Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Atherogenic traits, living habits, signs of preclinical disease, and susceptibility all contribute to cardiovascular disease. High low-density lipoprotein is positively related to coronary heart disease, and high high-density lipoprotein is inversely related. Systolic or diastolic hypertension at any age in either sex contributes powerfully. The impact of diabetes is greater for women and varies with the number of accompanying risk factors. High-normal fibrinogen values further escalate risk of these atherogenic factors. An atherogenic life-style is typified by a diet excessive in fat, calories, and salt; sedentary habits; unrestrained weight gain; and cigarette smoking. Moderate alcohol use may be beneficial. Use of oral contraceptives beyond age 35 years and in conjunction with cigarette smoking predisposes one to thromboembolism. Type A behavior carries an increased risk, and men married to more highly educated women and to women in white-collar jobs are more vulnerable. Signs of preclinical ischemia include silent myocardial infarction, left ventricular hypertrophy on ECG, blocked intraventricular conduction, and repolarization abnormalities. Measures of innate susceptibility include a family history of early cardiovascular disease. Quantitative combination of risk factors provides optimal prediction, including persons with multiple marginal abnormalities. Preventive management should also be multifactorial and requires a commitment to behavior modification and alteration in life-style.
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PMID:New perspectives on cardiovascular risk factors. 330 Feb 33

A simple, sensitive HPLC method using fluorescence detection was developed for determination of adenosine in fetal venous perfusates of dual-perfused cotyledons from human term placentas. Maternal and fetal circuits of in vitro placental cotyledons were perfused with physiological salt solution containing dextrose and dextran (Earle's medium). Conditions were established for optimal formation of fluorescent 1,N6-ethenoadenosine from adenosine and chloroacetaldehyde in Earle's medium and for optimal resolution of 1,N6-ethenoadenosine by reversed-phase HPLC of the reaction mixture. The yield of 1,N6-ethenoadenosine was enhanced by dilution and acidification of the sample matrix. Perfusate samples in autosampler vials were diluted 40% with water and reacted with chloroacetaldehyde for 40 min at 100 degrees C; replicate 100-microliters injections were made automatically from each reaction mixture for HPLC analysis with fluorescence detection on a column packed with 3 microns octadecylsilica (Hypersil). Calibration curves were prepared similarly from 4-100 nM adenosine in Earle's medium. Alternatively, perfusate samples were diluted twofold with dilute phosphoric acid to give a final pH of 5.4 before reaction with chloroacetaldehyde, and replicate 50-microliters injections were made automatically for HPLC; calibration curves were prepared from 2-400 nM adenosine in Earle's medium. 1,N6-Ethenoadenosine was well resolved from Earle's-derived artifactual peaks on chromatography with either a linear or a concave gradient of methanol in ammonium phosphate buffer. Total run times were 15 and 19 min, respectively. Sensitivity of measurement of adenosine was 2-4 nM. Derivatization of adenosine using the acidified reaction mixture gave a limit of detection of 100 fmol of adenosine per injection. Application of the method to analysis of adenosine in fetal venous perfusates of eight dual-perfused cotyledons, each from a different placenta, gave a range of 3.5-52 nM adenosine. Ischemia, imposed by cessation of maternal perfusion, caused a two- to sixfold increase in fetal venous perfusate adenosine concomitant with an increase in fetoplacental perfusion pressure; perfusion pressure and perfusate adenosine returned to baseline levels on reperfusion of the maternal circuit. This facile method of determination of perfusate adenosine should allow investigation of the role of placental adenosine release in regulation of fetoplacental vascular resistance and should be applicable to study of adenosine released by other isolated perfused organs.
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PMID:Determination of adenosine in fetal perfusates of human placental cotyledons using fluorescence derivatization and reversed-phase high-performance liquid chromatography. 340 8

The influence of long-term infusion of the calcium-entry blocker diltiazem on postischemic acute renal failure was investigated in conscious dogs monitored by implanted instruments. In 18 uninephrectomized beagle dogs on a salt-rich diet, an electromagnetic flow probe and an inflatable plastic cuff were placed around the renal artery. Acute renal failure was induced by inflating the cuff for 180 min in the conscious animal. Group A (n = 5, control) received an intraaortic injection of 0.9% NaCl (5 ml/day) from the 3rd day before until the 7th day after ischemia and group B (n = 6, posttreatment) an intra-aortic injection of diltiazem (5 micrograms X min-1 X kg-1) beginning at the end of ischemia until the 7th day. Group C (n = 7, pre- and posttreatment) received diltiazem from the 3rd day before until the 7th day after ischemia. In group A, renal blood flow dropped from 149 +/- 16 (preischemic) to 129 +/- 29 ml X min-1 on the 1st day after ischemia. In contrast, renal blood flow increased on the 1st postischemic day in both treatment groups by 29 +/- 15% (group B, P 0.05) and 14 +/- 13% (group C). In the following days, there was no significant difference in renal blood flow between groups A, B and C. In group B, the reduction of the glomerular filtration rate was similar to that in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The influence of long-term infusion of the calcium antagonist diltiazem on postischemic acute renal failure in conscious dogs. 351 3

Bile formation is an active secretory process involving bile salt-dependent and -"independent" mechanisms. This study was performed to determine the effect of selected periods of warm ischemia on biliary secretion. Rats were studied using an in situ liver perfusion system after stabilization of bile flow with intravenous sodium taurocholate. Bile flow remained stable in control livers and ceased during ischemic periods of 15 or 25 min. After reperfusion of 15-min ischemic livers, bile flow was depressed but returned to normal by 45 min of reperfusion. After 25 min of ischemia, bile flow remained depressed. A similar depression in bile salt secretion was observed. These studies indicate that both bile flow and bile salt secretion reflect the degree of ischemia in this isolated perfused system, and further use of this model for the investigation of biliary flow as an index of ischemic injury is warranted.
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PMID:Bile flow--an index of ischemic injury. 358 26

Furfuryl amine salt of 4-chloro-N-(2-furylmethyl)-5-sulfamoyl anthranilic acid was shown to exert more pronounced diuretic and saluretic action in rats, mice and dogs than that of furosemide. The previous administration of furfuryl amine salt of furosemide promoted normalization of the excretory processes of the kidney and increased survival rate of rats in ischemia of the single kidney. The antiedema activity of the drug was found to be much more pronounced than that of furosemide.
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PMID:[Pharmacological activity of the furfuryl amine salt of 4-chloro-N-(2-furylmethyl)-5-sulfamoyl anthranilic acid]. 381 48

The unique architecture and organization of medullary vasculature permit regional regulation of medullary hemodynamics by vasoactive hormones and are conducive to the operation of the countercurrent multiplication system. Recent studies suggest that an increase in inner medullary blood flow causes medullary solute washout, which in turn decreases passive sodium transport in the thin ascending limb of Henle's loop. In canine models of chronic sodium retention accompanied by activation of the renin-angiotensin system, glomerular filtration rate (GFR), renal blood flow (RBF), and intracortical blood flow distribution were similar to those in normal dogs; however, papillary plasma flow (PPF) was markedly reduced and papillary tissue solute content was increased significantly both during hydropenia and after saline loading. During euvolemic diuresis with loop diuretics, there was an increased renin release associated with a marked reduction in PPF, despite an increase in total RBF. Direct intrarenal infusion of angiotensin II (AngII) (at a dose not affecting GFR and RBF) induced ipsilateral sodium retention, conservation of urinary concentration, and papillary ischemia. These studies provide evidence for regional regulation of medullary hemodynamics by AngII, possibly contributing to sodium retention in chronic salt-retaining states.
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PMID:Contribution of angiotensin to the control of medullary hemodynamics. 395 61

Eicosapentaenoic acid is converted by cyclo-oxygenase to the prostacyclin, PGI3. Consequently eicosapentaenoic acid might protect the brain from the impairment in cerebral blood flow that follows temporary cerebral arterial occlusion. We studied the effect of 90% pure eicosapentaenoic acid, given intravenously, on cerebral blood flow, brain water and prostaglandins after ischemia in gerbils. Ischemia was produced by bilateral carotid occlusion for 15 min followed by reperfusion for 2 h. In experimental gerbils, 0.833 mg or 0.167 mg of eicosapentaenoic acid (Na salt) was given intravenously followed by a continuous infusion of 1 mg h-1. Control gerbils were given 0.167 mg of linoleic acid (Na salt) intravenously followed by a continuous infusion of 1 mg h-1 or a saline infusion. Regional cerebral blood flow was measured by the hydrogen clearance method and brain water by the specific gravity technique. Brain diene prostaglandins were measured by radioimmunoassay. In control gerbils cerebral blood flow decreased significantly during reperfusion and remained depressed after 2 h of reperfusion. In eicosapentaenoic acid treated gerbils blood flow decreased initially but after 2 h of reperfusion blood flow was significantly higher than in control gerbils. Brain edema and brain diene prostaglandins were not significantly different between control and experimental groups. Our study indicates that eicosapentaenoic acid, given intravenously, improves cerebral blood flow after ischemia and reperfusion. We speculate that this effect may be due to the formation of the prostacyclin, PGI3.
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PMID:Effect of intravenous eicosapentaenoic acid on cerebral blood flow, edema and brain prostaglandins in ischemic gerbils. 609 43

The protective effects of the beta-adrenergic blocking drugs, propranolol and atenolol, were tested in a model of global ischemia and assessed electron microscopically. Cats isolated hearts were perfused retrogradely with arterial blood drawn from donor cats. After a period of equilibration, isolated hearts were rendered globally ischemic for 1 h and subsequently reperfused for another hour. Hearts were then flushed with physiological salt solution followed by perfusion-fixation with cacodylate-buffered glutaraldehyde, containing ionic lanthanum. Lanthanum was included as a probe of myocardial membrane integrity. Left ventricular subendocardial samples were processed and examined electron microscopically. Nontreated hearts, which underwent normothermic ischemia and reperfusion, displayed extensive ultrastructural damage. Nonischemic and donor cat control myocardial tissue appeared normal in all respects. Hearts that received either propranolol or atenolol maintained their ultrastructural integrity, resembling controls. Ionic lanthanum proved to be reliable as a marker of membrane integrity and permeability, as nontreated hearts displayed intracellular deposition of the marker, indicating that deteriorations of membrane integrity occurred. The results suggest that beta-adrenergic blockade may be valuable in preserving myocardium subjected to ischemia and reperfusion.
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PMID:Protective effects of beta-adrenergic blockade in isolated ischemic hearts. 610 35

The effects of amino acids aspartate (Asp) and glutamate (Glu) on recovery of contractile function and preservation of compliance were studied in globally ischemic, isolated, blood-perfused cat hearts. Ischemia-induced declines in contractility and compliance were measured with an intraventricular fluid-filled balloon. Asp and Glu were delivered to isolated hearts in physiological salt solution (PSS) containing 10 mM glucose, just prior to, and intermittently during (every 15 min for 1 min) 1 h of normothermic ischemia. Isolated hearts which received Asp and Glu showed recoveries of left ventricular (LV) developed pressure of 79 +/- 8 and 50 +/- 7% of their preischemic values, respectively, compared to 34 +/- 7% in hearts perfused only with PSS. These alterations of contractile function were paralleled by changes in LV compliance. The addition of amino-oxyacetate, and aminotransferase inhibitor, to Asp- containing PSS markedly attenuated the beneficial effects of this amino acid. The results indicate that certain amino acids can protect the ischemic myocardium, presumably through effects on intermediary metabolism.
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PMID:Comparative effects of aspartate and glutamate during myocardial ischemia. 611 86

Severe head injury often produces complex intracranial displacements of the brain, resulting in widespread, often microscopic lesions. These are responsible for two types of edema: vasogenic edema, with outflow of molecules and fluid into the extracellular spaces by rupture of the blood-brain barrier and vasoplegia, and cytotoxic edema, with swelling of astrocytes due to membrane lesions. The connexions between these two types of edema are still obscure. Alterations in membrane phospholipids may impede function of Na-K pump enzymes, causing accumulation of water in the cell. Cerebral edema is responsible for intracranial hypertension and tentorial herniation, which in turn increase edema through venous compression, ischemia, and hypoxia. The least controversial anti-edema therapeutic measures include relative fluid and salt restriction, mannitol if called for, neuroplegia, in particular with diazepam and Gamma-OH, and assisted ventilation.
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PMID:[Post-traumatic cerebral edema. Physiopathology and treatment]. 632 13


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