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)

Dexamethasone (6 mg/kg) given intravenously to anesthetized cats exerted no significant hemodynamic effect on control open-chest cats or in cats subjected to acute myocardial ischemia by coronary artery ligature. However, dexamethasone normalized elevated S-T segments toward preischemic values, and prevented much of the increase in plasma CPK activity following coronary artery ligation. Moreover, dexamethasone prevented loss of CK activity within ischemic myocardial tissue five hours after the onset of ischemia. Dexamethasone also reduced the extent of ischemic damage as assessed by a nitro-blue tetrazolium staining technique, providing anatomic verification of the reduced ischemic damage. Moreover, dexamethasone prvented the swelling and vacuolization of myocardial lysosomes in the ischemic region, indicating a stabilization of lysosomal membranes within the heart. These data indicate that lysosomal disruption is an important consequence of myocardial ischemia and that early treatment with dexamethasone prevents the loss of myocardial lysosomal and cellular enzymes as reflected in normalization of the ECG and plasma CK 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:Mechanism of the beneficial effect of dexamethasone on myocardial cell integrity in acure myocardial ischemia. 739 11

We evaluated retrospectively the benefit of prophylactic nitroglycerin (TNG) infusions during elective coronary artery bypass grafting (CABG) in 73 patients. In all patients anesthesia was maintained with high dose fentanyl. Thirty-seven patients were infused TNG 0.3 microgram.kg-1.min-1 during surgery and 36 patients were not. The TNG-infused patients demonstrated lower perfusion pressure during cardiopulmonary bypass (CPB) and higher incidence of inotropic administrations than the uninfused patients. Serum myocardial creatine phosphokinase (CPK-MB) levels of TNG-infused patients were higher than those of TNG-uninfused patients on the first postoperative day. We speculate that inotropic administrations under low myocardial perfusion pressure at the time of weaning from CPB induces myocardial ischemia which in turn causes an increase in serum CPK-MB level. We conclude that prophylactic administration of TNG does not prevent perioperative ischemia during CABG.
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PMID:[Clinical evaluation of prophylactic nitroglycerin infusion during coronary artery bypass grafting]. 777 30

This study aimed at the exploration of the relationship between Na(+)-H+ exchange system and myocardial ischemia-reperfusion injury (MRI) in an attempt to provide a theoretic basis for the prevention and treatment of MRI. We used the isolated working guinea pig hearts as the experimental model to mimick cardiopulmonary bypass, which included 120 min hypothermic ischemic cardioplegic arrest followed by 60 min normothermic reperfusion. The hearts were divided into 2 groups: the control group receiving St. Thomas' Hospital Solution (STS) and the treated group receiving STS + amiloride, a Na(+)-H+ exchange blocker. The results showed that during reperfusion, [Na+]i and [Ca2+]i overloads, poor recovery of cardiac function, increases in CPK release and OFR generation, reduction of ATP content and serious damage of ultrastructure were seen in group 1; whereas there were no [Na+]i and [Ca2+]i overloads and better recovery of cardiac function accompanied by improved results of biochemical assay and less damage of ultrastructure was found in group 2. Our study indicates that amiloride can inhibit Na(+)-H+ exchange system in cardiac cells during early reperfusion period, which prevents [Na+]i overload produced by Na(+)-H+ exchange, and stops Na(+)-Ca2+ exchange activated by high level of [Na+]i, thus attenuating [Ca2+]i overload caused by Na(+)-Ca2+ exchange and myocardial injury. Therefore, we conclude that Na(+)-H+ exchange blocker, amiloride, can exert significant protective effects on MRI and its use may prove to be a new clinical approach to prevention and cure of MRI.
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PMID:Studies on the role of sodium/hydrogen exchange system in myocardial ischemia-reperfusion injury. 778 66

Paeonol 60 mg.kg-1 ip, was given to rats for 15 days. On the 16th day myocardial ischemia reperfusion injury was produced in the rat heart by occlusion of the left coronary artery and the release of the occlusion. The results showed that paeonol significantly improved myocardial SOD activity (5.8 +/- 0.6.mg-1 compared with reperfusion control 3.4 +/- 0.9, P < 0.01), reduced the MDA content (11.4 +/- 1.7 nmol.mg-1 versus 17 +/- 1.3, P < 0.01) and cardiac CPK release (1523 +/- 478.5 U.L-1 versus 2355 +/- 626.5, P < 0.01). The myocardial ultrastructure was also protected keeping them from the oxygen free radical damage. It appears that paeonol is an efficient protective agent against ischemia reperfusion damage in the rat heart.
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PMID:[Anti-ischemia reperfusion damage and anti-lipid peroxidation effects of paeonol in rat heart]. 804 13

A 53-year-old woman was admitted to the hospital for chest pain with headache, nausea and vomiting, two and a half hours after an intramuscular injection of 6 x 10(6) units of IFN (interferon) alpha 2a, in the 11th week of IFN treatment for chronic hepatitis C. The electrocardiogram (ECG) showed ST depression and T inversion in leads II, III, aVF and V3-V6, as commonly seen in myocardial ischemia. However, emergency coronary angiography (CAG) did not show stenosis or spasms clearly, serum CPK was always within the normal limits, Tc-99m PYP scintigraphy and T1-201 scintigraphy did not show any abnormal uptake or defect, and the echocardiogram did not show any abnormality. She recovered from chest pain and the ischemia-like changes seen on the ECG, after IFN treatment was stopped, and she rested for 7 days from this treatment and other treatment using nitrites and a calcium-antagonist. After recovery, the ECG during exercise and hyperventilation showed changes similar to those seen on admission. From these findings, this case was considered to be precipitated by spasms of coronary microvessels, which were not noticeable in CAG. The cause was thought to be complicated by IFN treatment, because this episode appeared after IFN injection, and improved after stopping IFN treatment.
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PMID:[A case of chronic hepatitis C complicated by ischemia-like changes seen on the electrocardiogram during interferon treatment]. 835 43

The protective effects of captopril were evaluated in vitro on isolated perfused rat hearts after a global ischemia of 20 min. The hearts were randomly allocated in 2 groups. In the first one (n = 6) captopril was added at a concentration of 270 microM. The second one was utilized as control (n = 6). Aortic flow and minute work respectively decreased on reperfusion by 35% and 49% in captopril group and by 65% and 71% in controls (p < 0.001). No changes occurred in heart rate. Aortic systolic pressure and coronary flow decreased in the 2 groups, but not significantly. Myocardial enzyme release during reperfusion showed significant lower levels of CPK and LDH in the captopril group as compared to controls (p < 0.001 after 41 min). The occurrence of serious ventricular arrhythmias was considerably higher in controls with respect to the captopril group. Irreversible ventricular fibrillation occurred only in control hearts (50%). These data indicate that captopril exerts a protective effect during myocardial ischemia and reperfusion by preventing serious ventricular arrhythmias, reducing enzymatic release and a lower decrease in cardiac performance, without an increase in heart rate.
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PMID:[The myocardial protective effects of cardiac tissue ACE inhibition in experimental ischemia-reperfusion in isolated rat hearts]. 839 28

This report describes a 63 year-old man who suffered an acute myocardial infarction after carbon monoxide exposure. When evaluated in the Emergency Room the patient was completely conscious and did not experience any chest pain. The electrocardiogram showed non-specific T wave abnormalities in inferolateral leads. The only sign consistent with a possible myocardial involvement was a slight increase in serum CPK. The electrocardiogram taken 12 hours later revealed a Q-wave inferior myocardial infarction, and CPK levels showed a typical elevation in the following 24 hours. The coronary angiography, performed about two weeks after admission, documented multiple obstructions in the main coronary branches. In the presence of a reduced coronary reserve, the onset of a prolonged myocardial ischemia might have been secondary to a decreased oxygen transport capacity of the blood, which lead to a decreased amount of oxygen available to the tissues. According to their experience, the authors emphasize the importance of a careful electrocardiographic and enzymatic monitoring of all patients in the first hours after CO exposure, because the typical chest pain may be absent.
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PMID:[Silent myocardial infarction caused by acute carbon monoxide poisoning]. 840 20

Toxic manifestations of digitalis are one of the most prevalent adverse drug reactions encountered in clinical practice. The estimated incidence is about 20% in hospitalized patients in the USA. The authors describe a rare case of myocardial "catecholamine necrosis" (anteroseptal myocardial infarction) during accidental digitalis intoxication. A male patient, 75 years old, suffering from cirrhosis and ascites, take on by mistake a tablet of digoxin 0.25 mg. four times at day for eleven days. He hadn't heart disease in the past. At the eleventh day the patient showed a deep tiredness and so he was submitted to a clinical examination and electrocardiogram. The ECG demonstrated an anteroseptal myocardial infarction in the second-third electrical stage. The patient was hospitalized. The successive examination revealed: very high plasma digitalis concentrations; an increase of the serum levels of CPK and LDH; a significant increase of plasmatic and urinary catecholamine levels which return to normal values after fifteen days; apical akinesia at the echocardiographic examination; no signs of residual myocardial ischemia to the echo-dypiridamole stress test; normal coronary artery to the coronary arteriography and absence of coronary artery spasm to the ergonovine test. Furthermore the abdominal echography and the abdominal computerized tomography didn't reveal surrenal disease but showed an important liver disease. The patient was free from other cardiac events in the follow-up. Generally, during the digitalis intoxication we observe various rhythm and conduction disturbances. Instead in this case no serious arrhythmias were registered and the main expression of the drug toxicity was an anteroseptal myocardial infarction with undamaged coronary artery. Also the usual extracardiac symptoms and signs of the digitalis intoxication were absent in this case. All these observations can be explained with the pathological increase of the cathecholamine levels, indirectly induced by digitalis; with the direct toxic effect of the drug at the myocardic level; with the contemporary absence of ionic disturbances; with the concomitant liver disease. The direct toxic effect of the digitalis produced an increase in calcium ions availability for the electromechanical coupling and an increase of the intramyocardial pressure; the increase of the adrenergic activity determined contemporary an increase in the oxygen consumption of the myocardial cells, a rise of vascular tone and coronary artery tone and a reduction of the duration of the diastole. All these factors provoked a "primary and secondary" ischemia which evolved toward a real "cathecholamine necrosis" and produced a myocardial infarction. This hypothesis explains the myocardial infarction in absence of injury at the coronary arteriography and without coronary spasm at the ergonovine test; moreover it explains the transient increase in cathecholamine plasma levels observed in the acute phases an normalized after fifteen days. The "cathecholamine necrosis" is an anatomical definition, nevertheless in our opinion it gives account of the rare clinical situation observed.
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PMID:[An unusual case of "catecholamine necrosis" caused by accidental digitalis poisoning]. 855 67

Although the protective effects of the calcium antagonists on ischemic and reperfused myocardium have been investigated, there have been only a few reports regarding their efficacy in relation to the degree of ischemic myocardium. This study was undertaken to investigate the efficacy of diltiazem, a calcium antagonist, in relation to the degree of ischemic myocardial injury in an isolated working rat heart. Three different models of ischemic injury were designed; Group A: 30 min global ischemia with a single dose infusion of St. Thomas' cardioplegic solution (STS), Group B: 60 min global ischemia with multidose infusion (every 30 min) of STS and Group C: 60 min global ischemia with multidose infusion (every 15 min) of STS. These groups received only STS, while Groups A-D, B-D and C-D (the treated groups) received the same solution with diltiazem (0.5 mumol/l). The recovery of post-ischemic cardiac function and the CPK leakage during reperfusion were evaluated, and the two groups were compared. For 30 min global ischemia, the addition of diltiazem to STS significantly improved the percentage recovery ratio of aortic flow (63.2 +/- 8.6% vs 79.9 +/- 5.9%, control vs. diltiazem, p < 0.01) and reduced CPK leakage during reperfusion (87.5 +/- 35.8 IU/20 min/g dry wt vs. 41.7 +/- 14.5 IU/20 min/g dry wt, control vs. diltiazem, p < 0.05). However, no differences in the post-ischemic functional recovery and CPK leakage were noted between the groups for 60 min global ischemia. In conclusion, for myocardial preservation, the addition of diltizaem to St. Thomas' cardioplegic solution was less effective for the 60 min global ischemia. Regarding severe myocardial ischemia, it was suggested that, inhibitation or suppression of calcium channel by diltizaem might insufficient to obtain additional protection of the St. Thomas' cardioplegic solution. Therefore, it would be necessary to control calcium entry through another pathway during ischemia and reperfusion.
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PMID:[The experimental study of myocardial protection for warm myocardial ischemia in an isolated rat heart: the effect of a calcium antagonist]. 871 59

Coronary artery bypass grafting (CABG) for patients with ischemic heart disease and hypothyroidism contains many controversies, such as a need of preoperative thyroid replacement therapy and the influences on thyroid function and hemodynamics. A 73-year-old man with three vessel disease including left main trunk lesion was admitted for CABG. Primary hypothyroidism was diagnosed after admission because of high CPK value. The CABG was performed safely with preoperative minimal thyroid replacement and his postoperative course was uneventful. We evaluated the change of perioperative thyroid hormones. At the start of the extracorporeal (ECC), values of T3 and free-T3 decreased progressively, but the change was small. On the other hand, values of T4 and free-T4 increased after the start of ECC. It is suggested that CABG for a patient with angina and hypothyroidism can be performed safely with minimal preoperative thyroid replacement therapy.
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PMID:[A case report on successful coronary artery bypass grafting (CABG) for angina pectoris combined with hypothyroidism]. 909 85


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