High serum total cholesterol (> or = 220 mg/dl) was the second most important risk factor for ICH (OR: 2.52; 95% CI: 1.23-5.14), and low total cholesterol (< 160 mg/dl) decreased the risk of ICH (OR: 0.47; 95% CI: 0.27-0.82). In contrast, heart disease decreased the risk of ICH, and there was no observed association between alcohol consumption, cigarette smoking, or diabetes mellitus and ICH. This study conducted in Izumo suggests that hypertension is the most important risk factor for ICH and contrary to most previous studies indicates that serum total cholesterol concentration is also positively associated with the risk of ICH. In contrast, heart disease may decrease the risk of ICH.
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PMID:Risk factors for primary intracerebral hemorrhage in patients in Izumo City, Japan. 1750 99

Multiorgan dysfunction ensuing from severe heatstroke includes hypotension, hepatic and renal failure, hypercoagulable state, activated inflammation, and cerebral ischemia and injury. We attempted to assess whether human umbilical cord blood-derived CD34+ cell therapy improves survival during experimental heatstroke by attenuating multiorgan dysfunction. Anesthetized rats, immediately after the onset of heatstroke, were divided into 2 major groups and given CD34- or CD34+ cells (1 x 10(5)-5 x 10(5)/mL/kg body weight) i.v. They were exposed to ambient temperature of 43 degrees C to induce heatstroke. Another group of rats were exposed to room temperature (26 degrees C) and used as normothermic controls. Hypotension, hepatic and renal failure (evidenced by increased serum urea nitrogen, creatinine, aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase levels in plasma), hypercoagulable state (evidenced by increased prothrombin time, activated partial thromboplastin time, and D-dimer, and decreased platelet count and protein C in plasma), activated inflammation (evidence by increased TNF-alpha levels in serum), and cerebral dysfunction (evidenced by intracranial hypertension, cerebral hypoperfusion and hypoxia, and cerebral ischemia and injury) were monitored. When the CD34- cell-treated or untreated rats underwent heat stress, their survival time values were found to be 19 to 23 min. Resuscitation with CD34+ cells significantly improved survival time (duration, 63-291 min). As compared with normothermic controls, all CD34- cell-treated heatstroke animals displayed hypotension, hepatic and renal failure, hypercoagulable state, activated inflammation, and cerebral ischemia and injury. However, CD34+ cell therapy significantly caused attenuation of all the above-mentioned heatstroke reactions. In addition, the levels of IL-10 in plasma and glial cell line-derived neurotrophic factors in brain were all significantly increased after CD34+ cell therapy during heatstroke. Our data indicate that CD34+ cell therapy may resuscitate persons who had a heatstroke by reducing multiorgan dysfunction or failure.
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PMID:Human umbilical cord blood-derived CD34+ cells cause attenuation of multiorgan dysfunction during experimental heatstroke. 1750 7

Hyperbaric oxygen has been found to be beneficial in treating heatstroke animals. We attempted to further assess the possible mechanism of therapeutic protection offered by hyperbaric oxygen in experimental heatstroke. Anesthetized rats, immediately after the onset of heatstroke, were randomized into the following groups and given: a) hyperbaric oxygen (100% O(2) at 253 kPa for 1 h); or b) normal air. They were exposed to 43 degrees C temperature to induce heatstroke. When the untreated rats underwent heat stress, their survival time values were found to be 20-24 min. Resuscitation with hyperbaric oxygen increased the survival time to new values of 152-176 min. All untreated heatstroke rats displayed cerebrovascular dysfunction (evidenced by hypotension, intracranial hypertension, and cerebral hypoperfusion, hypoxia, and ischemia), hypercoagulable state (evidenced by increased levels of activated partial thromboplastin time, prothrombin time, and D-dimer, but decreased values of platelet count and protein C in plasma), and tissue ischemia/injury (evidenced by increased levels of creatinine, serum urea nitrogen, aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase in plasma, and dihydrobenzoic acid, lipid peroxidation, and oxidized-form glutathione/reduced-form of glutathione ratio in hypothalamus). The cerebrovascular dysfunctions, hypercoagulable state, tissue ischemia/injury, and brain oxidative stress that occurred during heatstroke were all suppressed by hyperbaric oxygen therapy. The current results indicate that hyperbaric oxygen therapy may resuscitate rats that had a heatstroke by decreasing multiple organ dysfunction and brain oxidative stress.
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PMID:Hyperbaric oxygen improves survival in heatstroke rats by reducing multiorgan dysfunction and brain oxidative stress. 1750 57

Since the 1980's nitric oxide (NO), carbon monoxide (CO) and hydrogen sulfide (H(2)S), the endogenous gas molecules produced from metabolic pathway, have been realized as signal molecules to be involved in the regulation of body homeostasis and to play important roles under physiological and pathophysiological conditions. The researches on these endogenous gas signal molecules opened a new avenue in life science. To explore the new member of gasotransmitter family, other endogenous gas molecules which have been regarded as metabolic waste up to date, and their biological regulatory effects have been paid close attention to in the current fields of life science and medicine. Sulfur dioxide (SO(2)) can be produced endogenously from normal metabolism of sulfur-containing amino acids. L-cysteine is oxidized via cysteine dioxygenase to L-cysteinesulfinate, and the latter can proceed through transamination by glutamate oxaloacetate transaminase (GOT) to beta-sulfinyl pyruvate which decomposes spontaneously to pyruvate and SO(2). In mammals, activated neutrophils by oxidative stress can convert H(2)S to sulfite through a reduced form of nicotinamide-adenine dinucleotide phosphate (NADPH) oxidase-dependent process. The authors detected endogenous production of SO(2) in all cardiovascular tissues, including in heart, aorta, pulmonary artery, mesenteric artery, renal artery, tail artery and the plasma SO(2) content. As the key enzyme producing SO(2), GOT mRNA in cardiovascular system was detected and found to be located enriched in endothelial cells and vascular smooth muscle cells near the endothelial layer. When the normal rats were treated with hydroxamate(HDX), a GOT inhibitor, at a dose of 3.7 mg/kg body weight, the blood pressure (BP) went high markedly, the ratio of wall thickness to lumen radius was increased by 18.34%, and smooth muscle cell proliferation was enhanced. The plasma SO(2) level in the rats injected with 125 micromol/kg body weight SO(2) donor was increased to 721.98+/-30.11 micromol/L at the end of 30 seconds, while the blood pressure was decreased to the lowest point 65.0+/- 4.9 mm Hg at the end of 1 minute. The above results showed that endogenous SO(2) might be involved in the maintenance of blood pressure and normal vascular structure. In spontaneous hypertensive rat (SHR) animal model, exogenous supplement of SO(2) donor decreased the BP, the media cross-sectional area, and pressure of the media and the ratio of wall thickness to lumen radius in the SHR. Moreover, the proliferative index of aortic smooth muscle cells was decreased in the SHR treated with SO(2) donor compared with that in SHR. The above data showed that SO(2) could prevent the aortic structural remodeling by inhibiting the proliferation of aortic smooth muscle cells. The authors observed the direct vasorelaxant effects of SO(2) on the aortic ring pre-treated with norepinephrine (NE). SO(2) donor at a concentration of 25-100 micromol/L relaxed the aortic ring temporarily and slightly, but SO(2) donor at a concentration of 1-12 mmol/L induced relaxation of the ring in a concentration-dependent manner. Administration with nicardipine, an L-type calcium channel blocker other than glibenclamide, an ATP sensitive potassium channel (K(ATP) channel) blocker or removal of vascular endothelium could decrease the SO(2)-induced vasorelaxation. In hypoxic pulmonary hypertension animal model, SO(2) donor decreased the mean pulmonary artery pressure and the systolic pulmonary artery pressure (P<0.01), respectively as compared with hypoxic group, and alleviated obviously the hypoxic pulmonary vascular structural remodeling. The percentage of muscularized arteries of small pulmonary vessels was significantly decreased in hypoxia+SO(2) donor-treated rats compared with that of hypoxic rats (P<0.01), while the percentage of non-muscularized vessels was obviously higher in hypoxia with SO(2) donor-treated rats than that of hypoxic rats (P<0.01). Similarly, SO(2) obviously decreased relative media area and relative media thickness of small muscularized pulmonary arteries in hypoxic rats (P<0.01). The above data showed that SO(2) might play an important role in development of hypoxic pulmonary hypertension. Perfusion with SO(2) donor (10(-6)-10(-3) mol/L) to the isolated rat heart obviously inhibited the left ventricular peak rate of contraction ( + LV dp/ dtmax) , peak rate of relaxation (-LV dp/ dtmax) and difference of left ventricular pressure ( DeltaLVP) in a concentration dependent manner. Nicardipine, an L-type calcium channel blocker, could partly antagonize the inhibitory effect of SO(2) on the heart function. In a word, SO(2) could be endogenously generated in cardiovascular tissues and exert important cardiovascular effects such as vasorelaxant effect and negative inotropic effects. Moreover, SO(2) might play considerable roles in the regulation of systemic circulatory pressure, pulmonary circulatory pressure and vascular structural remodeling in the pathogenesis of hypertension and hypoxic pulmonary hypertension. On the basis of the above findings, we presumed that endogenous SO(2) might be a novel cardiovascular functional regulatory gasotransmitter. More studies on the significance of endogenous SO(2) in cardiovascular system under physiological and pathophysiological conditions need to be investigated.
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PMID:[Significance of endogenous sulfur dioxide in the regulation of cardiovascular system]. 1765 74

The dual endothelin receptor antagonist, bosentan, is an orally active therapy, which is effective in the treatment of pulmonary arterial hypertension (PAH). This review critically appraises the evidence for the efficacy of bosentan in idiopathic and familial PAH, in PAH associated with connective tissue disease and in PAH which may develop in association with other conditions. Data from the pivotal placebo controlled studies and their open labeled extensions as well as long term survival and quality of life data is presented. Data is also presented on the potential benefit of bosentan in patients with inoperable chronic thromboembolic pulmonary hypertension. The safety and tolerability of bosentan as well as drug interactions are discussed. Dosage recommendations in adults and pediatrics are presented. An algorithm is provided to guide the reader in monitoring potential increases in alanine and aspartate transaminase levels that may occur with bosentan use and the dose adjustments that are recommended as a result of any increase in the levels of these enzymes are shown. Finally, the role of bosentan as part of combination therapy in PAH is examined.
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PMID:Review of bosentan in the management of pulmonary arterial hypertension. 1820 Aug 8

Atenolol is a beta(1)-selective drug, which exerts greater blocking activity on beta(1)-adrenoreceptors than on beta(2)-adrenoreceptors, with the S-enantiomer being more active than R-enantiomer. The aim of this study was to investigate the proteins with differential protein expression levels in the proteome of vascular smooth muscle cells (A7r5) incubated separately with individual enantiomers of atenolol using an iTRAQ-coupled two-dimensional LC-MS/MS approach. Our results indicated that some calcium-binding proteins such as calmodulin, protein S100-A11, protein S100-A4, and annexin A6 were down-regulated and showed relatively lower protein levels in cells incubated with the S-enantiomer of atenolol than those incubated with the R-enantiomer, whereas metabolic enzymes such as aspartate aminotransferase, glutathione S-transferase P, NADH-cytochrome b(5) reductase, and alpha-N-acetylgalactosaminidase precursor were up-regulated and displayed higher protein levels in cells incubated with the S-enantiomer relative to those incubated with the R-enantiomer. The involvement of NADH-cytochrome b(5) reductase in the intracellular anabolic activity was validated by NAD+/NADH assay with a higher ratio of NAD+/NADH correlating with a higher proportion of NAD+. The down-regulation of the calcium-binding proteins was possibly involved in the lower intracellular Ca2+ concentration in A7r5 cells incubated with the S-enantiomer of atenolol. Ca2+ signals transduced by calcium-binding proteins acted on cytoskeletal proteins such as nestin and beta-tropomyosin, which can play a complex role in phenotypic modulation and regulation of the cytoskeletal modeling. Our preliminary results thus provide molecular evidence on the metabolic effect and possible link of calcium-binding proteins with treatment of hypertension associated with atenolol.
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PMID:Comparative proteomics analysis of vascular smooth muscle cells incubated with S- and R-enantiomers of atenolol using iTRAQ-coupled two-dimensional LC-MS/MS. 1827 Jan 96

Two approaches to calculation of the qualitative measures for assessing the functional state level of human body are considered. These approaches are based on image and fuzzy set recognition theories and are used to construct diagnostic decision rules. The first approach uses the data on deviation of detected parameters from those for healthy persons; the second approach analyzes the degree of deviation of detected parameters from the approximants characterizing the correlation differences between the parameters. A method for synthesis of decision rules and the results of blood count-based research for a number of diseases (hemophilia, thrombocytopathy, hypertension, arrhythmia, hepatic cirrhosis, trichophytia) are considered. An effect of a change in the functional link between the cholesterol content in blood and the relative rate of variation of AST and ALT enzymes in blood from direct proportional (healthy state) to inverse proportional (hepatic cirrhosis) is discussed. It is shown that analysis of correlation changes in detected parameters of the human body state during diagnostic process is more effective for application in decision support systems than the state space analysis.
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PMID:[Quantitative measures for assessing the functional state of the human body during diagnostic procedure]. 1850 6

The black widow spider (BWS), which is a member of the arthropod family, is widely distributed on earth. Black widow spider bites can cause a wide variety of signs or symptoms in humans, but the cardiovascular manifestations are relatively rare except hypertension/hypotension and bradycardia/tachycardia. We report on a 65-year-old man who experienced myocarditis after BWS envenomation, which is extremely rare. He complained of chest pain after the BWS bite, and electrocardiography (ECG) was consistent with a 0.5-mm ST-segment elevation in leads II, aVF, and V3 through V6 and accompanying augmentation in T-wave amplitude in leads V3 through V6 without reciprocal changes. Creatine kinase-MB, troponin-I, and aspartate aminotransferase levels peaked at 98 IU/L, 6.1 ng/mL, and 62 U/L, respectively. His ECG readings and cardiac enzymes returned to normal with supportive treatment, and he was discharged with complete recovery. To the best of our knowledge, the present case is the third in the literature reporting myocarditis and the first reporting ST-segment elevation and accompanying augmentation in T-wave amplitude after BWS envenomation. In addition to usual measures, we recommend ECG and cardiac-specific enzyme followup for every patient envenomated by BWS for potentially fatal cardiac involvement.
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PMID:Myocarditis after black widow spider envenomation. 1853 3


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