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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects on sarcoplasmic reticulum (SR) Ca2+ transport of solutions mimicking the important intracellular milieu changes associated with short-term hypoxia (hypoxic solutions, as described by Kammermeier et al. J. Mol. Cell. Cardiol. 14: 267, 1982) were examined. SR Ca2+ content was estimated by measuring the magnitude of the caffeine-induced contracture in saponin-skinned rat papillary muscle. SR Ca2+ uptake was inhibited by hypoxic solutions only at loading times less than or equal to 30 s. This inhibition was primarily due to the increase in Pi. The hypoxic solutions had no effect on Ca(2+)-induced Ca2+ release from the SR. We also tested the effects of ATP-free (rigor) solutions that mimic the intracellular environment during late hypoxia and ischemia. Elevating Pi or ADP alone in rigor solution had no effect on SR Ca2+ content. However, elevating Pi and ADP (+/-Mg2+) produced a 44-48% reduction in SR Ca2+ content. This reduction is most likely due to reversal of the SR Ca2+ pump. We conclude that the changes in milieu with short-term hypoxia can depress contractility in intact cardiac muscle by inhibiting SR Ca2+ uptake. During long-term hypoxia or ischemia, these milieu changes can elevate intracellular Ca2+ by reversing the SR Ca2+ pump.
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PMID:Intracellular milieu changes associated with hypoxia impair sarcoplasmic reticulum Ca2+ transport in cardiac muscle. 188 12

Although previous work has implicated activation of ATP-sensitive K+ currents (IK,ATP) in action potential duration (APD) shortening and increased cellular K+ efflux during hypoxia, ischemia, and metabolic inhibition, no prior study has directly assessed the tissue levels of ATP at which IK,ATP activates in intact cardiac muscle. Accordingly, we correlated changes in tissue high-energy phosphate levels during substrate-free hypoxia with activation of IK,ATP in intact voltage-clamped rabbit papillary muscles. During 10 min of hypoxia, the outward K+ current measured in response to a voltage-clamp pulse step from -50 to 0 mV increased from 8.57 +/- 0.27 to 15.67 +/- 1.41 microA (P less than 0.05, n = 6), and APD decreased from 452 +/- 54 to 292 +/- 56 ms (P less than 0.05, n = 6). Glibenclamide (10 microM), a specific IK,ATP blocker, prevented both of these changes. In a parallel set of experiments, papillary muscles were freeze-clamped and assayed for tissue ATP. In these muscles, 10 min of hypoxia resulted in a comparable degree of APD shortening (441 +/- 24 to 297 +/- 18 ms, P less than 0.05, n = 12), and tissue ATP levels fell from 13.2 +/- 1.3 to 9.7 +/- 0.7 mumol/g dry wt (P less than 0.05, n = 12). These results directly demonstrate that IK,ATP is activated and causes APD shortening during hypoxia in intact cardiac muscle despite only a modest (approximately 25%) decline in tissue ATP content.
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PMID:Activation of cardiac ATP-sensitive K+ current during hypoxia: correlation with tissue ATP levels. 190 1

The goal of studies was to define diagnostic possibilities of echocardiography. 1250 patients with myocardial infarction and aggravations of ischemia were examined in the conditions of resuscitation and intensive care unit. The application of echoCG gives the possibility to determine with great accuracy the state of transport function of myocardium, pinpoint a location of cardiac muscle affection and measure its gravity, make a diagnosis of myocardial infarct aggravations at an early period, control the efficiency of treatment which is provided.
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PMID:[The potentials of echocardiography in the diagnosis of acute cardiovascular diseases]. 204 6

In the present study we examined the regulation of the cardiac muscle mitochondrial ATPase both in situ and in vitro in intact and sonicated mitochondria from rabbit, pigeon, and rat. We chose to study these three species because each is representative of one of the three classes into which all species thus far studied may be placed with respect to the in situ activity of their cardiac muscle mitochondrial ATPase inhibitor and with respect to the amount of ATPase inhibitor present in their cardiac muscle mitochondria (1). Class A species (rabbit) contain a full complement of ATPase inhibitor and show a marked ATPase inhibition during ischemia. Class B species (pigeon) also contain a full complement of inhibitor but exhibit only a low level of ATPase inhibition in situ. Class C species (rat) contain only low levels of inhibitor and, like class B species, don't appear to utilize the inhibitor they possess during ischemia in situ. We found that, while hearts from all three species developed a marked cytosolic acidosis during ischemia, only rabbit exhibited a marked ATPase inhibition in situ. In in vitro experiments in which matrix pH values close to 6.2 and delta psi values close to zero were measured in intact mitochondria from all three species, matrix pH appeared to be an important factor regulating ATPase inhibition in rabbit, but it had little effect upon ATPase--inhibitor interaction in pigeon and rat despite the lack of membrane potential. However, a pH-dependent further release of ATPase inhibitor was observed in sonicated pigeon heart mitochondria only. This latter observation suggests that, while slow heart-rate heart mitochondria appear to be designed for ATPase down regulation during ischemia by inhibitor binding to the ATPase, fast heart-rate heart mitochondria appear to be designed primarily for ATPase up regulation by a further release of inhibitor from the enzyme.
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PMID:Regulation of the mitochondrial adenosine 5'-triphosphatase in situ during ischemia and in vitro in intact and sonicated mitochondria from slow and fast heart-rate hearts. 214 Dec 43

The availability and the now routine use of thrombolytic agents are important advances for therapeutic cardiology and the emergency care of patients experiencing AMI. The progression from ischemia to necrosis of cardiac muscle now can be aborted in a portion of this population by initiating thrombolytic infusions. Early use of thrombolysis in these patients has reduced acute myocardial infarction mortality and morbidity significantly. Although thrombolytic therapy has changed the course of treatment and survival after AMI, there may be time when this approach is contraindicated or unsuccessful. Alternative treatments that may be considered when thrombolytic agents cannot be given, or fail to ameliorate ischemia, are emergent percutaneous transluminal coronary angioplasty or coronary artery bypass graft surgery. Future interventional procedures such as intracoronary stents, atherectomy devices, and lasers may be considered as emergent treatment in the near future. It is important to have reviewed when these alternative invasive procedures, some of which are currently experimental, might be considered. Indeed, interventional procedures such as intracoronary stents, atherectomy devices, and laser delivery systems eventually may be accepted as primary therapies for the patient who arrives in the emergency department with an AMI. In the meantime, thrombolytic therapy administered as urgently as possible to appropriate patients with myocardial infarction is the most important goal.
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PMID:Invasive cardiac procedures after myocardial infarction: which procedure when and its relationship to thrombolysis. 214 12

With the use of microelectrodes, intracellular pH (pHi), surface pH (pHs), and intracellular Na+ activity (aiNa) were measured in isolated guinea pig papillary muscles during normal superfusion and during a reversible condition of simulated ischemia. Acid loading by NH+4 prepulse or by CO2-HCO3- addition during superfusion with pH 7.4 solutions caused internal acidification followed by a recovery of pHi, which could be inhibited by amiloride. pHi recovery was associated with an amiloride-sensitive peak rise of aiNa and membrane hyperpolarization, indicative of Na(+)-H+ exchange. Peak increase of aiNa was absent if the pH of the superfusion solution was concomitantly lowered. Imposed ischemia after control superfusion caused membrane depolarization and acidification of pHi and pHs. The change of pHs consistently was larger than that of pHi. aiNa decreased from 5.5 to 4.6 mM after 10-min ischemia. Enlarging the pHi (and pHs) decrease in ischemia by prior reduction of the tissue buffer capacity (CO2-HCO3(-)-free superfusion) was unable to induce a rise of aiNa during the subsequent ischemic period. Amiloride had no significant effect on aiNa during ischemia. It is concluded that the important acidification of pHs reduces the rate of pHi regulatory Na(+)-H+ exchange and thereby contributes to a longer maintenance of the Na+ electrochemical gradient in ischemic cardiac muscle.
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PMID:Acidification and intracellular sodium ion activity during stimulated myocardial ischemia. 216 81

It is difficult to associate the ATP-sensitive potassium (K-ATP) channel of cardiac muscle with hypoxia/ischemia induced action potential shortening because this occurs before intracellular ATP falls to levels associated in vitro with channel opening. This leaves the cardiac K-ATP channel without any obvious physiological function. We have quantitatively examined the relationship between action potential duration and K-ATP channel activity in enzymatically isolated ventricular myocytes of the guinea-pig. In whole-cell voltage-clamp recording experiments when the K-ATP channel opener SR 44866 (2-10 microM) stimulated an outward membrane current greater than 50 pA at 0 mV membrane potential (the equivalent of 30 open K-ATP channels or 1% of the cell K-ATP channel population) action potential duration was reduced by more than 50%. In the majority of cell-attached membrane patch recordings metabolic inhibition stimulated K-ATP channel open probability of 1-2% which continued for long periods (7-25 min) before cell contracture and coincident major K-ATP channel activation (open probability 65%). Our quantitative analysis thus shows that physiologically relevant activity of K-ATP channels in cardiac muscle is confined to a very small percentage of the possible cell K-ATP current and thus intracellular ATP would not have to fall very far before the opening of K-ATP channels would influence cardiac excitability.
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PMID:Action potential duration and activation of ATP-sensitive potassium current in isolated guinea-pig ventricular myocytes. 222 7

Perioperative myocardial infarction is a major complication of revascularization surgery of the heart which can negatively affect both the quality and duration of the patient's life. The aim of the paper is to contribute to the understanding of the problem which involves the definition, incidence, pathogenesis, diagnosis, complications, therapy and prognosis of perioperative myocardial infarction. One of the basic factors implicated in the development of perioperative derangement of the cardiac muscle is closely analyzed, namely insufficient protection of the myocardium with subsequent ischemia-reperfusion induced myocardial damage. Pitfalls of electrocardiographic diagnosis are pointed out and the rather complicated interpretation of increased enzyme levels following cardiac surgery is discussed. Complications, management, as well as early and late prognosis of patients with perioperative myocardial infarction are also dealt with.
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PMID:[Perioperative myocardial infarct in association with surgical treatment of coronary heart disease]. 222 48

Based on the therory of promoting flow of qi and dispersing blood stasis, the KUO GUAN QU YU LING coronary--dilating and stagnation--dispersing) powder in capsules were prepared for the treatment of 60 cases of coronary heart disease. After a 30 day course of treatment, cardiac ischemia was improved in 64.7% and the symptom of angina pectoris was relieved in 61.7% of the patients. This drug also acted to reduce blood lipids and to improve left cardiac function. Pharmacological study indicated that this preparation improved the tolerance of cardiac muscle against anoxia and prevented ventricular fibrillation and cardiac damage from ischemia.
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PMID:Observations on the treatment of coronary heart disease by kuo guan qu yu ling. 236 65

In the experiments on anesthetized cats and dogs it was shown that calcium antagonists nimodipine and flunarisine possessing the predominant action on the cerebral vessels exert a significant effect on the blood supply and the activity of the cardiac muscle. Administration of the drugs causes bradycardia, increases the total coronary blood flow. Nimodipine enhances the contractile function of the myocardium, flunarisine fails to change it. Under ischemia of the cardiac muscle the drugs increase the blood supply of only the intact zones of the left ventricle without influencing positively the blood supply of the ischemic focus itself.
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PMID:[A comparative study of the effect of nimodipine and flunarizine on the intact and ischemic myocardium]. 238 72


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