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

Studies in cats suggest alpha-adrenergic contributions to arrhythmias during myocardial ischemia and reperfusion. The validity of this concept in other species, however, remains uncertain. Thus, 106 chloralose-anesthetized open-chest dogs undergoing a 25 min coronary artery occlusion followed by reperfusion received saline (n = 52), prazosin (1 mg/kg, n = 26), phentolamine (5 mg/kg, n = 18), or phentolamine (same dose) + propranolol (1 mg/kg, n = 10). Alpha-blockade was confirmed by alpha-agonist dose-response studies. In phentolamine-treated dogs, arterial pressure and heart rate were kept constant to prevent exacerbation of ischemia. Control and treated groups were comparable with respect to variables known to affect arrhythmias, such as size of occluded and reperfused vascular beds, coronary collateral flow, severity of ischemia estimated from intramyocardial CO2 tension, and peak reactive hyperemia. During coronary occlusion, the number of single premature ventricular complexes was reduced by phentolamine (P less than 0.01), but not by prazosin or phentolamine + propranolol; no treatment affected the total number of couplets, ventricular tachycardia episodes and ventricular ectopic complexes, or the incidence of ventricular tachycardia and ventricular fibrillation. During coronary reperfusion, arrhythmias did not differ in control and treated groups. Thus, selective alpha 1-(prazosin), nonselective alpha 1- and alpha 2-(phentolamine), and combined alpha- and beta-blockade (phentolamine + propranolol) failed to attenuate complex arrhythmias induced by acute myocardial ischemia and reperfusion. Alpha-adrenergic mechanisms appear unimportant in the genesis of these arrhythmias in the canine model.
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PMID:Effect of alpha-adrenergic blockade on arrhythmias induced by acute myocardial ischemia and reperfusion in the dog. 615 73

Digitalis sensitivity of the heart is increased in patients with ischemic heart disease. Whether this elevation of digitalis sensitivity occurs as the result of ischemia-induced changes in the cardiac tissue and whether changes in the sarcolemmal Na,K-adenosine triphosphatase (ATPase) or reserve capacity of the sodium pump are responsible for the increased digitalis sensitivity were examined using isolated heart preparations obtained from guinea pigs. Ligation of the left anterior descending coronary artery (LAD) in Langendorff preparations 40 min before perfusion with a toxic concentration (either 1.8 or 2.5 microM) of digoxin decreased the time to the onset of arrhythmias. LAD-ligation by itself did not cause arrhythmias. The time to the onset of arrhythmias during digoxin perfusion was slightly longer in preparations obtained from reserpine-treated animals; however, the reserpine pretreatment failed to alter the effect of LAD ligation on digitalis sensitivity, indicating that the release of catecholamines is not involved in the sensitization. The effects of ischemia on Na,K-ATPase and sodium pump activities, glycoside binding to the enzyme and reserve capacity of the sodium pump were examined in globally ischemic Langendorff preparations. The preparations were perfused with a Krebs-Henseleit bicarbonate buffer solution (pH 7.4) saturated with a 95% O2-5% CO2 gas mixture at a control flow rate of 2.5 ml/g of tissue per min or at 5 or 0% of the control flow rate. After 6 hr of zero perfusion, Na,K-ATPase activity and the number of specific ouabain binding sites were reduced in ventricular muscle homogenates. However, the remaining Na,K-ATPase was not altered in its sensitivity to dihydrodigoxin-induced inhibition or affinity of binding sites for ouabain, sodium or potassium. Similar results were observed after reperfusion following 2 or 5 hr of zero perfusion. A 5% perfusion for 2 or 6 hr, or zero perfusion for 2 hr failed to affect Na,K-ATPase activity in muscle homogenates. Sodium pump activity in ventricular slices, estimated from the ouabain-sensitive 86Rb+ uptake, was unchanged after 5% perfusion or zero perfusion for 2 hr, but was significantly reduced after a 20-min reperfusion following 2 hr of zero perfusion. Reserve capacity of the sodium pump, as estimated from the differences in 42K+ uptake by right ventricular strips under 1.5 and 7 Hz stimulation, was unaffected by 2 hr of 5% perfusion. These results indicate that coronary artery occlusion enhances the arrhythmogenic action of digitalis in isolated heart preparations. This change in digitalis sensitivity produced by 40 min of occlusion cannot be explained by reductions in Na,K-ATPase activity or sodium pump reserve capacity as 2 hr of zero perfusion does not alter Na,K-ATPase or sodium pump activity in ventricular tissue.
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PMID:Ischemia-induced enhancement of digitalis sensitivity in isolated guinea-pig heart. 630 6

Recent experimental and clinical data have stimulated interest in the use of alpha-adrenergic antagonists in acute myocardial infarction. We evaluated nicergoline, a new relatively selective alpha 1-antagonist which uniquely lowers heart rate. Open-chest dogs, randomized to control (n = 25) or intravenously treated group (n = 20; 0.5 mg/kg bolus, then 0.10 to 0.15 mg/kg/min), underwent coronary artery occlusion (CAO) followed after 25 minutes by coronary artery reperfusion (CAR). Nicergoline decreased heart rate by 47 +/- 5 bpm and mean aortic pressure by 39 +/- 4 mm Hg. Following CAO, nicergoline reduced total coronary collateral resistance (radiolabeled microspheres; 698 +/- 75 vs 2167 +/- 530 mm Hg/ml/min/gm, p less than 0.05), increased the ischemic zone/nonischemic zone flow ratio (0.14 +/- 0.04 vs 0.06 +/- 0.02, p less than 0.05), and reduced the rise in intramyocardial CO2 tension in the ischemic zone (mass spectrometry, p less than 0.001). Furthermore, the drug decreased the rate of ventricular tachycardia (VT; 191 +/- 13 vs 243 +/- 3 bpm, p less than 0.001) and the incidence of ventricular fibrillation (VF; 1 of 20 [5%] vs 7 of 25 [28%], p less than 0.05). Following CAR, nicergoline did not significantly reduce the incidence of VF but did lower rate (154 +/- 8 vs 212 +/- 10 bpm, p less than 0.001) and incidence (p less than 0.05) of VT. Thus nicergoline reduced severity of ischemia and afforded protection against arrhythmias induced by myocardial ischemia and reperfusion. The observed reduction in heart rate may have contributed importantly to these beneficial effects. Clinical investigation of this potentially useful vasodilator seems warranted.
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PMID:Beneficial effects of the alpha-adrenergic antagonist nicergoline during acute myocardial ischemia and reperfusion in the dog. 641 40

The basic physiologic characteristics of acid-base equilibria during hypothermia were briefly reviewed. By graphic analysis, four possible clinical strategies for managing the acid-base status of the patient undergoing H-CPB were documented. The effect of hemodilution on buffer capacity was charted in a manner applicable to common current operative procedures. During hypothermia for cardiac operations as presently conducted, the perfusionist is in control of the temperature of the body and the perfusion preservation of the body and brain; the surgeon must assume responsibility for preservation of the heart. The literature pertinent to the relationship of the acid-base state to the functions and structural preservation of the heart and brain during the conditions of cooling to and rewarming from deep hypothermia associated with cardiopulmonary bypass, aortic cross clamping, cardioplegia and total circulatory arrest have been reviewed. The evidence is overwhelming that myocardial anoxia caused by aortic occlusion or total circulatory arrest at any temperature to 15 degrees C. result in progressive acidosis which, of itself, is myotoxic. In contrast, alkalinity is ionotropic. Myocardial ischemia, in both adults and infants, should be prevented and treated by alkaline perfusion cooling and by frequent coronary perfusion of a cardiopreservative solution which is extremely cold (4 to 8 degrees C.), oxygenated, has a pH of 7.8, slightly hyperosmolar and which has a hematocrit of 20 per cent (imidazole, erythrocytes and plasma protein colloid), a cardioplegic ionic pattern and energy substrates. Reperfusion of the heart should begin at a 37 pH of 7.8. Evidence is strong that the use of CO2 added to any gas mixture is harmful. It increases myocardial acidosis; it does not increase cerebral blood flow during hypothermia. Protection of the unperfused brain of an infant should emphasize prevention of circulatory arrest prolonged to more than 40 minutes. Temporary reperfusion at that time limit should be used. Probably the best general management of the body for H-CPB is alpha-stat, which preserves biologic neutrality. The uncorrected analyzer reads pH 7.4 and Pco2 at any temperature. However, the need for preservation of the hypoxic heart is overwhelming and, thus, the best acid-base management for cardiac hypothermic operations is significant respiratory alkalosis. The most appropriate sites for the collection of blood samples for gas analysis and measuring temperatures were discussed; "body temperature" is the most unreliable parameter measured. The major characteristics of an "ideal" cardiopreservative solution were described.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The importance of acid-base management for cardiac and cerebral preservation during open heart operations. 642 51

The gaseous microemboli (GME) production and gas transfer characteristics of two series of bubble oxygenators (Harvey H-1500 and Bentley BOS-10) were evaluated during clinical perfusion in 33 adult patients during open heart surgery for acquired valvular and ischaemic heart disease. For each oxygenator series, patients were divided into two groups, depending upon the method of measurement (intermittent or continuous) of the arterial PO2(PaO2). Using the data available, the perfusionist altered the gas:blood flow ratio in an attempt to maintain the PaO2 within the normal range. In the first group (I = intermittent), where PaO2 data were available only intermittently, the PaO2 values were well above normal, and large numbers of GME were detected in the arterial blood. In the second group (C = continuous), where the PaO2 data were available continuously, there was significantly better control of the PaO2 (P less than 0.001 and P less than 0.01 for the H-1500 and BOS-10, respectively) and significantly fewer GME (P less than 0.01 and P less than 0.05 for the H-1500 and BOS-10, respectively). The Bentley BOS-10 oxygenator used a lower gas:blood flow ratio to achieve physiological levels (range 9 to 13 kPa at 37 degrees C) of PaO2 than did the Harvey H-1500 oxygenator, but there was no difference in the number of GME detected. The lower gas:blood flow ratios for the BOS-10 oxygenators in group C resulted in significantly higher PaCO2 values well outside the physiological range (4 to 6 kPa at 37 degrees C) during the rewarming phase (mean PaCO2 = 7.6 +/- 0.8 kPa) of cardiopulmonary bypass than did the H-1500 oxygenator (mean PaCO2 = 6.3 +/- 0.7 kPa). Mean values for the PaCO2 for both oxygenators during other phases of bypass (cooling and hypothermia) were within the physiological range. If the CO2 retention was corrected by increasing the gas:blood flow ratio the PaO2 values and GME counts became elevated.
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PMID:A clinical evaluation of the gas transfer characteristics and gaseous microemboli production of two bubble oxygenators. 644 73

During the global myocardial ischemia of cardiac arrest and during regional myocardial ischemia due to local impairment of coronary blood flow, intramyocardial carbon dioxide tensions (Pmco2) of ischemic myocardium increase to levels exceeding 400 Torr. The mechanism of such myocardial hypercarbic acidosis is as yet incompletely understood, specifically whether these increases in Pmco2 are due to increased oxidative metabolism, decreased CO2 removal, or buffering of metabolic acids. We therefore measured Pmco2 and the total CO2 content of rat hearts harvested before, during, and after resuscitation from cardiac arrest. Pmco2 significantly increased from an average of 63 to 209 Torr during a 4-min interval of untreated ventricular fibrillation. This was associated with concurrent decreases in intracellular pH from an average of 7.03 to 6.02 units. The total CO2 content of the myocardium simultaneously decreased from 17.0 to 16.5 mmol/kg. Accordingly, increases in Pmco2 and [H+] were observed in the absence of increases in the total CO2 content and therefore the calculated myocardial bicarbonate. These observations in the rat model implicate buffering of metabolic acids by bicarbonate rather than increases in CO2 production or decreases in CO2 removal as the predominant mechanism accounting for myocardial hypercarbia.
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PMID:Mechanisms of myocardial hypercarbic acidosis during cardiac arrest. 761 73

In anesthetized dogs intraduodenal administration of m-nifedipine (m-Nif) 0.4 mg.kg-1, coronary flow increased from 708 +/- 72 to 880 +/- 150 ml.min-1.kg-1 (+24%) at 5 min, to 1976 +/- 350 ml.min-1.kg-1 (+179%) at 30 min, and to 998 +/- 250 ml.min-1.kg-1 (+41%) at 4 h. At the dose of nifedipine (Nif), coronary flow increased from 778 +/- 91 to 1080 +/- 90 ml.min-1.kg-1 (+39%) at 3 min and to 1836 +/- 280 ml.min-1.kg-1 (+136%) at 90 min. m-Nif was more 43% potent than Nif and the duration of action of m-Nif was longer. m-Nif reduced heart rate by -39%, while Nif reduced only -11%. m-Nif increased coronary sinus O2 content and reduced MVO2, and no difference was seen between these 2 drugs. However, the rate of CO2 production with m-Nif was reduced to a greater degree than that of Nif. The results indicated that m-Nif was more beneficial in alleviating myocardial ischemia than that of Nif.
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PMID:[Effects of m-nifedipine and nifedipine given intraduodenally on coronary flow, myocardial oxygen, and carbon dioxide metabolism in dogs]. 801 68

Non-invasive evaluation of systemic hemodynamics during exercise in ischemic heart disease (IHD) was attempted by simultaneous measurement of cardiac output by the CO2 rebreathing method and indirect blood pressure in 44 males and 7 females with suspected IHD who underwent left ventriculography and coronary angiography. Thirty-nine of the 51 patients had abnormalities in the regional left ventricular systolic function (asynergy) and/or 75% or more stenosis of the major coronary arteries (IHD group). The other 12 patients were free of these findings, and injection of acetylcholine into the coronary arteries did not induce spasm. These patients were used as the control group. There were no differences in cardiac index (CI), mean blood pressure (MBP), or total peripheral resistance index (TPRI) at rest between the 2 groups. The IHD group had significantly lower CI (p < 0.01) and significantly higher TPRI (p < 0.05) during 25 and 50W exercise than the control group. There were no differences in MBP. A discriminant function using the change in CI (delta CI: l/min/m2) and the percent change in TPRI (% delta TPRI: %) during 25W exercise could predict IHD or control patients with probabilities of 82 and 83%, respectively. D = 3.66-1.39 x (delta CI)-6.67 x 10(-3) x (% delta TPRI), where D > or = 0.3 indicates IHD, and D < 0.3 indicates control. These results suggest that IHD patients have abnormal systemic hemodynamics during mild upright ergometer exercise, even though the resting hemodynamics are nearly normal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Non-invasive evaluation of hemodynamics during mild upright exercise using the CO2 rebreathing method]. 804 93

7 healthy pigs, anesthetized with ketamine/azaperon/thiopentone and ventilated with O2/N2O by volume control, underwent anterior resection of the descending colon by laparoscopic view. During operation of pneumoperitoneum by inflating CO2 to an abdominal pressure of 14 mm Hg was installed. Immediately (+2 min) after the onset of insufflation, both systemic and pulmonary arterial pressure increased. However, pulmonary artery pressure started to decrease after 10 min, whereas systemic arterial pressure remained elevated until the end of the experimental protocol. Left ventricular (LV) pressure and LV dp/dt increased in parallel with the systemic arterial pressure. Peak inspiratory pressure and central venous pressure increased in parallel with the abdominal pressure. Blood gas analysis of arterial and pulmonary blood demonstrated increased pCO2 associated with mild acidosis. Arterial pO2 did not change significantly indicating that the decreased pulmonary distensibility did not endanger the oxygenation. Pulmonary pO2 and pulmonary O2 saturation increased early (+10 min) after start of insufflation and were stable during the 2 h of observation indicating either increased cardiac output or decreased O2 extraction. We conclude that the sharp initial rise of both arterial pressures could be the effect of a mechanical action, whereas sustained hemodynamic alterations would involve complex regulatory mechanisms like an increase of sympathetic activity, baroreceptor control, or a response to acidosis. The acute and, in the systemic circulation, stable increase of ventricular afterload should be considered in patients with underlying cardiac diseases such as ischemic heart disease or valvular dysfunction or in patients taking drugs which interfere with normal compensatory processes.
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PMID:Hemodynamic changes during prolonged laparoscopic surgery. 813 42

Bacterial endocarditis caused by Actinobacillus actinomycetemcomitans (AA) is an extremely rare disease. AA, a gram negative cocco-bacillus, normally resides in the oral cavity. It is involved mostly in local oral cavity infections, but severe systemic infections caused by it have been reported. We describe a 63-year-old man with endocarditis caused by AA which probably originated from a dental abscess. The course of the disease was complicated by acute myocardial ischemia, apparently caused by coronary artery embolism. To enable growth of this bacterium, blood cultures should be maintained for 2-3 weeks in a CO2-rich atmosphere.
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PMID:[Actinobacillus actinomycetemcomitans endocarditis]. 834 5


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