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)

1. An experimental comparative study on isolated guinea pig hearts was carried out to determine the effect of dipyridamole added to the reperfusion solution on myocardial recovery after global ischemia. 2. After 20 min of normothermic ischemia two groups of solutions: (1) Krebs solution; (2) Krebs + dipyridamole 20 micrograms/l (10 experiments in each group) were used for reperfusion. 3. Postischemic myocardial functions (heart rate, ventricular contractility, heart work) and tissue enzymes (CPK-MB, LDH) were compared with their preischemic values. 4. Addition of dipyridamole 20 micrograms/l to reperfusion solution improved postischemic myocardial functions and decreased myocardial injury.
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PMID:Dipyridamole induced myocardial recovery after global ischemia. 151 53

We report a case of unstable angina in an active phase of polymyositis. A 51 year-old man was admitted with a diagnosis of polymyositis and unstable angina with ST elevation on prolonged rest chest pain. Rest anginal attack which had been refractory to conventional antianginal medications was controlled by high dose of glucocorticosteroid. Electrocardiography revealed multifocal premature ventricular contraction. Since silent ischemia on exercise persisted, percutaneous transluminal coronary angioplasty (PTCA) was performed on a stenotic lesion in the left anterior descending artery. Since there was recurrent anginal attack, re-PTCA was carried out at the same site. He was discharged in a good condition. This case is considered to be associated with cardiac involvement of polymyositis because of ventricular arrhythmia, persistent increased serum levels of CPK-MB, and the marked benefits of corticosteroid against unstable angina. In addition, clinical manifestations, coronary arteriographic findings, and increased plasma levels of thrombin-antithrombin III complex suggest that cardiac involvement in polymyositis accelerates intracoronary thrombus formation and/or coronary spasm.
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PMID:[A case of unstable angina pectoris associated with an active phase of polymyositis]. 158 49

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

Fifty healthy males aged from 19 to 34 years were examined. Experiments were conducted on 30 male mice weighing 200-250 g. After 10- and 20-minute ischemia of the upper limb the concentration of cAMP and cGMP in its venous blood increases in direct proportion to the duration of ischemia. Increase of the level of cyclic nucleotides (CN) in the blood does not depend on hypersecretion of catecholamines. Increase of the CN level coincides in time with increase of blood CPK. The mechanisms of changes in the blood CN level in ischemia are discussed.
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PMID:[Blood cyclic nucleotide content in acute regional ischemia of the extremities]. 162 31

The calcium-entry blocker isradipine was tested in a closed-chest pig model for chronic myocardial infarction. Ischemia was evoked in anesthetized pigs (25-35 kg) by inflating a catheter balloon in the left anterior descending coronary artery for at least 45 min. Hemodynamic monitoring and signal averaging of X, Y, and Z electrocardiographic leads were performed (150 beats, filtered at 50 Hz). After reperfusion, all animals developed an accelerated idioventricular rhythm and high creatine kinase (CPK) plasma levels. Coronary venous purines and catecholamines increased transiently. Two hours after reperfusion, heart rate was elevated from the initial 87.5 +/- 6.3 to 126 +/- 6.4 beats/min (p less than 0.01) and the pressure-rate product (PRP, an index of oxygen demand) from 9,530 +/- 630 to 11,950 +/- 790 mm Hg/min (p less than 0.05). After 2 weeks, six surviving pigs had a decreased stroke volume (98 +/- 18 versus the initial 124 +/- 14 microliters/kg, p less than 0.05), a prolonged high-frequency signal-averaged QRS duration (81.2 +/- 6.5 versus 65.7 +/- 2.9 ms, initially; p less than 0.05), and ventricular tachycardias (VTs), inducible by programmed electrical stimulation (PES). After the infusion of isradipine (1 microgram/kg/min for 30 min), the cardiac index increased from 92 +/- 14 to 133 +/- 8.7 ml/min.kg (p less than 0.02). Even at a higher heart rate, the PRP dropped from 12,600 +/- 1,900 to 10,560 +/- 1,400 mm Hg/min (p less than 0.05). Sustained monomorphic tachycardias were inducible in five pigs before and in three pigs after isradipine, and no deterioration of the signal-averaged electrocardiogram parameters was found.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of isradipine on hemodynamic parameters and ventricular tachycardia in healed myocardial infarction. 168 21

Although the difficulty of preserving hypertrophied myocardium from induced arrest during aortic clamping has long been recognized, the difference of response to ischemia between the two types of hypertrophy induced by pressure-loading (P) and by volume overloading (V) has not been fully elucidated. In the present study, to assess the two types of hypertrophied myocardium we investigated the 44 patients undergoing valve replacement; the 23 patients of aortic stenosis (AS) without aortic regurgitation (AR), and the 21 patients of AR without AS. The patients of AS (group-P) were divided into two groups regarding the thickness of posterior wall of left ventricle; over 15 mm in P-1 and under 15 mm in P-2. The patients of AR (group-V) were also divided into two groups, which is, preoperative LVEDVI over 250 ml/m2 in V-I and under 250 ml/m2 in V-2. In all four groups myocardial temperature was kept about 5 degrees C with GIK and continuous cold blood coronary perfusion during aortic clamping time. There was no operative death. Postoperative serum enzymes (GOT and CPK) in P-1 were higher than in P-2. Per cent increase of LVEF in P-1 were greater than P-2 and V-1 greater than V-2, respectively. Postoperative catecholamines needed for P-1 was greater than P-2.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Protection of the two types of severely hypertrophied myocardium induced by pressure-loading and by volume overloading]. 183 32

The significance of transient increase in ST-segment elevation immediately after reperfusion in acute myocardial infarction (AMI) was assessed by 12-lead electrocardiography. The study population consisted of 18 patients with initial anterior AMI, whose totally-occluded left anterior descending arteries were reperfused within 6 hours after the onset of symptoms. The ST-segment elevation was defined as that of more than 0.2 mV in the V3 lead immediately after reperfusion. Collateral circulation, timing of reperfusion, CPK release, left ventricular ejection fraction and mean % 201Tl uptake in the infarct regions were compared between patients with and without ST elevation. Eleven patients (61%) had ST-segment elevation (0.61 +/- 0.29 mV). Well-developed collaterals were observed in 43% of patients without ST-segment elevation (p < 0.05) but not in those with ST elevation. ST-segment elevations were accompanied by delays in timing of reperfusion (3.7 +/- 1.2 hrs vs 2.5 +/- 0.9 hrs, p < 0.05), higher peak CPK values (6,190 +/- 3,156 IU/l vs 3,222 +/- 2,053 IU/l, p < 0.05) and lower mean % 201Tl uptake (54.2 +/- 11.4% vs 73.9 +/- 11.3%, p < 0.01). We concluded that transient increase in ST-segment elevation immediately after reperfusion may relate to poorly-developed collaterals and prolongation of ischemia; i.e., severe ischemia before reperfusion, and therefore may reflect myocardial reperfusion injuries.
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PMID:[Transient increase in ST-segment elevation immediately after reperfusion in acute myocardial infarction]. 184 33

To assess the value of myocardial substrate in the occurrence of ischemic-reperfusion damage, isolated, electrically paced rabbit hearts were perfused for 60 min under aerobic condition (25 ml/min with oxygenated Krebs-Henseleit solution containing glucose 11 mM). Thereafter the hearts were made ischemic for 30 min by reducing coronary flow to 3 ml/min. During ischemia, 3 different substrates were used glucose 11 mM (Group I), palmitate 1.2 mM (Group II) and palmitate 1.2 mM + glucose 11 mM (Group III). The hearts were then reperfused (25 ml/min) for 30 min under aerobic condition using glucose 11 mM as the only substrate. In the presence of glucose with or without palmitate (Group I and III) ischemic damage was mild. Recovery of the developed pressure was 95% and there was no contracture during ischemia and or reperfusion. During ischemia and reperfusion there was a small release of CPK, GSSG and GSH. In the presence of palmitate (Group II) ischemic and reperfusion damage was profound. Recovery of developed pressure was reduced (25%) and diastolic pressure significantly increased (68 +/- 5.1 vs 3 +/- 1.5, 5 +/- 1.8 mmHg). These mechanical data were concomitant with an important release of CPK (580 +/- 50 vs 180 +/- 35, 210 +/- 48 mU/min/gww) and oxidised glutathione (0.38 +/- 0.3 vs 0.05 +/- 0.001, 0.09 +/- 0.003 nmoles/min/gww). In addition the redox state of the cells of the Group II was significantly shifted through the oxidative state at the end of ischemia and of reperfusion. These results indicate that palmitate as substrate increases the deleterious effects of ischemia; glucose is able to overcome the negative effects of palmitate.
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PMID:[Toxicity of fatty acids during myocardial reperfusion: a new possible mechanism of action]. 191 18

The course of 357 balloon inflations performed during 38 angioplasties for single-vessel coronary artery disease was prospectively studied using continuous ECG recording. Ischemic ECG changes appeared during 91 percent of the inflations at a mean of 20 +/- 8 seconds after inflation and resolved in 97 percent of those at a mean of 11 +/- 5 seconds after deflation. Elevation of the plasma CPK level was found in six patients who had ischemic ECG changes for at least 7.8 minutes. The duration of ischemia did not exceed 5.4 minutes in any of the patients without CPK elevation. Resolution of the ischemic changes was delayed in patients with CPK elevation and in last vs initial inflations. We conclude that in patients with noninfarcted myocardium, ECG changes follow coronary occlusion and reflow very rapidly, detecting these coronary events with a high sensitivity. Lack of rapid regression predicts lack of reperfusion, and persistence of ischemia for more than 7.8 minutes is sufficient to cause myocardial necrosis.
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PMID:Ischemia and reperfusion during intermittent coronary occlusion in man. Studies of electrocardiographic changes and CPK release. 198

In the majority of patients with intestinal infarction, it is generally agreed that the occlusion of mesenteric arteries or vein is the primary etiologic factor; however, some showed no evidence of thrombosis, embolization or vasculitis as the causative factor. In many patients, this particular type of infarction is the terminal event of the episode. From October 1977 to December 1986, 24 patients with mesenteric infarction were investigated following cardiovascular surgery in our institute. Among them, 15 were diagnosed with organic vascular occlusion; however, the other 9 showed no evidence of thromboembolism or any other organic vascular occlusive lesion of mesenteric vessels and were diagnosed as non-occlusive mesenteric infarctions. All of these patients were in severe cardiac failure (LOS) postoperatively. There was no typical symptom, although abdominal fullness and diarrhea were the major and consistent findings. In blood chemical analysis, the enzymatic levels such as serum GOT, LDH and CPK were significantly elevated and discrepancy between serum GOT and serum GPT was observed. In this clinical situation, it was difficult to establish a correct diagnosis mainly because of the few signs and symptoms present relating to the mesenteric infarction. On the other hand, when the correct diagnosis was made, these patients were too critically ill to be treated conservatively. The outcome of these patients was grave and all of them died which showed 100% of mortality rate. The conservative management did not produce favorable progress, which accelerated LOS and prevented patients from recovering from cardiac failure. The aggressive surgical approach to this particular type of acute mesenteric ischemia might have offered an improved prognosis from these catastrophic events.
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PMID:[Non-occlusive mesenteric infarction following cardiovascular surgery]. 202 11


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