Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rabbit hearts were perfused at a pressure of 60 cm H2O with 37 degrees C Tyrode solution aerated with 5% CO2 in O2. The effluent from the heart was collected in four consecutive 10-min periods. The samples were analyzed for prostaglandins of the E series (PGE), using thin layer chromatography for identification and assay on the superfused rat stomach strip for quantitative estimation. Three different series of experiments were performed, the hearts in each series during the second effluent collection period being perfused under conditions of either hypoxia (Tyrode solution aerated with 5% O2 and 5% CO2 in N2), absence of glucose in the Tyrode solution, or hypotension/low perfusion flow (perfusion pressure lowered to 30cm H2O). In the series where glucose was omitted or hypotension/low perfusion flow was induced during the second effluent collection period, the outflow of PGE decreased exponentially throughout the four periods. In the series where hypoxia was maintained during the second effluent collection period, a marked increase in the outflow of PGE was noted after the end of hypoxia. Prostaglandins of the E series are powerful vasodilators, and the PG released may, by inducing coronary vasodilation, counteract the hypoxia. However, it has been shown that, in human plasma, conversion of arachidonic acid to PGE is parallelled by platelet aggregation. Therefore, if PG synthesis is also stimulated by hypoxia in man, myocardial ischemia must be considered as a possible mechanism for platelet aggregation and subsequent coronary thrombosis.
 ...
PMID:Hypoxia-induced prostaglandin release from rabbit heart. 120 90

Seventy-two healthy young individuals were subjected to controlled, moderate hyperventilation with room air and with 4.9 percent CO2 in air, and monitored electrocardiographically. Significant summed frontal T-wave changes with hyperventilation (sigmaT1,2,3 larger than or equal to 1.5 mm) were observed in 12 patients. Six subjects (8.3 percent) showed T-wave depression. It was reversed in five patients by hyperventilation with 4.9 percent CO2 in air. T-wave elevation, observed in six subjects, was reversed in four patients by hyperventilation with 4.9 percent CO2. A short period of hyperventilation with an air mixture containing 4-5 percent CO2 is suggested as a means of screening patients under suspicion of ischemic heart disease exclusively on the basis of ECG changes.
 ...
PMID:Hyperventilation-induced T-wave changes in the limb lead electrocardiogram. 123 20

The extracellular pH (pHo) and intracellular pH (pHi) were simultaneously measured with H(+)-sensitive microelectrodes in the rabbit papillary muscle during normal arterial perfusion and no-flow ischemia. The preparation was kept in an artificial gaseous atmosphere (N2 and CO2 during ischemia) without a surrounding fluid layer. Cylindrical muscles of small diameters (less than 1.0 mm) were selected to prevent major diffusion gradients of CO2 within the muscle cylinder during ischemia. In normal perfusion with CO2/HCO3(-)-buffered blood at PCO2 of 35 mm Hg, pHi was 7.03 +/- 0.03. During early ischemia, extracellular acidification was much more prominent than intracellular acidification. Consequently, the transmembrane pH gradient reversed (pHo less than pHi) at approximately 8 minutes. At 14 minutes of ischemia, pHo was 6.64 and pHi was 6.93. A moderate increase in PCO2 from 35 to 67 mm Hg before ischemia enhanced intracellular acidification in ischemia. Simulation of CO2 accumulation (increase of PCO2 in the surrounding atmosphere), as encountered in midmural ventricular layers during in vivo ischemia, produced a significant decrease of pHo (6.30 versus 6.64) and pHi (6.65 versus 6.93) at 14 minutes of ischemia. The presence of red blood cells in the intravascular space after arrest of coronary perfusion showed a pronounced effect on extracellular and intracellular acidosis. If the muscles were perfused with CO2/HCO3(-)-buffered perfusate in the absence of red blood cells, the changes of pHo and pHi were significantly larger (pHo, 6.00 versus 6.64; pHi, 6.46 versus 6.93 at 14 minutes) during ischemia. Actively developed force during ischemia was not significantly influenced by conditions modulating pHi. It decreased by 82% after 5 minutes, even when no significant change of pHi was recorded. By contrast, ischemic contracture was dependent on intracellular acidification. It developed earlier in the absence of red blood cells or with low extracellular buffer capacity. It is concluded that during acute myocardial ischemia 1) extracellular acidification exceeds intracellular acidification, 2) the decrease in pHi is inhomogeneous because of local variation in CO2 accumulation and diffusion, 3) the decrease in pHi is relatively small in the presence of red blood cells, and 4) the development of ischemic contracture but not the early decline in active tension is sensitive to changes in pHi.
 ...
PMID:Changes in extracellular and intracellular pH in ischemic rabbit papillary muscle. 162

In order to understand the pathophysiology of myocardial stunning, reversibility, accumulation and continuity of ischemic myocardial damage after reperfusion should be studied. Then, to analyze these three factors, myocardial function, metabolism and morphology under ischemia and reperfusion were studied in anesthetized, open-chest dogs. When myocardial ischemia was induced by occlusion of the left anterior descending coronary artery, percentage regional systolic shortening (%SS) of ischemic myocardium sharply decreased and became stable 10 min after occlusion. After reperfusion, ischemic myocardium showed active shortening after within 30-min occlusion, but did not after more than 60-min occlusion. During 90-min of ischemia, extracellular K+ concentration (Ke) steeply increased for first 10 min and was almost stable for next 10 min. Then, Ke straightly increased till 90 min. Metabolic rates, calculated from myocardial tissue CO2 and pH, steeply increased for first 20 min and sharply decreased for next 10 min. After 30 min, these two variables were almost stable, near zero. By electron-microscopy with cytochemistry, distribution of Na/K ATPase to myocardial cell membrane was observed to be almost after 15-min occlusion but distinctly sparse with destruction of cell membrane after 30-min occlusion. Therefore, irreversible myocardial damage appears after about 20-min ischemia and is almost complete after 60 min. Reversibility of damage to ischemic myocardium after reperfusion may mainly occur within 60-min ischemia. Although stunned myocardium in a narrow sense is may appear after reperfusion within less than 20-min of ischemia, stunned myocardium in a broad sense may appear within less than 60-min ischemia. When reversible myocardial ischemia (4- or 15-min occlusion) was repeated after short time intervals (20-min reperfusion), %SS of ischemic myocardium was gradually decreased with each ischemic episode. Active shortening of ischemic myocardium disappeared after more than two episodes of 15-min occlusion. Fluctuation of PCO2, pH and Ke of ischemic myocardium was gradually depressed with each occlusion. Metabolic viability of ischemic myocardium was cumulatively depressed by repeated brief occlusion. Naturally, myocardial damage was more severe after repeated 15-min occlusion than after 4-min occlusion. Accumulation of ischemic myocardial damage may arise as brief ischemia, which only induces reversible damage, is repeated. At last, continuity of ischemic myocardial damage was studied. The effect of 5-min occlusion to %SS of ischemic myocardium was apparently reversed after 90-min reperfusion. Early contractile failure was advanced even after very short duration of ischemia. Thus, myocardial function will be latently damaged.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:The pathophysiology of myocardial stunning: reversibility, accumulation and continuity of the ischemic myocardial damage after reperfusion. 165 10

The role of local accumulation and diffusion of CO2 to modify cellular loss and extracellular accumulation of K+ during the initial, reversible phase of myocardial ischemia was investigated in isolated, cylindrical papillary muscles of the rabbit. The muscles were blood-perfused through their vascular tree and placed in a (permanently flowing) humidified gas mixture with predetermined partial pressures of N2, O2, and CO2. Ischemia was produced by total arrest of perfusion and O2 withdrawal from the gas mixture. With surface PCO2 kept constant during ischemia, [K+]o varied markedly with muscle geometry. After 10 minutes of ischemia, K+ accumulation was approximately 2.5 mM in muscles with a radius of 0.35 mm and approximately 14 mM in muscles with a radius of 0.9 mm, indicating that a large fraction of K+ accumulation was dependent on diffusion of a volatile metabolite. Computer simulation of CO2 accumulation and diffusion within a tissue cylinder suggested a close phenomenological relation between PCO2 and [K+]o in ischemia. This was confirmed by the finding that an increase of tissue PCO2 in small cylinders before or during ischemia by externally applied CO2 produced an increase in K+ accumulation. The importance of CO2 diffusion for local inhomogeneities in K+ within the same preparation was demonstrated by showing [K+]o gradients with simultaneous or consecutive measurements between the papillary muscle cylinders and the adjacent septum and within 300 microns from the surface of the papillary muscle cylinders. These gradients predict an inhomogeneity of impulse conduction that might contribute to the genesis of ventricular arrhythmias. Besides the demonstration that accumulation and diffusion introduce inhomogeneities of [K+]o in ischemia, our results suggest that a significant component of cellular ischemic K+ loss is associated with production and extrusion of metabolic acid. On the basis of previous measurements of pHo and pHi in identical conditions, possible mechanisms of ischemic cellular K+ loss are discussed.
 ...
PMID:Early changes in extracellular potassium in ischemic rabbit myocardium. The role of extracellular carbon dioxide accumulation and diffusion. 173 38

The cardiopulmonary effects of constant-flow ventilation were investigated in dogs with normal heart function (control-phase, n = 14) and after development of acute myocardial ischaemia (ischaemia phase, n = 14). Heated, humidified and oxygen-enriched air was continuously delivered with an inspiratory flow rate of 1.21.kg-1.min-1 via two catheters positioned within each mainstem bronchus. Continuous positive pressure ventilation with a positive end-expiratory pressure of 0.5 kPa (5 cmH2O) was used as a reference. During control, neither continuous positive pressure ventilation nor constant-flow ventilation showed impairment of cardiopulmonary performance. Oxygenation and CO2 removal were more efficiently achieved by continuous positive pressure ventilation (P less than or equal to 0.05). Acute myocardial ischaemia was induced by occlusion of the left anterior descending (LAD) coronary artery; measurements during the ischaemia phase were performed 60 min following LAD occlusion. Myocardial ischaemia resulted in moderate changes of cardiac output, left ventricular end-diastolic pressure and dP/dtmax. Both modes of ventilation were well tolerated in the ischaemia phase, and cardiovascular performance revealed no significant differences between continuous positive pressure ventilation and constant-flow ventilation. Haemodynamic parameters could be more precisely assessed during constant-flow ventilation. Oxygenation deteriorated, but hypoxaemia did not occur in any animal and CO2 elimination remained unchanged. It is concluded that 'non-conventional' ventilation by continuous intrabronchial gas flow maintains adequate gas exchange with no adverse effects on haemodynamics in dogs with acute myocardial ischaemia. Constant-flow ventilation may be advantageous in the experimental setting to study cardiac function without cyclic heart-lung interaction due to airway pressure alterations.
 ...
PMID:Cardiopulmonary effects of constant-flow ventilation in experimental myocardial ischaemia. 178 43

Pharmacologic action of antiarrhythmic agents in hypoxia was studied with the microelectrode using the guinea pig papillary muscle. Tyrode solution saturated with 95% O2 and 5% CO2 provided normoxic condition and that with 95% N2 and 5% O2 hypoxic condition. The parameters measured were as follows: 1) Vmax: the maximum rate of rise of the action potential, 2) ERP: effective refractory period, 3) ERP/APD90%: the ratio of effective refractory period to action potential duration at 90% repolarization. [1] When the papillary muscle was perfused more than 15 minutes with the hypoxic solution, irreversible changes ensued inevitably. Accordingly, a perfusion with the hypoxic solution for 15 minutes was succeeded by that with the normoxic solution for 30 minutes. This was then followed by another perfusion with the hypoxic solution. [2] Flecainide was examined in 7 cases. The rate of the depression of Vmax by flecainide was significantly (p less than 0.01) increased in hypoxia (16.3 +/- 4.2%) than in normoxia (7.4 +/- 2.0%). There were no significantly differences in the rate of the change of ERP between both conditions. The rate of ERP/APD90% was significantly (p less than 0.01) increased by flecainide during hypoxia (2.2 +/- 0.8%) than during normoxia (0.1 +/- 2.1%). [3] The depression of Vmax and the increase of ERP/APD90% by flecainide occurred in a dose-dependent manner in normoxia. it was concluded that the depression of Vmax by flecainide over the concentration of 2 micrograms/dl were ascribed to its inhibitory effect on the fast Na channel and that its depressive effects were enhanced during hypoxic condition. This inhibitory action was regarded as the main antiarrhythmic action of flecainide. From the above results, it is expected that flecainide could be effective in the treatment of ventricular arrhythmias in the ischemic heart disease.
 ...
PMID:[A design of the electrophysiological model on the action of antiarrhythmic agent in hypoxic condition and the electrophysiological study of flecainide]. 190 36

A Commercially available, non-invasive system for estimation of cardiac output by the CO2-rebreathing method (Sensormedicus MMC4400) was evaluated to determine its reliability in clinical practice. Values of cardiac output were obtained at rest and during mild to moderate bicycle ergometer work in patients with ischemic heart disease or hypertension. Cardiac output measured by the CO2-rebreathing method was significantly correlated with that measured simultaneously by dye dilution or thermodilution methods. Cardiac output values determined by the CO2-rebreathing method were the same as those obtained by the two invasive methods in reproducibility. When cardiac output and Vo2 were normalized for body weight, they were significantly correlated with each other. This result was obtained both by the CO2-rebreathing method, and by the two invasive methods. These results indicate that MMC4400 will provide a value for cardiac output substantially the same as that obtained by using more laborious invasive methods. Clinical use of the CO2-rebreathing method has been limited by technical difficulties. However, the recently developed non-invasive cardiac output measurement system (MMC4400) uses a microcomputer to analyze the results, and the operator can determine the values for cardiac output easily. Furthermore, it simultaneously measures VO2, VCO2 and VE, so the operator can estimate the measured values for cardiac output with background information on ventilatory gas analysis. Determination of cardiac output through the use of the CO2-rebreathing method is suitable particularly for exercise studies, and it is expected to be a useful device, in the near future, for evaluating cardiac function of patients with primary cardiac diseases.
 ...
PMID:[Non-invasive measurement of cardiac output by the CO2 rebreathing method and its reliability in clinical practice]. 190 14

The effects of intermittent coronary sinus occlusion (ICSO) on the size of myocardial infarction and reperfusion hemorrhage was evaluated. In Protocol 1, 8 dogs with ICSO and 8 controls underwent 4h of occlusion of the left anterior descending coronary artery. The same number of dogs underwent 4h of occlusion followed by 1h reperfusion in Protocal 2. The ICSO was started 1h after the ligation and continued through the occlusion period. There was no difference between the ICSO and the control group in hemodynamics and regional myocardial blood flow using hydrogen clearance method. However, ICSO did accelerate the rate of decline in intramyocardial CO2 tension. The half life of CO2 tension was 256 +/- 106 min in the control group but 139 +/- 34 min in the ICSO group (p less than 0.01). Lactate extraction rate showed the improving tendency during ICSO period. The ICSO resulted in a 50% and 80% reduction on an average in the size of infarct and reperfusion hemorrhage, respectively. We conclude that ICSO has prospective effects on myocardial ischemia with promise for clinical application.
 ...
PMID:Effects of intermittent coronary sinus occlusion on experimental myocardial infarction and reperfusion hemorrhage. 212 46

It is traditional practice to treat acute hyperventilation (thought to be due to anxiety) by having patients rebreathe into a brown paper bag. The author reports three cases in which this treatment, erroneously applied to patients who were hypoxemic or had myocardial ischemia, resulted in death. This clinical experience motivated a study of the effects of paper bag rebreathing in normal volunteers. Subjects deliberately hyperventilated to an average end-tidal CO2 concentration of 21.6 (SD, 3.2) mm Hg and then continued to hyperventilate into a no. 4 Kraft brown paper bag containing the calibrated sensors for a Hewlett-Packard 47210A capnograph and a Teledyne TED 60J digital oxygen monitor. Fourteen men and six women with an average age of 36 years (SD, 6.1) were tested. Results are reported as mm Hg. After 30 seconds of rebreathing, mean change in O2 from room air was -15.9 (SD, 4.6) and mean CO2 was 38.7 (SD, 6.2); at 60 seconds, -20.5 (6.0) and 40.2 (6.4); at 90 seconds -22 (6.8) and 40.5 (6.4); at 120 seconds -23.6 (6.8) and 40.7 (6.5); at 150 seconds -25.1 (1.2) and 41 (7.3); and at 180 seconds -26.6 (8.4) and 41.3 (7.5). A few subjects achieved CO2 levels as high as 50, but many never reached 40. The mean maximal drop in O2 was 26 (8.8); seven subjects had drops in oxygen of 26 mm Hg at three minutes, four had drops of 34 mm Hg, and one had a drop of 42 mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Hypoxic hazards of traditional paper bag rebreathing in hyperventilating patients. 249 28


1 2 3 4 5 6 7 Next >>