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)

Isolated working rat hearts were made ischemic by introducing a one-way aortic ball valve. After the ischemic period the hearts were perfused in a retrograde non-working way for 30 min. Flow rates, glycogen, ATP, and creatine-phosphate went down during the time of ischemia, whereas tissue lactate accumulated. For shorter periods of ischemia these values were normalized but after 30 min of ischemia the hearts seemed to be irreversibly damaged. There was a leakage of GOT, GPT, LDH, and CPK from all hearts when ischemic from 5 to 30 min. Different factors that might be of importance for the degree of ischemic injury were tested. The injury tended to be more severe at higher heart rates. Addition of adrenaline 10(-6)M resulted in excessive myocardial damage. A variation of pH from 7.1 to 7.7 did not alter the effects of the ischemic injury. One group of rats were injected with adrenaline for 8 weeks to simulate chronic stress. When hearts from these rats were made ischemic they were more prone to fail compared to controls. The failing hearts, on the other hand, had a lower leakage of enzymes, possibly due to a less severe myocardial damage. A high mechanical performance and a normal noradrenaline content of the hearts are key factors for the development of myocardial infarction, as indicated by this study.
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PMID:Factors of importance for the degree of ischemic injury in the isolated rat heart. 0 96

It was found that following occlusion of the coronary artery in dogs, the rate of increase in K+ concentration in blood plasma draining directly from the focus of ischemia is greater in cases complicated by ventricular fibrillation. Fibrillation always occurs against the background of a decrease in pH and an increase in the K+ level in blood plasma draining from the focus of ischemia. It is suggested that inhibition of the development of disorders of acid-base and ion equilibrium in the myocardium would be an effective means of preventing ventricular fibrillation in the acute stage of myocardial infarction.
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PMID:[pH changes and the K+ and Na+ concentration in the blood of the coronary vein in experimental myocardial infarct complicated and not complicated by ventricular fibrillation]. 4 60

An accurate postmortem method of planimetrically estimating the extent of myocardial infarction was employed in 16 cases. Delineation of necrotic myocardium was enhanced by a macroscopic staining technique, which utilizes a tetrazolium dye. Comparison of infarct size with peak serum creatine phosphokinase levels showed a general correlation between the two that was not statistically significant. Two markedly disparate cases serve to emphasize the need for clinical awareness of the temporal relationship between myocardial infarction and creatinine phosphokinase analysis as well as the possibility of other anatomic sources of elevation of serum enzyme levels. Comparison of infarct sizes in cardiogenic shock and nonshock patients confirms the existence of a significant relationship between a larger myocardial infarct and shock. However, the data from several patients in the group again emphasize the possibility of maintaining a reasonable blood pressure in the face of a massive myocardial infarction or, more importantly, of manifesting "cardiogenic" shock when only a small amount of left ventricular damage has been sustained. The latter possibility may be related to other anatomic events, e.g., bowel infarction, hemorrhage, or possibly right ventricular ischemia, infarction, or dysfunction.
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PMID:Myocardial infarct size: clinicopathologic agreement and discordance. 7 21

Circulatory variables and arterial partial pressure for oxygen (PaO2) were compared in 91 anesthetized patients who received infusions of either nitroglycerin (TNG) or nitroprusside (SNP) to induce hypotension for the purpose of decreasing intraoperative blood loss. At comparable systolic arterial blood pressures, the mean and diastolic arterial blood pressures were significantly higher with TNG. Electrocardiographic changes suggestive of ischemia occurred in 18 patients who received SNP, whereas none were detected in patients given TNG. Both drugs significantly decreased PaO2 and rate-pressure product, an indirect index of myocardial oxygen consumption. No untoward response to TNG occurred. No clinical evidence of myocardial infarction, renal damage, or cerebral vascular complication was encountered in the postoperative period in any patient. Thus, TNG is an effective hypotensive drug that may prove superior to currently available agents.
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PMID:Nitroglycerin as a hypotensive drug during general anesthesia. 9 6

The quantitative potassium and sodium contents in the separate regions of the heart and m. rectus abdominis in cases of sudden and violent death were investigated. The disturbances of the electrolyte metabolism of potassium and sodium were established to be the earliest changes in coronary disease (acute coronary insufficiency resulting from functional disturbances of the coronary circulation and myocardial infarction). The decrease of the quantitative potassium contents and sodium increase in myocardium depend on the ischemia duration and the stage of the myocardial lesion. The highest potassium decrease was observed in the left ventricle and right auricle. Not very high but even decrease of potassium and sodium contents in the separate heart regions was observed in the deceased by electrocution and strangulation, the decrease being most negligible in the deceased by electrocution. The changes observed in potassium and sodium contents are not pathognomic signs of coronary disease. Only the sharp, focal decrease of the contents of those element is a reliable sign of myocardial infarction.
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PMID:[Quantitative K and Na levels in different parts of the heart in cases of sudden death from coronary disease, acquired heart valve defects and violent death]. 13 71

1. Influence of ischemia on the biochemical properties of the sarcoplasmic reticulum (SR) was studied in the experimental myocardial infarction in the dog. 2. Ca2+ -uptake rate of SR decreased at around 90 minutes after coronary occlusion. This reduction was roughly in parallel with the reduction in the Ca+ -Mg2+ -stimulated ATPase activity. However, Ca2+ -binding rate of SR was kept within the range of that of the non-infarcted tissue through the time course of myocardial infarction. 3. Ca2+ -Mg2+ -stimulated ATPase activity decreased at around 3 hours after coronary occlusion to about 50% of that of the non-infarcted portion. 4. In SDS gel electrophoresis, the protein band with the largest molecular weight among three major components decreased at 3 hours after coronary occlusion, which is suggestive of ATPase. At 48 hours after coronary occlusion, the protein with the smallest molecular weight in the major proteins also decreased. 5. Ca2+ -uptake rate, Ca2+ -Mg2+ -stimulated ATPase activity and the substructural changes return to the normal level and pattern at around 28 days after coronary occlusion.
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PMID:Studies of the cardiac sarcoplasmic reticulum in myocardial infarction. 15 53

Polarization-microscopic and micrometric investigations of the myocardium during infarction at autopsy and in experimental ischemic conditions, has shown that one of the earliest and most typical morphological signs of ischemic myocardium is sarcomere relaxation. The latter is expressed by the loss of contractility of muscle cells in life time and in strongly frozen corpses, and due to the effects of fixatives. Increase of the percentage of relaxed sarcomeres parallels the duration of experimental ischemia and the time after myocardial infarction. This allows the indirect calculation of irreversible cell change.
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PMID:The relaxation of sarcomeres in ischemic injury of myocardium. 15 33

The evolution of experimental myocardial infarction in the Rat with or without revascularization has been studied histochemically and histoenzymatically in 56 animals sacrified after 1, 6, 12, 24, 48 hrs and 7 days. Following permanent ischemis (14 animals), there appeared an extended transversal infarction marked by the complete disappearance of all phosphorylase activity (P-ase) after the first hour. During the first 6 hrs, changes appeared in succinodeshydrogenase (SHD) and cytochrome oxydase (Cyt-Ox). Glucose-6-phosphodeshydrogenase (G6PDH) presisted until lysis of the necrotic focus. It was possible to define a perinecrotic marginal area in which Pase activity is absent and SDH is granular "G3 in nature, characterized by continuous remodeling in the first 48 hrs. Following temporary ischemia (42 animals) the evolution was marked by rapid tissue reactions and early regression of the marginal zones. After 48 hrs and 7 days of survival, the planimetric evaluation of the infarcted area shows a definite reduction in the size of the infarctus in 50% of cases following removal of the ligature after 6 hrs, and in 66% of cases following removal of the ligature after 1 hr. It would appear probable that the revitalization of certain myocardial areas may extend from the marginal zones as is suggested by the reappearance in these zones several hrs after revascularization of P-ase and SDH activity. On the other hand, it is also true that the early restoration of blood flow does not always prevent the occurrence of an extended infarction. Certain recent observations have shown microcirculatory changes which are secondary to anoxia and should be studied further.
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PMID:[Histochemical and histoenzymatic study of experimental myocardial infarction in the rat by temporary and permanent ligation of the left coronary artery (author's transl)]. 16 14

The relation between the accumulation of pyrophosphate and technetium-99m in myocardium with reversible and irreversible ischmic injury was studied in dogs subjected to transitory or persistent coronary arterial occlusion. Among four dogs with coronary occlusion maintained for less than 20 minutes, none had either increased MB creatine kinase (CK) (the "myocardial" CK isoenzyme) activity serum or a positive 99mTc stannous pyrophosphate image. Seven dogs with coronary occlusion maintained for 30 or more minutes had elevated serum MB CK activity, and five of the seven had positive (abnormal) images. Thus, although false negative images may occur occasionally despite myocardial damage, both increased serum MB CK and abnormal images generally accompanied prolonged coronary occlusion. In contrast, ischemia without infarction was not associated with abnormal images. Both 99mTc and 32P labeled pyrophosphate were accumulated extensively and proportionally in myocardium from zones of infarction, and uptake of both tracers was comparable although modest in isolated mitochondria. Similar results were obtained after myocardial infarction in animals with induced profound leukopenia. Thus, phagocytosis of the radiopharmaceutical agent by leukocytes migrating into the infarct is not an essential mechanism accounting for uptake. These results indicate that abnormal images reflect uptake of pyrophosphate, associated with 99mTc, by irreversibly injured myocardium rather than leukocytic infiltration involved in the inflammatory response in the heart.
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PMID:Mechanisms contributing to myocardial accumulation of technetium-99m stannous pyrophosphate after coronary arterial occlusion. 18 32

The effect of curantil on the values of energy metabolism in different parts of the myocardium was studied on dogs with experimental myocardial infarction. Tissue respiration, the activity of Krebs' cycle enzymes, cytochrome oxidase, pentose phosphate cycle and glycolysis, and the content of glycogen and adenyl components were studied. It was established that curantil has a positive effect on energy processes, particularly in myocardial areas not involved in ischemia. It is suggested that activation of tissue oxidation enzymes, which improves oxygen utilization and increases ATP production, is among the mechanisms of the curantil effect. It is noted that curantil stimulates the synthesis of glycogen and inhibits its decomposition. The accumulation in the myocardium of AMP, the precursor of adenosine possessing a marked coronarolytic effect, is an important aspect of the drug's action.
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PMID:[Metabolic shifts in acute period of myocardial infarct and the possibility of their correction with curantil]. 22 32


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