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)

Hepatic blood flow was monitored in cats during myocardial ischemia (MI). Increased plasma CPK activity, the S-T segment of the electrocardiogram, and hepatic flow was reduced by 5 h to 40% of control. The results suggest that MI can influence organs distant from the original ischemic episode.
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PMID:Hepatic blood flow in acute myocardial ischemia. 52 Apr 66

Nitroglycerin (NTG) traditionally has bben avoided in the treatment of pain caused by acute myocardial infarction because of the belief that NTG-induced decrease in arterial pressure and concomitant reflex increase in heart rate might extend the ischemic process. However, recent experimental and clinical investigations cast doubt on this concept. For example, when the left anterior descending coronary artery is acutely occluded in normal dogs or in dogs when chronic coronary occlusions and extensive collaterals, NTG reduces ST-segment evevation (and presumably myocardial ischemia). This salutary effect occurs despite lowering of systemic arterial pressure, as long as excessive reflex tachycardia does not result; the magnitude of ischemia reduction is potentiated when methoxamine or phenylephrine are administered simultaneously to abolish the NTG -induced hypotension and reflex tachycardia. NTG and methoxamine treatment also results in 1) reduction of infarct size as (as assessed by gross morphologic examinations and myocardial CPK levels) in dogs subjected to 5 hours of coronary occlusion, and 2) increase in ventricular fibrillation (VF) threshold and reduction of the incidence of spontaneously occurring VF in dogs with acute coronary occlusion. Finally, the effectiveness of NTG during acute myocardial iinfarction (AMI) in man has been studied. Multiple precordial electrodes were used to measure changes in the degree of ST-segment elevation; these changes were used as an index of alterations in myocardial ischemic injury. Patients with normal pulmonary capillary wedge pressures ( less than 15 mm Hg) did not benefit consistently from NTG alone; however, when phenylephrine was administered with NTG (to abolish NTG-induced arterial pressure reduction and reflex increase in heart rate), ST-segment elevation diminished consistently. In patients with elevated wedge pressures ( greater than 15 mm Hg), NTG alone consistently reduced ischemia; addition of phenylephrine often partially reversed this benefit. Thus, administration of NTG, alone or with phenylephrine, appears to reduce myocardial ischemic injury during AMI in man; however, the response to phenylephrine depends upon the presence or absence of LV failure prior to treatment. These experimental and clinical results suggest this form of therapy may be use in reducing infarct size in man, although additional studies are necessary to determine the functional significance of these acute electrophysiologic alterations.
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PMID:Protection of ischemic myocardium by nitroglycerin: experimental and clinical results. 81 59

Repeatedly bred male rats which develop arteriosclerosis spontaneously were subjected to unilateral nephrectomy, 1% saline drinking water, and 2 mg subcutaneous injections of deoxycorticosterone acetate per animal weekly for 7 weeks to induce severe hypertension (+/- 175 mmHg systolic). Acute cerebral ischemia was induced by ligating one carotid artery. Two days later, experimental animals were subjected to acute myocardial ischemia by injecting them subcutaneously with a single dose of isoproterenol (25 mg/100 g body weight). All of the experimental animals died within 4 hours of the injection of isoproterenol. During this same period, blood pressure, body weight, thymus, kidney, and testicular weights were reduced, whereas heart and adrenal gland weights increased markedly. Serum enzymes (CPK, SGOT, and LDH), lipids (triglycerides and free fatty acids), glucose, BUN, and corticosterone rose progressively. Fatty infiltration of the liver, adrenal hyperplasia, myocardial thrombi, renal degenerative changes, and cerebral edema became progressively more severe. A hypothalamic-pituitary-adrenal axis component may be involved in the reaction to the stress of acute cerebral or myocardial ischemia, which is intensified when the two ischemias are combined, and chronic hypertension may exacerbate both.
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PMID:Acute cerebrovascular and myocardial ischemia superimposed upon chronically hypertensive and arteriosclerotic male Sprague-Dawley rats. 90 14

In the light of 4 personal observations of PPPRINZMETAL's angina, a review has been conducted of the literature in the 15 years since the condition was first described. Although the formal diagnostic criteria for this form of angina simultaneously clinical, biological and electrical - anginal attacks occurring at rest, often at night, during which elevation of the ST segment is recorded which disappears at the end of the attack without any significant rise in enzyme levels (SGOT and CPK) - the frontiers of the syndrome appear to have widened since PRINZMETAL's description: - Severe proximal stenosis of the coronary arteries is not obligatory; they may be only slightly damaged or even healthy. - Prinzmetal's angina is by no means always "spontaneous" but is often induced, either by psychic factors, which explain the fixed time of the attacks, or by organic factors, e.g. cold drinks (Observation No.2). In this event it would appear safer to speak of angina or rest as opposed to angina of effort. - In contrast to what PRINZMETAL thought, effort tests may sometimes induce angina-type pain with elevation of the ST segment, and here the borderline between this syndrome and conventional angina with ST segment elevation after effort test (5% of cases) is less clear-cut. The two nosologic entities probably reflect the same physiopathological situation, i.e. acute myocardial ischemia, and may represent the same affection in different phases of development. The prognosis is equally bad. - Attacks of rinzmetal's angina are often accompanied by severe and sometimes fatal disorders of rhythm, and this influences the therapeutic approach. - The coronary spasm posited by PRINZMETAL and others before the advent of coronarography is indeed, in the majority of cases, the immediate cause of myocardial ischemia and anginal pain, without any preliminary increase in the energy requirements of the heart as in the conventional anginal attack. - A vasoactive substance present in the circulating blood at the beginning of the affection, which may be degraded and subsequently disappear and may be secreted by the pathologic coronary artery, was demonstrated in observation No. 4: this may, in conjunction with vagal hypertonia, be the causative factor in coronary spasm. Study of its pharmacodynamic properties is now in progress.
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PMID:[Prinzmetal's angor. Apropos of 4 cases. Review of the literature]. 108 Aug 80

Dexamethasone exerted no significant hemodynamic effect in sham-operated cats or in cats subjected to acute myocardial ischemia. However, the glucoccortcoid did normalize elevated S-T segments toward pre-ischemic values, and prevented much of the increase in plasma CPK activity following coronary artery ligation. Moreover, dexamethasone prevented loss of CPK activity and restricted the loss of lysosomal hydrolase within ischemic myocardial tissue. These data indicate that lysosomal disruption is an early consequence of myocardial ischemia and that treatment with dexamethasone prevents the loss of myocardial lysosomal and cellular enzymes as reflected in normalization of the ECG and plasma CPK activity of ischemic cats. In this way, dexamethasone may act to retard the spread of the developing infarct within the ischemic myocardium.
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PMID:Effects of dexamethasone on myocardial cells in the early phase of acute myocardial infarction. 113 39

Reversible short-term and local myocardial ischemia in non-anaesthetized dogs involved a functional (if changing the activity of CPK) and morphologic aftereffect. At the same time it is possible to find some mechanisms of compensation (in chronic experiment).
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PMID:[The sequelae of transient myocardial ischemia in chronic experiments]. 137 93

Serum cardiac myosin light chain I (LCI) levels were quantitated using a radioimmunoassay kit in patients suspected of dilated cardiomyopathy (DCM). In this study, 55 patients were evaluated between 1986 and 1991. They were composed of 40 males and 15 females, and their age was 27-75 years (51 +/- 11 years). The patients with renal dysfunction were excluded due to their serum creatinine levels (greater than 2.0 mg/dl). 1) After cardiac catheterization, endomyocardial biopsy and echocardiography, 44 patients were diagnosed as DCM, 2 as ischemic heart disease, 2 as chronic myocarditis, 1 as restrictive cardiomyopathy, 1 as dilated hypertrophic cardiomyopathy, 1 as cardiac amyloidosis, 2 as myopathy, 1 as polymyositis and 1 as hypothyroidism. 2) Only two patients with DCM had elevated LCI. Besides, two patients with myopathy or hypothyroidism had elevated LCI. 3) In the follow-up, one patient died suddenly 6 months later and another showed normal value of LCI four years later. 4) LCI elevation in DCM was not related to either the severity of heart failure or cardiac function and it showed no finding of 201Tl myocardial defect or elevated CPK. 5) The mechanism for elevated LCI in myopathy is related to a cross-reaction with myosin light chain in the skeletal muscle. In hypothyroidism, it may be related to decreased clearance of normal LCI concentration or increased myosin light chain from damaged skeletal muscle. In conclusion, it is evident that the measurement of LCI is not helpful in clinical assessment of patients with DCM, but may be useful in detection of secondary cardiomyopathy.
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PMID:[Clinical assessment of serum myosin light chain I in patients with dilated cardiomyopathy]. 143 84

Dauricine (Dau) 5 mg.kg-1 and verapamil (Ver) 0.15 mg.kg-1 iv followed by infusions of 0.1 and 0.01 mg.kg-1.min-1, respectively, for 30 min, depressed the elevated coronary venous blood LDH and CPK after LAD occlusion. Dau produced antagonistic effects on acute myocardial ischemia-induced ventricular ectopic activities (VE) and ventricular tachycardia (VT). The incidences of VE and VT in Ver group and ventricular fibrillation (VF) in both groups tended to descend. The results suggested that Dau and Ver produced marked protective effects on myocardial infarction and antagonized the acute ischemic arrhythmia.
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PMID:Protective and anti-arrhythmic effects of dauricine and verapamil on acute myocardial infarction in anesthetized dogs. 144 8

A 63 year old female, who was admitted to a psychiatric hospital for schizophrenia, was referred to our emergency room because of sudden loss of consciousness and convulsions. On arrival, she was drowsy and hypoxemic. Her chest X-ray showed cardiomegaly with pulmonary edema. ECG showed marked ST depression in precordial leads and serum chemistry revealed marked elevation of CPK, GOT and LDH along with hyponatremia and hypochloremia. She was immediately admitted to CCU on suspicion of acute non-transmural myocardial infarction complicated with congestive heart failure. After fluid restriction and intravenous infusion of dopamine she passed large amount of urine, and her consciousness level, electrolyte imbalance and ECG change, improved gradually. Although serum CPK level increased as high as 32,307 IU/ml, there were no signs of left ventricular asynergy on UCG and CPK isozyme analysis performed later revealed more than 99% of serum cCPK was MM-type. We concluded that water intoxication was the cause of the ECG change and the elevated serum CPK, GOT and LDH levels. There are few reports on elevated CPK level in association with water intoxication, in which rhabdomyolysis is speculated as the cause of CPK elevation. But there is no report on ECG change complicated with water intoxication. In our case, electrolyte imbalance caused by water intoxication seemed to play a major role in ST depression and QT prolongation. Although water intoxication is a rare disorder in the general population, it is not infrequent among patients with psychiatric diseases. Care must be taken when such patients present ECG change and serum enzyme elevation mimicking ischemic heart disease.
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PMID:[A water intoxication patient who showed remarkable ST depression and suspected ischemic heart disease]. 152 80

The aim of this work was to ascertain whether free radicals play a causal role in the injury occurring in myocardial ischemia and reperfusion. To this purpose we observed whether spin-trapping compounds protect the heart when used at a concentration capable of reacting with free radicals. The lipophilic spin trap alpha-phenyl-t-butyl nitrone (PBN) was used because it is taken up by the myocites. Isolated Langendorff rat hearts were subjected to ischemia according to two schemes: "Model A" = 30 min zero-flow ischemia followed by 30 min reperfusion; "Model B" = 60 min of low-flow ischemia (10% of the individual value; N2 saturated) followed by 30 min reperfusion. Treated groups received in addition 5.0 mM PBN which was supplied continuously. The following parameters were measured throughout the experiment: contractile performance (RPP); coronary flow (CF); CPK; phosphocreatine (PCr), ATP, inorganic phosphate (Pi), intracellular pH (pHi). The pathology obtained by "Model A" is more severe than that of Model B, and partly irreversible. During the ischemic phase in "Model A", contractility, PCr and ATP dropped to near zero; during initial reflow CPK rose about 13-fold and Pi rose 2.5-fold, while pHi decreased to 6.1. During reperfusion, a partial recovery of PCr, Pi and pHi was observed, while RPP and ATP did not increase; PBN treatment improved significantly PCr and CPK, while the other parameters were unaffected. During ischemia, "Model B" hearts showed a drop of contractility to near zero, of PCr to 35%, of ATP to 50%; CPK rose 7-fold and Pi 1.5-fold; pHi was not modified. During reperfusion, all parameters recovered in part, with exception of Pi. PBN developed a marked protective activity on all tested parameters, which gained a nearly normal value. The results of the present investigations show that the lipophilic spin trap PBN partly protects the heart from the ischemia/reperfusion injury, thus confirming that free radicals play a causal role in this pathology; the continuous loading of the tissue with the drug can be an important factor for obtaining the protective effect.
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PMID:Protective activity of the spin trap tert-butyl-alpha-phenyl nitrone (PBN) in reperfused rat heart. 161 68


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