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)

A 31-year-old woman with systemic lupus erythematosus (SLE), diabetes mellitus, and chronic renal failure developed digital ischemia, myocardial dysfunction, abnormal ECG, and elevated CPK levels. Radiographic studies revealed calcification of the peripheral vasculature although coronary angiography was unremarkable. An endomyocardial biopsy demonstrated intra and extracellular myocardial calcification without evidence of vasculitis or primary myocarditis. A diagnosis of calciphylaxis, as a result of secondary hyperparathyroidism, was made. This case demonstrates that calciphylaxis can mimic the cardiovascular manifestations of SLE. Early differentiation of these disparate diseases is important because treatment strategies employed in SLE may exacerbate calciphylaxis.
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PMID:Systemic lupus erythematosus: calciphylaxis induced cardiomyopathy. 769 81

Aiming at investigating biochemical markers of Primary Graft Nonfunction (PNF) in Orthotopic Liver Transplantation (OLT) an experimental work is made on 21 Large-White pigs randomly distributed in three groups of seven, and two additional groups of seven donors each. In Group I the supra and infrahepatic cava, the portal vein and the hepatic artery were clamped. After 30 minutes the caval and portal clamps were released and 30 minutes later the arterial clamp was also removed. In Group II (viable), OLT was performed. The Collins solution was used as preservation fluid, keeping the cold ischemia time under 2 hours. In Group III (Non-Viable), an OLT was carried out 24 hours of cold ischemia with Collins solution. Blood samples are taken in 8 different moments along the procedure to determinate the values of AST, ALT, LDH, FA, Bilirubin, Uric Acid, Cholesterol, Triglycerides, Urea, Creatinine, Glucose, Total Protein, Calcium, Phosphorus, CPK and Aldolase. The last 5 samples were drawn after reperfusion. In the Group III we found, in the samples drawn after reperfusion of the graft, significant increases in 5 of these parameters, AST, ALT LDH, Aldolase and Uric Acid. We consider that these 5 parameters may be of value in the early diagnosis of PNF of the graft, being the AST and ALT the most reliable, with the higher specificity for the same sensitivity.
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PMID:[Biochemical indicators of primary graft dysfunction in experimental orthotopic liver transplantation]. 776 81

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

The present paper has shown the effects of myocardial protection of isolated rat heart which were infused with different kinds of cardioplegia, and made to be arrested in the state of ischemia and absence of oxygen for 120 min. The heart rate, left ventricular constraction pressure and cardiac output volume, the myocardium water content and calcium content and pathological examination of myocardium were observed. The isolated rabbit heart under the circumstances of ischemia and absence of oxygen at 37 degrees C for 20 min Observations of the different kinds of cardioplegia. was observed that the different pH and oxygen content between artery and vein of the heart during the infusion of cardioplegia, the value of left ventricular constraction pressure multiplied by heart rates after reperfusion with autologous artery blood for 20 min. The values of CPK and MDA in right atrial blood, the ATP and CP volume of myocardium and pathologic study of myocardium were carried out. The results demonstrated that the warm blood cardioplegia had a better myocardial protection effect in supplying sufficient oxygen to myocardium during heart arrest, preserving and increasing energy store; controlling reperfusion in jury after ischemia, buffering acidosis and preserving heart status function. Therefore it has great value for improving the safety of the patients with complex and high risk heart diseases in perioperation.
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PMID:[Experimental study of myocardium protection with warm blood cardioplegia]. 784 50

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

The aim of this study was to clarify the role of oxygen-derived free radicals and the effect of free radical scavengers on skeletal muscle ischemia/reperfusion injury. Male Wistar rats were divided into a complete ischemia group (C-group) and an incomplete ischemia group (IC-group) and each animal was subjected to 2 h of ischemia and 1 h of reperfusion. In an attempt to decrease reperfusion injury, the rats were given free radical scavengers either as allopurinol 50 mg/kg for 2 days or as superoxide dismutase 60,000 units/kg plus catalase 500,000 units/kg. Tissue malondialdehyde, a product of lipid peroxidation, was measured as an indicator of free radicals, with higher levels indicating higher concentrations of free radicals. The malondialdehyde level in the gastrocnemius muscle after 1 h of reperfusion increased significantly in both groups when compared to the levels before and 2 h after ischemia, although there was no significant difference between the two groups. The water content of the gastrocnemius muscle and serum creatinine phosphokinase MM isoenzyme (CPK-MM) in both groups, and GOT in the C-group, increased significantly after 1 h of reperfusion when compared the values before and 2 h after ischemia. In the C-group, these values were significantly higher than in the IC-group. The administration of free radical scavengers suppressed the increase in malondialdehyde in the gastrocnemius muscle after reperfusion in both groups. The increase in water content and CPK-MM after reperfusion was also suppressed by free radical scavengers in the IC-group, but not in the C-group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of oxygen-derived free radicals and the effect of free radical scavengers on skeletal muscle ischemia/reperfusion injury. 811 19

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

The aim of this study is to investigate the efficacy of HTK solution in the 120 minutes cross-clamping method in comparison with conventional intermittent cardioplegia using GIK solution. Fifty-four open heart surgery were performed with cardioplegic solution using either HTK solution (HTK) or GIK solution (GIK). In the HTK, HTK (3L) was infused for the initial dose and 1L was added every 60 min after 120 min of cross-clamping. In GIK, 1L of GIK solution was intermittently infused initially and then every 30 min together with continuous cold blood perfusion. The effect of two cardioplegic solution was evaluated by postoperative cardiac function (CI, %SF), released enzymes (CPK), histology and dosage of catecholamine. Postoperative CI was 3.67 +/- 0.76 in HTK, and 4.34 +/- 1.04 in GIK (NS). % SF was 26.0 +/- 5.26 in HTK and 25.6 +/- 0.76 in HTK, and 4.34 +/- 1.04 in GIK (NS). %SF was 26.0 +/- 5.26 in HTK and 25.6 +/- 9.2 in GIK (NS). The CK-MB (IU/dl) level after reperfusion was significantly decreased in HTK at 60 and 180 min after reperfusion. Histology at 60 min of ischemia revealed a significant increase of edema of mitochondria in GIK. Postoperative catecholamine dose was 2.65 +/- 1.3 in HTK and 10.3 +/- 3.4 in GIK (p < -0.01). PH of myocardium was well maintained around 7.4 during cross-clamping in HTK, however, it was decreased in GIK. In conclusion, The HTK method offers a reliable cardiac protection due to effective buffering using Histidine in comparison with GIK.
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PMID:[Efficacy of myocardial preservation using HTK solution in continuous 120 min cross-clamping method--a comparative study with GIK method]. 840 3

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


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