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)

Left thoracotomy and femoro-femoral cardiopulmonary bypass has been used for reoperation in five patients requiring coronary bypass graft into the inferolateral surface of the heart. Five patients had refractory angina pectoris and angiographic occlusion of lateral wall native vessels or previous occluded vein grafts and all had positive exercise test. Four of the five had patent internal mammary to the LAD. Following supine positioning and removal of the saphenous vein and isolation of the femoral artery and femoral vein, a left fifth interspace thoracotomy was made, the patient heparinized and cannulated for cardiopulmonary bypass, the pericardium opened, the heart dissected free, and either the internal mammary artery dissected off the left chest wall or saphenous vein grafts used to bypass the appropriate lesions. The proximal inflow was the descending thoracic aorta making tunnels for the vein grafts through the posterior pericardium. All of the patients did well in the postoperative period. This technique is recommended for reoperations in patients with documented inferolateral ischemia as the primary cause of symptomatology with mitigating circumstances against an anterior approach.
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PMID:Left thoracotomy and femoro-femoral bypass for reoperative revascularization of the posterior coronary circulation. 297 83

Defibrotide (D) is a natural polydeoxyribonucleotide from mammalian lungs with profibrinolytic and antithrombotic activities. D also has PGI2-stimulating and tissue plasminogen activator (TPA)-releasing activities, but has no anticoagulant properties. The protective effects of D were demonstrated very recently in a model for non-lethal ischemia in the cat. In the experiments reported here Defibrotide was tested in a model for acute myocardial ischemia leading to ventricular fibrillation (VF) and death of the cat. Occlusion of the coronary artery (LAD) at its origin induced VF and death in 17 of 20 control cats. When cats were treated with D (32 mg Kg-1, bolus i.v., + 32 mg Kg-1 h-1, i.v., after LAD occlusion) 19 of 20 animals survived until the end of experiments. D also prevented changes in plasma and myocardial CPK, hemodynamics and ECG. D was compared with a variety of pharmacological agents which are used clinically for specific cardiovascular diseases. The ability of D to promote considerable generation of PGI2 from vascular walls plus its ability to prevent the decreases in CPK-activity and ATP in the myocardial tissue may have roles in its beneficial effects against ischemic heart in the cat. However, the mechanism/s of the substantial protective effect of D against cardiac death has still to be clarified.
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PMID:Protective activity of defibrotide against lethal acute myocardial ischemia in the cat. 308 10

We assessed the histochemical, ultrastructural and cytochemical effects of reperfusion on ischemic myocardial cells during the early and late reperfusion phases in two groups of dogs. Group A were 8 dogs undergoing 1 hour occlusion of LAD, and Group B were 14 dogs undergoing 1 hour occlusion of LAD followed by 2 hour reperfusion period. The results of the histochemical study (PAS stain) demonstrated that in Group A, a patchy distribution of glycogen occurred primarily in the subepicardial region. Three-dimensional analysis of this distribution revealed peninsulas of glycogen running parallel with a vessel. The cells in Group B, mainly subepicardium, showed a moderate glycogen content which was more extensive than those in Group A. The ultrastructural changes were assessed after a 60-minute ischemia and subsequent recovery (after 5 minutes and 120 minutes of reflow) using transmural biopsy specimens. Each myocardial cell was graded from 0-4 according to the degree of ischemic injury and recovery. The degree of ischemic damage varied in intensity from slight to severe, in both the subepicardium and the subendocardium. Ca++-ATPase activity was examined cytochemically in myocardial cells of Group B. After 60-minute occlusion, the moderately ischemic cells (especially in the subepicardium) that were without amorphous dense bodies or marked sarcolemmal lifting-off made significantly greater ultrastructural recovery (p less than 0.05) with restoration of Ca++-ATPase activity on sarcoplasmic reticulum and mitochondria after 120 minutes of reflow. This occurred even though after 5 minutes of reflow the cell showed temporary deterioration such as contraction bands, vacuoles and severe destruction of some mitochondria.
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PMID:Histochemical, ultrastructural and cytochemical study of reperfusion effect on ischemic myocardial injury. 315 16

The characterization of thromboxane A2 as vasoconstrictor and potent stimulus of platelet aggregation has led to attempts to overcome these effects obviously unfavourable in ischemia. As an attractive approach, we examined potentially protective results of thromboxane synthetase inhibition on canine myocardium stressed by transient ischemia, using as inhibitor the imidazole derivative UK 38.485. On anaesthetized open-chest mongrel-dogs (n = 5) repeated ischemia (3 min) was produced by proximal, intermittent occlusion of the LAD artery. In each experiment 3-4 control occlusions were compared to 3-4 occlusions under therapy. The efficiency of the drug (5 mg/kg body weight, i.v., 30 min before therapy occlusion) was examined (a) by quantification of the energy deficit occurring as the difference between oxygen demand and uptake during occlusion, (b) by the amounts of potassium, inorganic phosphate, and lactate released in the postischemic reperfusion and (c) by changes of the regional myocardial wall function in the central- and peripheral ischemic zone. Compared to control, premedication with UK 38.485 led to a reduced energy deficit (-39.1%; p less than 0.01) combined with a significant decrease in the release of potassium (-15.7%; p less than 0.001), inorganic phosphate (-20.2%; p less than 0.002), and lactate (-20.7%; p less than 0.01). Regional myocardial wall function was improved in the central and peripheral ischemic region as demonstrated by a significantly reduced systolic bulging. The protective effects seem to be mainly due to enhanced flow to ischemic areas.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interference with the prostaglandin system as a therapeutical concept to protect the myocardium during ischemic stress: experimental studies with inhibition of thromboxane synthesis. 318 78

In six anesthetized dogs with myocardium partially damaged by ischemia (LAD occlusion), the effect of an i.v. bolus injection of 0.05 mg molsidomine/kg body weight followed by a 6-h i.v. infusion of 0.5 micrograms molsidomine/kg/min on the volume of myocardial ischemia, the relative remaining blood flow in the ischemic area, and the dynamics of the left ventricle were examined by means of computer tomography. The extent of the ischemic volume in the group treated with molsidomine was by far lower than in the control group; this difference was significant if one takes into account the individual heart size. The relative remaining blood flow in the ischemic region was not influenced by molsidomine. The reduction of preload and afterload resulted in corresponding changes in left ventricular areas, segments of these areas, the long axis, thickness of myocardium, ejection fraction and stroke volume. Aortic pressure was lowered insignificantly, heart rate remained nearly unchanged. Plasma analyses of molsidomine. SIN 1 and SIN 1C show that the applied dosage was sufficient to reach a constant concentration over the whole period of observation in the dog.
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PMID:The influence of molsidomine on myocardial ischemia and ventricular dynamics. An in-vivo study in anesthetized dogs by means of computer tomography. 341 34

The value and limitations of stress 201T1 myocardial single photon emission computed tomography (SPECT) for diagnosing ischemic heart disease (IHD) was studied. Using a dual-head rotating gamma camera system, stress SPECT and conventional planar imaging were performed for 138 patients while they were examined by symptom-limited graded bicycle ergometer exercise. All patients underwent selective coronary arteriography and left ventriculography, and 93 had myocardial infarction (MI), 30 had effort angina (EA) and 15 were normal (control). Sensitivities for detecting IHD (SPECT: planar = 96%: 89%, p less than 0.01), individual coronary arterial lesions (left anterior descending artery = LAD, 84%: 68%, p less than 0.005; left circumflex artery = LCX, 60%: 47%, NS; right coronary artery = RCA, 88%: 69%, p less than 0.01), multivessel disease (= LAD + LCX and/or RCA, 53%: 31%, p less than 0.025), and three vessel disease (60%: 13%, p less than 0.005) were significantly higher by SPECT than by planar imaging. In addition, detection of ventricular aneurysms by SPECT was possible with a reasonably high sensitivity (94%) and specificity (84%). Signs of aneurysm included 1) an extensive anterior permanent defect, 2) a large left ventricular cavity, and 3) widening of the angle composed by the septal and lateral walls toward the apex in transaxial images. Sensitivity for detecting IHD was significantly lower in patients without MI (i.e., EA) than in patients with MI (MI: EA = 100%: 83%, p less than 0.005). Sensitivity for detecting individual coronary arterial lesions was lower in the absence than in the presence of MI (LAD; 77%: 87%, LCX; 38%: 68%, RCA; 71%: 90%, respectively), with multivessel disease than with single vessel disease, and with mild than with severe grade of stenosis. Sensitivity for detecting multivessel disease was lower in patients without MI than in those with MI (31%: 61%, respectively), and in anterior MI than in posteroinferior MI, or both MIs (36%: 69%: 100%, respectively). Stress-induced ischemia of infarcted area (anterior MI, 36%; posteroinferior MI, 24%) and ventricular aneurysm (anterior MI, 21%; posteroinferior MI, 0) masked other coronary arterial stenoses in patients with previous MI. We concluded that stress 201T1 myocardial SPECT was a useful non-invasive technique for detecting IHD and individual coronary arterial lesions, multivessel disease (especially posteroinferior MI and anterior + posteroinferior MI), three vessel disease and ventricular aneurysms. However, there were limitations in detecting multivessel disease in patients with anterior MI and EA.
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PMID:[Stress Tl-201 myocardial single photon emission computed tomography in diagnosing ischemic heart disease: its value and limitations]. 350 47

This study examined the relation between left ventricular (LV) function and the severity of acute myocardial ischemia in a conscious dog model. The LV ejection fraction (EF) was measured by multigated equilibrium radionuclide angiography, and regional myocardial blood flow was measured with radioactive microspheres before and 10 minutes after distal and then proximal occlusion of the left anterior descending (LAD, 13 dogs) or left circumflex (LC, 13 dogs) coronary artery. Two methods were used to evaluate the extent of ischemia. The first method determined the mass of myocardium that was ischemic based on different degrees of reduced blood flow. The second method estimated the severity of ischemia expressed as blood flow deficit resulting from each coronary occlusion. Global LV function was very sensitive to ischemia, and the relation between change in function and the degree of ischemia were described best by linear functions. The best linear correlation between mass of ischemic myocardium and percent reduction in EF resulted from the ischemic region defined as all tissue with 25% or greater reduction in blood flow, r = 0.84 for LAD (Y = 0.96X + 1.8) and r = 0.75 for LC (Y = 0.53X + 2.0) occlusions. Defining ischemic mass by more severe reduction in blood flow resulted in exclusion of ischemic myocardium that affected function. The myocardial blood flow deficit also correlated linearly with percent reduction in EF, r = 0.89 for LAD (Y = 1.31X + 2.7) and r = 0.81 for LC (Y = 0.83X - 0.1) occlusions. The slope of the regression lines using both analyses of ischemia were significantly greater (p less than 0.01) for LAD than LC occlusions, indicating that for comparable degrees of ischemia LAD as compared to LC occlusion decreased EF to a greater extent. Calculation of EF from attenuated corrected volumes resulted in small changes in LAD, but not LC, EF and did not account for the disproportionate effects of LAD and LC ischemia. In a separate group of studies (n = 18) EF measured by radionuclide angiography after LAD or LC occlusions correlated well with biplane contrast angiography r = 0.93, SEE 5.1. These data suggest that disproportionately greater effects of LAD compared to LC ischemia on global EF in the dog are due primarily to different pathophysiologic responses to ischemia.
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PMID:Relation between myocardial perfusion and left ventricular function following acute coronary occlusion: disproportionate effects of anterior vs. inferior ischemia. 356 88

Two fatty acid blocking agents, oxfenicine (33 mg/kg) and 4-bromocrotonic acid (0.34 mg/kg/min for 70 min), were used to selectively adjust levels of long-chain acyl CoA and carnitine in aerobic and ischemic myocardium. The purpose of the study was to test whether the shift in these amphiphiles was associated with alterations of mechanical function in intact myocardium. The extracorporeally perfused swine heart preparation was used. Hearts were perfused at aerobic levels for 40 min following which flow to the anterior descending (LAD) circulation was reduced by 50% for the final 30 min of perfusion. All hearts were perfused with excess fatty acids to raise serum levels to 1.37 +/- 0.16 mumol/mol throughout the studies. Oxfenicine and 4-bromocrotonic acid affected a 20% (P less than 0.05 and P less than 0.05, respectively) further decline in 14CO2 production from labelled palmitate as compared with placebo hearts during regional ischemia. Accompanying this were downward shifts in acyl carnitine (-27 delta %, NS in aerobic tissue; -70 delta %, P less than 0.001 in ischemic tissue) and acyl CoA (-13 delta %, NS in aerobic tissue; -33 delta %, P less than 0.01 in ischemic tissue) for oxfenicine and upward shifts of acyl carnitine (+212 delta %, P less than 0.001 in aerobic tissue; -9 delta %, NS in ischemic tissue) and acyl CoA (+78 delta %, P less than 0.001 in aerobic tissue; +29 delta %, P less than 0.025 in ischemic tissue) for 4-bromocrotonic acid. These adjustments in amphiphiles were further associated with improved function (+55 delta % increase in max LV dP/dt, P less than 0.05) in oxfenicine-treated hearts and depressed function (+87 delta % increase in LVEDP, P less than 0.05) in 4-bromocrotonic acid-treated hearts. Thus, at comparable conditions of coronary flow, left ventricular pressure, and fatty acid availability and oxidation between treatments, depletion or build-up of CoA and carnitine esters as affected by selective inhibitors of fatty acid metabolism were causally linked to improved or impaired cardiac performance in intact hearts.
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PMID:Effects of the fatty acid blocking agents, oxfenicine and 4-bromocrotonic acid, on performance in aerobic and ischemic myocardium. 362 84

Decreasing pleural pressure impedes the ejection of blood from the left ventricle (LV), may lead to decreased LV compliance because of interdependence effects and leads to increased transmural LV systolic and diastolic pressure. Previous work from this laboratory has shown that patients with coronary artery disease (CAD) often develop akinetic segments of the LV wall during the Mueller maneuver. In the presence of increased LV transmural pressure regional akinesis could be caused either by the development of regional ischemia or by mechanical inhibition of motion of an area of nonfunctional myocardium as would be caused by previous myocardial infarction (MI). The present study was designed to distinguish between these two mechanisms by determining if the presence of CAD alone is sufficient to lead to regional akinesis or if prior MI is necessary. We used first pass radionuclide ventriculography (RVG) in the 30 degrees LAD supine position to measure LV ejection fraction (EF), end-diastolic (EDV) and end-systolic (ESV) volumes, heart rate and to assess regional wall motion during the Mueller maneuver. This was done in four groups of subjects: 13 normal subjects, 25 patients with CAD but no prior MI, 13 patients with prior nontransmural MI and 36 patients with prior transmural MI. All subjects had angina pectoris and underwent contrast coronary arteriography. Most also underwent routine contrast left ventriculography as well. There were no significant differences among the three patient groups as regards medications, extent and severity of CAD, and response to routine exercise tolerance testing. EF decreased significantly in the three patient groups (4%-9%, p less than 0.01) but not in the normals during the Mueller maneuver. Heart rate increased (5-10 bpm, p less than 0.05) in the normals and in patient groups 2 and 4. EDV decrease in all four subject groups (8%-10%, p less than 0.01), while ESV remained unchanged. Akinesis of the LV wall developed during the Mueller maneuver only in one group-2 patient, but did so in 17/36 patients with prior transmural MI (group 4, p less than 0.001). One-half of the akinetic LV wall segments seen during the Mueller maneuver on RVG were not seen on routine contrast ventriculography. We tested the effects of posture (supine versus upright) on the response to the Mueller maneuver in six normal subjects and found no changes in the response of EDV and ESV to the Mueller maneuver.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Mueller maneuver and LV function in coronary artery disease. 366 48

We studied the feasibility of using the impedance frequency curve method (IFM) to detect the myocardial physical heterogeneity of a cross-circulated isolated canine left ventricle with regional ischemia. The curve changed from a single-peak configuration to a double-peak configuration after the LAD coronary flow cessation and returned to the single-peak configuration with the reperfusion of LAD coronary flow. We concluded that IFM can be a useful tool to describe the physical heterogeneity of the ventricular muscle under the regional ischemia.
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PMID:The instantaneous impedance frequency curve of the ventricle with the regional ischemia. 373 10


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