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

Myocardial carbon dioxide tension and intramyocardial S-T segment voltage have previously been shown to provide useful quantitative indexes of the severity of regional myocardial ischemia. This study was designed to determine if (1) changes in intramyocardial S-T segment voltage and myocardial gas tensions, with the addition of atrial pacing, could be used to assess the functional significance of a coronary stenosis, and (2) if changes in S-T voltage recorded in intramyocardial electrodes proved a more sensitive indicator of ischemia than changes recorded in epicardial electrodes. In 12 open chest dogs, a variable constrictor and an electromagnetic flow probe were placed on the proximal left circumflex coronary artery. Myocardial carbon dioxide and oxygen tensions were recorded with mass spectrometry and unipolar intramyocardial S-T segment voltage with multicontact plunge electrodes. Intramyocardial S-T voltage and myocardial carbon dioxide tension showed parallel increases with atrial pacing in the presence of subcritical, critical and supercritical coronary stenoses. In the presence of a critical stenosis, S-T segment changes recorded in deepr myocardial layers were of greater magnitude than those recorded near the epicardial surface. These findings suggest that the severity of myocardial ischemia can be assessed by measuring intramyocardial S-T voltage or myocardial gas tensions at resting and paced heart rates. They also suggest that intramyocardial S-T voltage is a more sensitive indicator of the severity of pacing-induced myocardial ischemia than epicardial S-T changes. Application of this technique to patients undergoing coronary revascularization could allow intraoperative determination of the functional significance of questionable angiographic lesions and a more rational approach to the assignment of priorities to individual arteries when multiple bypasses are being considered.
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PMID:Functional significance of coronary arterial stenoses assessed by regional changes in intramyocardial S-T segment voltage and myocardial gas tensions with atrial pacing. 84 37

The effect of a critical coronary artery stenosis on myocardial blood flow and metabolism in the fibrillating heart was assessed by placing 10 dogs on cardiopulmonary bypass, venting the ventricle, inducing ventricular fibrillation, and applying critical stenosis to the left anterior descending coronary artery (LAD). Endocardial and epicardial blood flows were measured by the radioactive microsphere technique prior to the application of the stenosis and after one hour and 2 hours of fibrillation. Intramyocardial oxygen tension (PO2) and carbon dioxide tension (PCO2) were continuously monitored in the LAD-supplied myocardium by a mass spectrometer probe inserted at midmyocardial depth. Selective arterial-coronary venous lactate differences were determined at control, one hour, and 2 hours. At the end of the 2 hour period, vital dye injection defined the distribution of the LAD. Endocardial flow to the myocardium of the stenosed LAD was reduced by 50 per cent after one hour and by 70 per cent after 2 hours (p less than 0.05). Epicardial flow fell 40 per cent after one hour and 50 per cent after 2 hours (p less than 0.05). Endocardial and epicardial flow in the distribution of the unstenosed circumflex coronary artery remained unchanged. Changes in myocardial PO2 and PCO2 in the LAD-supplied myocardium indicated the development of severe ischemia in all 10 dogs and suggested myocardial infarction in 5. There was a conversion from lactate extraction to lactate production during the 2 hour period of ventricular fibrillation. From this study, it is concluded that the myocardium distal to a critical stenosis suffers a progressive reduction in flow during ventricular fibrillation which does not occur in regions supplied by unstenosed coronary arteries. Thus prolonged fibrillation in the presence of a flow-limiting coronary stenosis may play a role in the pathogenesis of myocardial infarction during coronary bypass surgery.
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PMID:Myocardial ischemia during cardiopulmonary bypass. The hazards of ventricular fibrillation in the presence of a critical coronary stenosis. 85 Apr 34

In a previous study from this laboratory, regional myocardial ischemia developed distal to a critical coronary stenosis in the fibrillating heart on cardiopulmonary bypass when myocardial perfusion was non-pulsatile. To assess the effect of pulsatile perfusion on the development of the fibrillation-induced ischemia, 10 dogs were placed on total cardiopulmonary bypass with the heart in the vented fibrillating state. A critical stenosis was applied to the left anterior descending artery (LAD). Pulsatile perfusion with a pulse pressure of 35 mm Hg and a pulse rate of 100/min was produced by a new method developed in this laboratory. During the 2 hours of bypass, ischemia in the LAD-supplied myocardium was assessed by changes in intramyocardial oxygen (PmO2) and carbon dioxide (PmCO2) tensions and by regional arterial-coronary venous lactate difference. With linear perfusion, regional ischemia in the LAD myocardium had been evidenced by a low PmO2 (8 +/- 3 mm Hg), a high PmCO2 (170 +/- 25 mm Hg) and regional lactate production (9.2 +/- 4.2 mg/100 ml). In contrast with pulsatile perfusion intramyocardial gas tensions remained stable during the 2 hours on bypass (PmO2 = 21 +/- 3 mm Hg, PmCO2 = 65 +/- 5 mm Hg, P less than 0.05 vs linear flow study) and lactate consumption was demonstrated (+17.7 +/- 2.9 mg/100 ml, P less than 0.001 vs linear flow group). With linear perfusion, myocardial blood flow to the LAD area had decreased 56 +/- 8% in the subendocardial layer and 46 +/- 7% in the subepicardial layer. In the dogs receiving pulsatile flow during bypass, regional LAD blood flow remained unchanged over the 2-hour bypass period and was significantly higher than the flow with linear flow (P less than 0.05). These data indicate that fibrillation-induced regional myocardial ischemia distal to a critical stenosis can be prevented by maintaining pulsatile perfusion during cardiopulmonary bypass.
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PMID:Regional ischemia distal to a critical coronary stenosis during prolonged fibrillation--improvement with pulsatile perfusion. 88 25

Plasma polyps can be found at the end of a normal pregnancy. Following NaF and MJA-intoxication, there is an extreme increase of plasma polyps. This accelerated formation can be prevented by the injection of Na-pyruvate and often the number of polyps can be reduced below the norm. 2,4-Dinitrophenol intoxication and breathing of hypoxic gas mixture (2,5% O2, 5% CO2, 92,5% N2) do not lead to increased plasma polyp formation. This proves, that it is not hypoxia, not an energy deficit secondary to separation of oxydative phosphorylation and not cardiac insufficiency leading to secondary ischemia which are responsible for the extreme increase in the number of plasma polyps following the injection of MJA and NaF.
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PMID:[The effect of 2,4-dinitrophenol, monoiodine acetate, sodium fluoride and hypoxia on the formation of plasma polyps in the placenta of guinea pigs (author's transl)]. 99 63

Responses of heart rate (HR), mean arterial blood pressure (MAP) ventilation (VE), and forearm blood flow (FBF) to different degrees of leg muscle ischemia were measured in eight subjects in a four-part experiment. Part I. Total circulatory occlusion (OCCL) of resting legs for 15 min had little or no effect on HR, MAP, VE, or FBF. Part II. OCCL of the legs for 3 min immediately after exercise at 50-250 W did not affect HR or end-tidal CO2; it lowered VO2 and VE and prevented recovery of MAP. Part III. OCCL beginning at end and 10, 20, 30 s before end of 7-min exercise (100-150 W) and continuing 3 min into recovery period produced sustained and graded increments (5-10 mmHg) in MAP, only small changes in HR, and accelerated recovery of VE while end-tidal CO2 remained constant. Part IV. OCCL at end and 30 s before end of exercise increased FBF 2.5-3.5 times; both skin and muscle vasodilated. Thus muscle ischemia preceded by exercise can raise MAP without affecting VE, whereas baroreflexes may lower HR and raise FBF. The results suggest the presence of muscle chemoreceptors whose major effect is on MAP.
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PMID:Human cardiovascular and respiratory responses to graded muscle ischemia. 99 57

Previous studies from this laboratory have demonstrated the usefulness of myocardial gas tensions as measured by mass spectrometry for the quantitative assessment of regional myocardial ischemia (Khuri et al., 1975a). Progressive increases in myocardial carbon dioxide tensions were noted when progressive reduction in coronary blood flow was created by means of a variable constrictor. The present study was designed to determine if changes in myocardial oxygen and carbon dioxide tension were greater in deep, compared to more superficial, myocardial layers. In eight anesthetized dogs, progressive reduction in circumflex coronary flow was associated with a progressive reduction in myocardial oxygen tension and a progressive increase in myocardial carbon dioxide tension and intramyocardial ST-segment voltage. Evidence of a transmural gradient in the severity of ischemia was present at all degrees of flow reduction. These results confirm the findings of previous metabolic studies, which demonstrated gradients in lactate and high-energy phosphates. Myocardial carbon dioxide tension, which can be monitored continuously by mass spectrometry, would appear to provide a useful means of quantitatively assessing changes in regional myocardial metabolism.
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PMID:Transmural gradients in myocardial gas tensions in regionally ischemic canine left ventricle. 103 74

The fetal mouse heart (FMH) in organ culture continues to beat for a period of weeks, but degenerative changes occur. Electron microscopy revealed formation of autophagic vacuoles containing damaged organelles in some cells after the first day, indicating focal cytoplasmic injury. This process was accelerated by transient deprivation of oxygen and glucose followed by resupply of oxygen and glucose. FMHs were maintained for up to four hours in glucose-free media in an atmosphere of 95% N/5% CO2 followed by resupply of O2 and glucose. Twenty-four hours later, many cells recovered without residual injury. Many others revealed autophagic vacuoles ranging from those in which organelles were readily identified to those characteristic of residual bodies. It appears that focal injury stimulates the endoplasmic reticulum to enclose the damaged components, permitting localized lysosomal digestion without causing injury to the entire cell. Autophagy has not been emphasized as an important mechanism in transient ischemia in adult myocytes, but it may play a role in repair of sublethal injury. The FMH organ culture provides an excellent model for studying the sequential autophagic changes in a system in which these events can be accelerated.
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PMID:Autophagy in cardiac myocytes. 103

A comparison of regional cerebral blood flow measurements made with beta- and gamma-emitting isotopes revealed good correspondence in areas of normal perfusion and reactive hyperemia but poor correspondence in areas of focal ischemia. After middle cerebral artery occlusion at normocapnia, there was a 65% reduction in regional cerebral blood flow from 1.40 plus or minus 0.27 ml/g min--1 to 0.49 plus or minus 0.10 ml/g min--1 in monkeys studied with 85Kr but only a 27% reduction in regional cerebral blood flow from 0.84 plus or minus 0.09 ml/g min--1 to 0.61 plus or minus 0.08 ml/g min--1 in monkeys studied with 133Xe. The lack of correlation within areas of focal, incomplete ischemia was attributed to an impairment of isotope delivery to the area of ischemia coupled with the inherent lack of spatial resolution of determinations made with 133Xe. This finding may partly explain the numerous discrepancies in experimental and clinical studies of the effects of alterations in the arterial partial pressure of CO2 on regional cerebral blood flow in areas of ischemia; it may also explain the failure of such studies to reflect the true severity of focal ischemia.
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PMID:Comparison of 85krypton and 133xenon cerebral blood flow measurements before, during, and following focal, incomplete ischemia in the squirrel monkey. 111 19

In isolated perfused rabbit hearts, coronary vasodilation, produced by reduced oxygen tension seems to be independent of myocardial prostaglandin biosynthesis. a) Anoxia (N2: CO2 95: 5 %) produced coronary vasodilation without causing prostaglandin-like substance (PLS) biosynthesis and release; b) the decrease in coronary resistance during hypoxia (N2:02:CO2 - 80:15:5 %) was sustained during myocardial perfusion with the low oxygen media despite the transitory nature of its PLS release; and c) indomathacin, which abolished basal or ADP stimulated myocardial PLS release, did not abolish the coronary vasodilation produced by ischemia, hypoxia, or anoxia.
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PMID:Relationship between oxygen tension, coronary vasodilation and prostaglandin biosynthesis in the isolated rabbit heart. 113 23

One hypothesis on the pathogenesis of post-ischemic-anoxic encephalopathy is impaired cerebral perfusion or the no-reflow phenomenon. Therapies aimed at preventing the development of this phenomenon are increased cerebral perfusion pressure (CPP) and hyperventilation or hypercapnia. Using a dog model in which we have described the progressive development of post-ischemic (PI) cerebral hypoperfusion after 15 minutes of global ischemia induced by aortic and vena cavae clamping, our aims in this study were to determine during the PI cerebral hypoperfusion period: (1) cerebrovascular reactivity to CO2, and (2) cerebral blood (CBF) autoregulation. Post-ischemic cerebral hypoperfusion to about 50% of normal was not accompanied by raised intracranial pressure (ICP) but cerebrovascular CO2 reactivity was markedly attenuated while maintaining some kind of autoregulatory phenomenon. Cerebral uptake of oxygen was not significantly affected by changing PACO2 from 20 to 60 torr at constant CPP or by changing CPP from 64 to 104 torr at constant PaCO2. These results suggest that increasing both CPP and hypocapnia/hypercapnia would not significantly attenuate PI neurological deficit after global cerebral ischemia. However, in two dogs inadvertently hemodiluted in the PI period, increasing CPP from 50 to 200 torr increased CBF by 200%, suggesting that hemodilution plus increased CPP may be effective therapy for amelioration of post-ischemic-anoxic encephalopathy. The significance of our findings on cerebrovascular CO2 reactivity and autoregulation with respect to the mechanism of the no-reflow phenomenon is discussed.
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PMID:Global ischemia in dogs: cerebrovascular CO2 reactivity and autoregulation. 115 79


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