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)

In the present study, we attempted to assess the mechanisms underlying the neuroprotective effect of hypervolaemic haemodilution in rat heatstroke. In anaesthetized rats treated with normal saline (NS) immediately after the onset of heatstroke induced by T (a) (ambient temperature) of 42 degrees C for 88 min, followed by T (a) of 24 degrees C for 12 min, the values for MAP (mean arterial pressure), ICP (intracranial pressure), CPP (cerebral perfusion pressure), CBF (cerebral blood blow), brain P O(2) (partial pressure of O(2)) and striatal glutamate, glycerol, lactate/pyruvate ratio, hydroxyl radicals and neuronal damage score were 42+/-3 mmHg, 33+/-3 mmHg, 9+/-3 mmHg, 109+/-20 BPU (blood perfusion units), 6+/-1 mmHg, 51+/-7 micromol/l, 24+/-3 micromol/l, 124+/-32, 694+/-22% of baseline and 2.25+/-0.05 respectively. In animals treated with 10% albumin immediately after the onset of heatstroke ( T (a) of 42 degrees C for 88 min), the values for MAP, ICP, CPP, CBF, brain P O(2) and striatal glutamate, glycerol, lactate/pyruvate ratio, hydroxyl radicals and neuronal damage score were 64+/-6 mmHg, 10+/-2 mmHg, 54+/-5 mmHg, 452+/-75 BPU, 15+/-2 mmHg, 3+/-2 micromol/l, 4+/-2 micromol/l, 7+/-3, 119+/-7% of baseline and 0.38+/-0.05 respectively. Apparently, the heatstroke-induced arterial hypotension, intracranial hypertension, cerebral hypoperfusion, cerebral ischaemia, brain hypoxia, increased levels of striatal glutamate, glycerol, lactate/pyruvate ratio and hydroxyl radicals, and increased striatal neuronal damage score values were all attenuated significantly by the induction of hypervolaemic haemodilution in rats immediately at the onset of heatstroke. These results demonstrate that the neuroprotective effect of hypervolaemic haemodilution is associated with a decrease in the elevation of glutamate, glycerol, lactate and free radicals in brain exposed to experimental heatstroke-induced cerebral ischaemia/hypoxia injury.
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PMID:Effect of hypervolaemic haemodilution on cerebral glutamate, glycerol, lactate and free radicals in heatstroke rats. 1468 77

The aim of the present study was to ascertain whether aminoguanidine attenuated intracranial hypertension and cerebral ischemic injury in experimental heatstroke. Urethane-anesthetized rats were exposed to heat stress (ambient temperature of 43 degrees C) to induce heatstroke. Control rats were exposed to 24 degrees C. Mean arterial pressure, cerebral perfusion pressure, and cerebral blood flow after the onset of heatstroke were all significantly lower than in control rats. However, colonic temperature, intracranial pressure, heart rate, cerebral inducible nitric oxide synthase (iNOS)-dependent NO, and neuronal damage score were greater after the onset of heatstroke. Aminoguanidine (30 micromol/kg, i.v.; 30 min before the start of heat exposure) pretreatment significantly attenuated the heatstroke-induced hyperthermia, arterial hypotension, intracranial hypertension, cerebral ischemia and neuronal damage, and increased iNOS-dependent NO formation in the brain. The extracellular concentrations of ischemic (e.g., glutamate and lactate/pyruvate ratio) and damage (e.g., glycerol) markers in the hypothalamus were also increased after the onset of heatstroke. Aminoguanidine pretreatment significantly attenuated the increase in hypothalamic ischemia and damage markers associated with heatstroke. Delaying onset of aminoguanidine administration (i.e., 0 or 30 min after the start of heat exposure) reduced the preventive efficiency on heatstroke-induced hyperthermia, arterial hypotension, intracranial hypertension, cerebral ischemia, and increased iNOS-dependent NO formation in brain. These results suggest that aminoguanidine protects against heatstroke-induced intracranial hypertension and cerebral ischemic injury by inhibition of cerebral iNOS-dependent NO production.
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PMID:Aminoguanidine protects against intracranial hypertension and cerebral ischemic injury in experimental heatstroke. 1515 51

The present study was conducted in order to evaluate the influence of hypertension on the triacylglycerol (TG) molecular species composition and other lipid classes of rat adipose tissue. In addition, the effect of two dietary oils, with a similar content in oleic acid but different TG moieties, was studied. Virgin olive oil (VOO) or high-oleic sunflower oil (HOSO) was added to a baseline diet (BD) and administrated to Wistar-Kyoto and spontaneously hypertensive rats (SHR) for 12 weeks. Both VOO and HOSO normalized the altered composition of TG molecular species and phospholipid (PL) fatty acids in SHR compared to animals fed BD, although the effect exhibited by VOO was greater. Rats fed HOSO showed a greater palmitic (p < 0.05) and lower linoleic acid (p < 0.05) incorporation into PL but a greater accumulation of linoleic acid-containing TG species, particularly dioleoyl-linoleoyl-glycerol, with a concomitant displacement of trilinolein. Both oils were capable of increasing the lipoprotein lipase (LPL) activity in normotensive rats, but only VOO did so in the SHR. Therefore, it was concluded that although oleic acid-rich diets improve some of the altered parameters of SHR adipose tissue, VOO is more effective than HOSO in this regard.
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PMID:Virgin olive oil normalizes the altered triacylglycerol molecular species composition of adipose tissue in spontaneously hypertensive rats. 1521 73

We recently observed that ANG II receptor blocker therapy improved the overproduction of triglyceride (TG) in fructose-fed rats and Zucker fatty rats with insulin resistance, which in turn suggests that ANG II may stimulate TG production. Accordingly, we investigated the effects of ANG II on TG production and the association with insulin resistance in normal rats. Male Wistar rats were continuously infused with ANG II (100 ng.min(-1).kg body wt(-1)) via an osmotic minipump for 14 days. ANG II infusion markedly elevated both the systolic and diastolic blood pressure. The plasma TG level increased twofold, but cholesterol was unchanged. ANG II infusion stimulated the TG secretion rate (TGSR) by twofold and increased the hepatic TG content by 31%. Lipogenesis determined by [2-(3)H]glycerol incorporation into hepatic TG was also significantly increased in ANG II-infused rats. The stimulatory effect of ANG II on TGSR was dose dependent and was not observed until 2 wk after the start of infusion. ANG II infusion significantly reduced insulin sensitivity index (SI) without affecting glucose effectiveness determined by Bergman's minimal model. The plasma TG level was positively correlated with TGSR (r = 0.88, P < 0.001) and inversely with SI (r = -0.80, P < 0.005). These results suggest that chronic ANG II infusion stimulates hepatic TG production, which is partly associated with simultaneous development of insulin resistance. Our results may suggest a new mechanism for the intimate association between hypertension and dyslipidemia.
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PMID:Chronic ANG II infusion increases plasma triglyceride level by stimulating hepatic triglyceride production in rats. 1521 64

Acute stroke presents an emergency that requires immediate referral to a specialized hospital, preferably with a stroke unit. Disability and mortality are reduced by 30% in patients treated in stroke units compared to those treated on regular wards, even if a specialized team is present on the ward. Systolic blood pressure may remain high at 200-220 mmHg in the acute phase and should not be lowered too quickly. Further guidelines for basic care include: optimal O2 delivery, blood sugar levels below 100-150 mg%, and lowering body temperature below 37.5 degrees C using physical means or drugs. Increased intracranial pressure should be treated by raising the upper body of the patient, administration of glycerol, mannitol, and/or sorbitol, artificial respiration, and special monitoring of Tris buffer. Decompressive craniectomy may be considered in cases of "malignant" media stroke and expansive cerebellar infarction. Fibrinolysis is the most effective stroke treatment and is twice as effective in the treatment of stroke than myocardial infarction. Fibrinolysis may be initiated within 3 h of a stroke in the anterior circulation. If a penumbra is detectable by "PWI-DWI mismatch MRI," specialized hospitals may perform fibrinolysis up to 6 h after symptom onset. In cases of stroke in the basilar artery, fibrinolysis may be performed even later after symptom onset. Intra-arterial fibrinolysis is performed in these cases using rt-PA or urokinase. Follow-up treatment of stroke patients should not only address post-stroke depression and neuropsychological deficits, but also include patient education about risk factors such as high blood pressure, diabetes mellitus, and cardiac arrhythmias.
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PMID:[Basics of acute stroke treatment]. 1586 21

Endothelial function is reduced by age, chronic heart failure, coronary artery disease, hypertension or type 2 diabetes, and it is shown that aerobic exercise may reverse this trend. The effect of a high aerobic training status on endothelial function in young, healthy subjects is however less clear. The present study was designed to determine whether endothelial function is improved in highly endurance-trained young women compared to sedentary, healthy controls. Brachial artery diameter was measured in 16 endurance-trained (age: 23.7 +/- 2.5 years, maximal oxygen uptake (VO2max): 60.6 +/- 4.5 ml/kg per min) and 14 sedentary females (age: 23.7 +/- 2.1 years, VO2max: 40.5 +/- 5.6 ml/kg per min) at rest, during flow-mediated dilation (FMD) and after sublingual glycerol trinitrate administration, using high-resolution ultrasound. FMD did not differ between the endurance-trained and the sedentary females (14.8% vs 16.4%, p = NS), despite a substantial difference in VO2max of 50% (p < 0.001). The endurance-trained group possessed however, a 9% larger resting brachial artery diameter when adjusted for body surface area. The results of the present study suggest that endothelial function is well preserved in young, healthy women, and that a high aerobic training status due to long term aerobic training does not improve the dilating capacity any further.
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PMID:Endothelial function in highly endurance-trained and sedentary, healthy young women. 1601 93

Antiphospholipid antibodies (aPLs) are characterized as heterogeneous and nonspecific autoantibodies directed against cardiolipin, ph-serine, ph-inositol, ph-acid, ph-glycerol, ph-choline, annexin V, and co-actor Beta2-glycoprotein I. aPLs occur during various autoimmune diseases, infectious diseases, neurological and kidney diseases, transplant loss, metabolic diseases, and drug abuse. They are also found in connection with reproductive failure. Antiphospholipid syndrome (primary or secondary) has to be treated according to the type and levels of aPLs as well as clinical symptoms (such as repeated pregnancy loss, preeclampsia, repeated missed abortions, unexplained hypertension, repeated delivery of hypotrophic fetuses) by a team of clinicians such as rheumatologists, reproductive immunologists, hematologists, and obstetricians. Based on clinical experience a low dose of heparin/fraxiparine or a low dose of aspirin and corticosteroids is used. This chapter contains up-to-date information about the clinical and laboratory significance of the antiphospholipid syndrome.
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PMID:Antiphospholipid antibodies and reproductive failure. 1612 43

We assess the effects of ipsapirone (a 5-HT1A receptor agonist), ketanserin (a 5-HT2A receptor antagonist), (-)-pindolol (a 5-HT1A receptor antagonist), and DOI (a 5-HT2A receptor agonist) on heatstroke in a rat model. Animals, under urethane anesthesia, were exposed to high ambient temperature of 42 degrees C until mean arterial pressure and local cerebral blood flow in the striatum began to decrease, which was arbitrarily defined as the onset of heatstroke. Normothermic controls were exposed to room temperature of 24 degrees C. In rats treated with normal saline immediately before the initiation of heat stress, the values for survival time were found to be 21 to 25 min. Systemic administration of ipsapirone (10 mg/kg) or ketanserin (2 mg/kg) immediately before the initiation of heat stress significantly increased the survival time to new values of 92 to 104 min. Combined treatment with ipsapirone and ketanserin had additive effects (survival time of 156-194 min). In contrast, systemic administration of (-)-pindolol (2 mg/kg) or DOI (2 mg/kg) significantly decreased the survival time to new values of 2 to 3 min. In vehicle-treated heatstroke rats, the values for core temperature, intracranial pressure, and the extracellular levels of cellular ischemia (e.g., glutamate and lactate/pyruvate ratio) or damage (e.g., glycerol) markers and neuronal damage scores in striatum were significantly higher than those of normothermic controls. On the other hand, the values for mean arterial pressure, cerebral perfusion pressure, cerebral blood flow, and brain partial pressure of O2 were significantly lower than those of normothermic controls. The heatstroke-induced hyperthermia, arterial hypotension, intracranial hypertension, cerebral hypoperfusion and hypoxia, and increased levels of cellular ischemia and damage markers in striatum were all significantly attenuated by prior administration of ipsapirone or ketanserin. The present results strongly suggest that previous activation of 5-HT1A receptors or antagonism of 5-HT2A receptors protects against heatstroke by reducing circulatory shock and cerebral ischemia, whereas prior antagonism of 5-HT1A receptors or activation of 5-HT2A receptors exacerbates heatstroke.
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PMID:Ipsapirone and ketanserin protects against circulatory shock, intracranial hypertension, and cerebral ischemia during heatstroke. 1620 18

Naltrexone, a nonselective antagonist of opioid receptors, is found to be beneficial in protecting against heatstroke. Further investigation using selective mu, delta, and kappa opioid receptor antagonists are needed to prove the involvement of specific receptors in heatstroke. Rats under sodium pentobarbital anesthesia were exposed to high ambient temperature of 43 degrees C to induce heatstroke. Control rats were exposed to 24 degrees C. In rats treated with normal saline 20 minutes before heat stress, the values for survival time were found to be 89-101 minutes. Intravenous administration of CTAP (a selective mu-opioid receptor antagonist; 50-200 microg/kg), but not nor-binaltorphimine (20-200 microg/kg; a kappa-opioid receptor antagonist) or ICI-174864 (50-500 microg/kg; a delta-opioid receptor antagonist), significantly increased the survival time to new values of 180-212 minutes. In vehicle-treated rats after heatstroke onset, the values for core temperature, intracranial pressure, and the extracellular markers for ischemia (eg, glutamate and lactate/pyruvate ratio) or damage (eg, glycerol) and neuronal damage scores in striatum were significantly higher than those of normothermic controls. In contrast, the values for mean arterial pressure, cerebral perfusion pressure, cerebral blood flow, and brain partial pressure of O2 were significantly lower than those of normothermic controls. The heatstroke-induced hyperthermia, arterial hypotension, intracranial hypertension, cerebral hypoperfusion and hypoxia, and increased levels of cellular ischemia and damage markers in striatum were all significantly attenuated by prior administration of CTAP. The data indicate that prior antagonism of mu-opioid receptors protects against circulatory shock and cerebral ischemia during heatstroke.
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PMID:Mu-opioid receptor blockade protects against circulatory shock and cerebral ischemia during heatstroke. 1630 98

The water channel protein PvTIP3;1 (alpha-TIP) is a member of the major intrinsic protein (MIP) membrane channel family. We overexpressed this eukaryotic aquaporin in the methylotrophic yeast Pichia pastoris, and immunogold labeling of cellular cryosections showed that the protein accumulated in the plasma membrane, as well as vacuolar and other intracellular membranes. We then developed an in vivo functional assay for water channel activity that measures the change in optical absorbance of spheroplasts following an osmotic shock. Spheroplasts of wild-type P. pastoris displayed a linear relationship between absorbance and osmotic shock level. However, spheroplasts of P. pastoris expressing PvTIP3;1 showed a break in this linear relationship corresponding to hypo-osmotically induced lysis. It is the difference between control and transformed spheroplasts under conditions of hypo-osmotic shock that forms the basis of our aquaporin activity assay. The aquaporin inhibitor mercury chloride blocked water channel activity but had no effect on wild-type yeast. Osmotically shocked yeast cells were affected only slightly by expression of the Escherichia coli glycerol channel GlpF, which belongs to the MIP family but is a weak water channel. The important role that aquaporins play in human physiology has led to a growing interest in their potential as drug targets for treatment of hypertension and congestive heart failure, as well as other fluid overload states. The simplicity of this assay that is specific for water channel activity should enable rapid screening for compounds that modulate water channel activity.
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PMID:In vivo functional assay of a recombinant aquaporin in Pichia pastoris. 1646 5


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