Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of enflurane with and without nitrous oxide on coronary haemodynamics and myocardial oxygenation were investigated in 11 patients with generalised atherosclerotic disease. Enflurane decreased systemic blood pressure (-50%) mainly by systemic vasodilation (SVR -41%) and to a lesser degree by impairment of cardiac performance (CO -27%). A change from 1MAC enflurane-nitrogen-oxygen (70/30) to 1MAC enflurane-nitrous oxide-oxygen (70/30) decreased blood pressure and cardiac output further (-16% and -14%). Enflurane-nitrogen-oxygen decreased coronary blood flow (-29%) and perfusion pressure (-47%). Coronary vascular resistance fell (-20%) along with decreases in myocardial oxygen consumption and extraction (-40% and -16%). Regional coronary blood flow measurements in four of the patients revealed maldistribution of blood flow. During enflurane-nitrous oxide-oxygen, myocardial oxygen consumption and extraction decreased further (-29% and -12%) without change in coronary blood flow or resistance. Myocardial ischaemia was observed in four patients during enflurane-nitrogen. During enflurane-nitrous oxide, ischaemia disappeared in two of the previously ischaemic patients and appeared in two not previously ischaemic. The regional blood flow maldistribution was abolished with nitrous oxide. It is concluded that enflurane is a powerful coronary vasodilator and in this respect slightly less potent than isoflurane. Enflurane may induce myocardial ischaemia by redistributing coronary blood flow and/or by producing hypotension. Nitrous oxide added to enflurane depresses cardiac function and augments the coronary vasodilatory effect of enflurane to a level at which coronary blood flow becomes totally pressure dependent.
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PMID:Effects of enflurane on coronary haemodynamics in patients with ischaemic heart disease. 652 84

Positron emission tomography (PET) performed after the administration of the positron-emitting radionuclides carbon-11 (11C), nitrogen-13(13N), oxygen-15(15O) and fluorine-18(18F) has permitted the improved noninvasive assessment of the regional myocardial metabolism of normal physiologic substrates and intermediates and their cogeners. In experimental animals, the rate of oxidation of 11C-palmitate correlates closely with other indexes of oxygen consumption, and the extraction of 11 C-palmitate (like that of 18F-fatty acids and 18F-fluordeoxyglucose) is markedly diminished in regions of myocardial ischemia. In both experimental animals and in patients, myocardial infarct site and size, determined by positron emission tomography after the intravenous injection of 11C-palmitate, correlate closely with the electrocardiographic infarct locus and enzymatically estimated infarct size as well as with the location and extent of regional left ventricular wall motion abnormalities. PET offers promise for assessment of flow as well despite the complexities involved. PET with 13NH3 appears to provide one useful qualitative index, although this tracer is actively metabolized. Because of the quantitative capabilities of positron emission tomography and the rapid progress which is being made in the development of fast scan, multi-slice, and gated instrumentation, this technique is likely to facilitate improved understanding and characterization of regional myocardial metabolism and blood flow in man under physiological and pathophysiological conditions.
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PMID:Cardiac positron tomography: current status and future directions. 697 Jan 58

The identification of metabolic and drug interventions able to reduce myocardial injury after coronary artery occlusion requires experimental models. The rat model of ischemic injury is technically simple, unexpensive, informative and accessible to quantitative studies. In this present study, 41 rats underwent temporary myocardial ischemia of variable duration using left coronary artery ligation. They were sacrificed at 48 hours, and the heart was immediately frozen in liquid nitrogen. Serial 8 micrometer sections of known intervals were tested for succinodehydrogenase (NBT stain). Gross sectional areas measured planimetrically were utilized to calculate total myocardial volume (Vmyocardium) and infarcted myocardial volume (Vinfarct) with the aid of a programmable calculator. The data showed a linear regression for Vinfarct/Vmyocardium according to the time of ischemia (p 0,001). We suggest to test the efficiency of metabolic and drug interventions on the regression curve of the necrotic tissue using a multiple linear analysis. Since ischemic changes evolve more rapidly in this model, the intervention under study should be set up at the time of coronary artery occlusion.
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PMID:Experimental myocardial infarction in the rat as a quantitative model for the study of anti-ischemic interventions. 731 11

The effects of thromboxane (Tx) inhibition or arachidonic acid (AA) infusion were studied in anesthetized cats during acute myocardial ischemia (MI). AA (7.2 mg kg-1 h-1) or imidazole (25 mg kg-1 h-1) infusions were initiated 30 min after occlusion of the left anterior descending coronary artery. Assessment of the degree of protection of the ischemic myocardium was made by measurement of S-T segment elevation, plasma and myocardial creatine phosphokinase (CPK) activities, and myocardial amino-nitrogen content. Assessment of Tx inhibition was performed by radioimmunoassay. Administration of imidazole inhibited the sevenfold increase in plasma thromboxane B2 (TxB2) levels occurring in MI (p less than 0.001 at 2-5 h), markedly decreased S-T segment elevations at 2-k h (p less than 0.025), significantly prevented the elevation in plasma CPK (p less than 0.05, at 4 and 5 h), the increase in TxB2 post-MI, significantly decreased (p less than 0.025) S-T segment evaluations at 2-5 h, caused a decrease in plasmaCPK levels (p less than 0.05 at 5 h), but did not prevent loss of myocardial CPK or amino-nitrogen. In summary, the administration of imidazole resulted in significant protection of the myocardium in all indices of ischemic damage measured, while AA infusion resulted in only a partial protection. The mechanism of the imidazole protection of ischemic myocardial tissue appears to be via inhibition of Tx synthesis althoug we cannot exclude a hemodynamic or cytoprotective mechanism. These results suggest that specific inhibition of Tx formation is beneficial during acute MI.
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PMID:Influence of thromboxane inhibition on the severity of myocardial ischemia in cats. 737 31

An 81-year-old man with a history of chronic pulmonary disease due to heavy smoking and ischemic heart disease had been suffering for the past few years from chronic constipation and urinary incontinence and was receiving medication for cardiopulmonary symptoms and urinary incontinence. He was admitted for repeated falling for a few months prior to admission. When put in the supine position, his blood pressure fell. He had bilateral pulmonary rales, consistent with lung disease, eccentricity of the left pupil (after cataract surgery), constriction of the right pupil, and absence of the pupillary light reflex. There was generalized hyperreflexia and a bilateral Babinski sign. He had normocytic, normochromic anemia; B12, folic acid and ferritin were within normal ranges, ESR was rapid, there was hyperglobulinemia (IgA and IgG), urea nitrogen and creatinine were increased but returned to normal after rehydration. ECG and chest X-ray were consistent with his cardiopulmonary status. Bone-marrow biopsy showed hypocellularity. IVP and barium enema were normal. Echocardiography revealed a possible old posterior wall myocardial infarction. CT-scan showed moderate cerebral and cerebellar atrophy, calcifications in the carotid and vertebral arteries, and small infarcts in both hemispheres. At this point, after an extensive survey of the literature, the diagnosis of Shy-Drager syndrome was proposed and proved by monitoring ECG and serum levels of noradrenaline during postural changes. He was treated with Fluorinef and there were no more episodes of postural hypotension. Several weeks after discharge he reported that he was feeling well and had not fallen since discharge.
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PMID:[Shy-Drager syndrome]. 775 2

Examinations are performed on 120 workers from the plant for nitrogen and 253 workers from the plant for phosphorous fertilizers. For comparison is used a control group of 103 persons having no professional contact with chemical noxa. The measuring of the arterial pressure and assessment of the arterial hypertension rate is performed after the standardised method of the World Health Organization (1984). The probability of ischemic disease of the heart is determined on the basis of the electrocardiographic changes (Minnesota code) and the data of the questionnaire of G. A. Rose (WHO, 1984). The results point out, that the arterial hypertension incidence and that of the ischemic disease of the heart in the exposed workers in both plants is insignificantly higher than that of the controls. There is no effect of the specialized length of service on the dissemination of the registered cardio-vascular diseases. The data of the carried out investigation show no presence of heightened risk of arterial hypertension and ischemic heart disease in workers from the nitrogen and phosphorous fertilizers production.
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PMID:[The incidence of arterial hypertension and ischemic heart disease in workers manufacturing nitrogen and phosphorus fertilizers]. 784 66

A comparative community-based study of serum lipids and other blood chemistry data in the elderly was carried out in two Japanese rural towns, Kahoku and Yaku. We studied the following blood chemistry factors; total proteins (TP), albumin (Alb), blood glucose (glucose), urea nitrogen (BUN), uric acid (UA), total cholesterol (T-Cho), high density lipoprotein (HDL-C) and lipoprotein (a) (Lp(a)). Subjects were the 312 eligible elderly aged over 75 years in Kahoku, and 172 similar elderly in Yaku. There were no significant differences in TP, Alb, glucose, BUN and UA of the elderly in the two areas. Mean HDL-C level was significantly lower and mean Lp(a) concentration was significantly higher in the elderly in Kahoku than in Yaku, Mean value of T-Cho did not differ significantly between the elderly in the two areas, however, the ratio of subjects whose T-Cho concentrations were over 220 mg/dl was significantly higher in Kahoku than in Yaku. These data suggested that the risk of atherosclerosis from the standpoint of view of serum lipids was higher in the elderly in Kahoku than in those in Yaku. Epidemiological data of Kochi and Kagoshima prefecture indicated that the mortality ratio from ischemic heart disease was higher in Kahoku than in Yaku, although that from cerebral infarction was lower in Kahoku than in Yaku. Comparative study of laboratory data in various districts is useful to investigate the relationship between lifestyle and diseases.
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PMID:[Comparative study of serum lipids and other blood chemistry factors in the elderly in Kahoku and Yaku]. 785 42

It is currently believed that reactive oxygen species are produced in the heart post-ischemia reperfusion, causing pathophysiological disorders. Studies reported in the literature dealing with this subject have generated contradictory findings. The aim of this study was to assess the catalytic activity of the superoxide anion-producing enzyme xanthine oxidase, and the level of lipid peroxides in isolated rat heart muscle undergoing ischemia of varying duration and severity followed by reperfusion. Three levels of ischemia were investigated: total, and partial at either 0.10 or 0.35 ml/min (residual flow rate). Three different periods of ischemia were examined in each case. After each period of ischemia, followed by 10 min of reperfusion, the heart was frozen in liquid nitrogen. Xanthine oxidase activity and lipid peroxide levels were assayed in the cardiac homogenate and in the centrifuged supernatant, respectively. In the different experimental protocols studied here, both cardiac xanthine oxidase and lipid peroxide levels remained statistically unchanged compared to the continuously perfused control hearts. Moreover, in a recent study (Boucher et al., FEBS Lett. 203, 261-264, 1992), we were unable to detect reactive oxygen species in perfusate upon reperfusion of ischemic rat hearts. These results suggest that changes in xanthine oxidase activity during myocardial ischemia-reperfusion, and lipid peroxidation, as assessed by measuring thiobarbituric acid reactants and lipid hydroperoxides, are not predominant phenomena in ischemia-reperfusion-induced injury, at least in the experimental model used in this study.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Xanthine oxidase activity and lipid peroxide content following different types of ischemia in the isolated rat heart. 794 21

Myocardial ischemia can be detected at the mitochondrial level by measuring shifts in nicotinamide adenine dinucleotide and its reduced form. Using a pulsed nitrogen laser and an optical multichannel analyzer, we monitored myocardial metabolism by measuring laser-induced nicotinamide adenine dinucleotide (reduced form) fluorescence in a large animal model of acute ischemia. Eight opened-chest sheep underwent occlusion of branches of the left anterior descending coronary artery, establishing a 15% infarct of the left ventricle. For the simulation of the clinical scenario, after 60 minutes of occlusion, the animals were supported by cardiopulmonary bypass, the aorta was crossclamped, and cold crystalloid cardioplegic solution was administered. The occlusion was removed after 10 minutes, and two additional doses of cardioplegic solution were delivered at 10-minute intervals. The aortic crossclamp was released, and a 30-minute period of reperfusion on bypass ensued. The hearts were then weaned off bypass and allowed to recover. Laser-induced fluorescence was measured inside, outside, and along the border of the infarct. Baseline measurements were made before occlusion, immediately after occlusion, and then at 5, 10, and 20 minutes after occlusion. The results show that immediately after occlusion there is a 200% +/- 30% (mean +/- standard deviation) increase in laser-induced fluorescence in the infarct zone, a 110% +/- 30% increase along the border, and no significant change in the area outside the infarct. The fluorescence in the infarct reaches a plateau in 5 minutes at 270% +/- 30%, whereas along the border it reaches a peak near end ischemia of 110% +/- 40%. With the first dose of cardioplegic solution, fluorescence increases outside the infarct and decreases inside the infarct and along the border to 120% +/- 30%, where it remains for all areas until the aortic crossclamp is removed. Fluorescence then drops to 70% +/- 20% and finally returns to baseline after 5 minutes of recovery. All of these shifts in laser-induced fluorescence were statistically significant (p < 0.01). The changes noted with doses of cardioplegic solution reflect the hypothermic and hyperkalemic effects on the myocardium. Laser-induced fluorescence provides a sensitive and specific method of monitoring myocardial ischemia during the operation. It also provides instantaneous feedback of metabolic changes that may be useful in evaluating the effects of different cardioplegic regimens and in monitoring reperfusion injury.
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PMID:Intraoperative myocardial ischemia detection with laser-induced fluorescence. 828 89

The purpose of this study was to define the physiologic responses of the heart and peripheral circulation to chronic anemia using noninvasive measurements while eliminating confounding biochemical, pharmacologic and physiologic variables. Stable chronic hemodialysis patients were studied at the University Hospital based chronic dialysis unit and echocardiography laboratory before and after therapy with human recombinant erythropoietin (rHuEPO). Subjects included maintenance hemodialysis patients free of left ventricular regional wall motion abnormalities discernible by echocardiography, rhythm disturbance, significant valvular or ischemic heart disease. Two-dimensional echocardiograms and simultaneous targeted M-mode echocardiograms, phonocardiograms and externally acquired subclavian artery pulse tracings were used to measure whole blood viscosity, arterial blood gases and ionized calcium, complete blood count, electrolytes, creatinine, blood urea nitrogen (BUN), and inorganic phosphate. All measurements were made immediately post-dialysis before and after therapy with rHuEPO. The interval between pre- and post-rHuEPO studies was 8.3 +/- 2.3 months. We found that post-dialysis hematocrit rose from 24.7 +/- 0.9 to 36.4 +/- 0.9%, hemoglobin from 83 +/- 3 to 121 +/- 3 g/liter and whole blood viscosity from 2.87 +/- 0.11 to 3.71 +/- 0.18 centipoise (all, P < 0.001 after therapy with rHuEPO). The remaining biochemical measurements did not change. Heart rate fell from 83 +/- 3 to 77 +/- 3 beats/min (P = 0.013). Left ventricular preload and afterload were not statistically different before and after rHuEPO. Total vascular resistance rose from 1313 +/- 84 to 1568 +/- 129 dynes.sec.cm-5, P = 0.029. Cardiac output and cardiac index fell by 12 and 15% (P = 0.024 and 0.030), respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiovascular consequences of correction of the anemia of renal failure with erythropoietin. 830 32


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