Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of 15 min periods of coronary occlusion on global and regional myocardial function, plasma creatine kinase (CK) and isoenzyme MB CK activity and subsequent myocardial necrosis were studied in 15 conscious dogs and 9 conscious baboons. Overall left ventricular (LV) function was assessed with measurements of LV systolic and diastolic pressures, rate of change of LV pressure, LV dP/dt. Regional LV function was assessed with measurements of regional segment length and velocity of shortening and/or regional LV wall thickening. An implanted hydraulic occluder on either the left anterior descending or circumflex coronary artery was inflated for 15 min. This induced complete loss of segment length shortening and systolic wall thickening (ultrasonic transit time technique). With release of the occlusion and reperfusion, recovery of regional mechanical function was delayed, but did occur after 6 hrs. Serial plasma enzyme activity revealed a significant increase in total CK as well as MB CK. At autopsy, neither gross pathological evidence (TTC-technique) nor histological evidence of myocyte necrosis was observed. Thus, in the conscious dog as well as in the conscious baboon, short episodes of intense myocardial ischemia do not result in a permanent deficit of myocardial function or necrosis. However, during the early phase of reperfusion, significant depression of regional mechanical function is observed associated with significant appearance of total CK and MB CK in the blood.
 ...
PMID:Effects of brief periods of myocardial ischemia on regional myocardial function and creatine kinase release in conscious dogs and baboons. 375 86

In eight open-chest anesthetized dogs, nitroglycerin (10 micrograms/kg per min) was infused intravenously for 2 h, beginning 10 min following ligation of the left anterior descending coronary artery. Oxygen supply, (radioactive microspheres), extraction (microspectrophotometry) and consumption were determined in subepicardial and subendocardial regions of both ischemic and non-ischemic myocardium, and compared to eight control hearts. In control, coronary occlusion reduced both subepicardial and subendocardial blood flow by 49.5% and 79.5% respectively. In the presence of nitroglycerin, depression of blood flow to the occluded regions was significantly less marked (-79.5% in control and -26.6% in the nitroglycerin group in the subendocardium). O2 extraction was significantly lowered by nitroglycerin in all areas. Regional O2 consumption was significantly lower in the control occluded than non-occluded regions; no regional O2 consumption differences were observed following nitroglycerin. In the occluded regions, nitroglycerin reduced the number of veins with very low O2 saturation. It is concluded that nitroglycerin improves the O2 supply/consumption balance in ischemia by redistribution of blood flow and possibly by alterations in local O2 consumption.
 ...
PMID:Improvement in regional myocardial O2 supply and O2 consumption by nitroglycerin during ischemia. 392 16

The slope of the left ventricular end-systolic pressure-volume relation has been proposed as a sensitive index of left ventricular function since it increases in response to positive inotropic agents and decreases with global depression of contractility. The effect of a segmental depression of left ventricular contractile function produced by circumflex coronary artery occlusion on the left ventricular end-systolic pressure-volume relation was evaluated in seven chronically instrumented dogs. Left ventricular volume was calculated from three ultrasonically measured, orthogonal left ventricular endocardial dimensions. Left ventricular pressure was measured with a micromanometer. The left ventricular end-systolic pressure-volume relation was generated by occlusion of the inferior vena cava, before and after inducing regional ischemia, in the presence of autonomic blockade with propranolol and atropine. The end-systolic data in each dog, before and after coronary occlusion, were fit to the equation, P = E(V - V0), with r greater than or equal to 0.95 in all cases. Coronary occlusion shifted the left ventricular end-systolic pressure-volume relation to the right in each animal. During regional ischemia, the volume intercept (V0) increased from 10.1 +/- 7.8 to 20.4 +/- 9.8 ml (mean +/- SD) (p less than 0.005). The slope (E) of the left ventricular end-systolic pressure-volume relation was relatively unchanged. It is concluded that in intact dogs, regional left ventricular ischemia resulting from coronary occlusion produces a rightward shift of the left ventricular end-systolic pressure-volume relation.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Effect of regional ischemia on the left ventricular end-systolic pressure-volume relation in chronically instrumented dogs. 396 14

The effect of synchronized coronary venous retroperfusion of arterial blood on cardiac function after experimental coronary occlusion was examined by two-dimensional echocardiography. In 18 closed chest anesthetized dogs, the proximal left anterior descending coronary artery was occluded for 6 hours with an intracoronary balloon catheter. Eight of these animals served as untreated controls. Ten were treated with synchronized retroperfusion initiated 30 minutes after occlusion, and treatment was interrupted for 5 minutes at 1 hour after occlusion for study of the rapidity of retroperfusion response. Quantitative echographic analysis yielded global ejection fraction and regional indexes of contraction in a low left ventricular short-axis section, including segmental systolic area change, systolic wall thickening and end-diastolic wall thickness. At 6 hours after occlusion, ejection fraction had decreased from 50.7 +/- 4.9% to 28.1 +/- 7.7% (mean +/- standard deviation) in control dogs, but was significantly (p less than 0.01) less depressed in treated dogs (from 55.9 +/- 5.2 to 41.8 +/- 9.3%). The ischemic zone fractional area change at 30 minutes of occlusion exhibited a marked depression in both groups, after which the dysfunction persisted in the control dogs, but was largely reversed with retroperfusion from 6.0 +/- 6.5 to 35.9 +/- 15.9% at 6 hours of occlusion (p less than 0.01). Brief interruption of retroperfusion 1 hour after occlusion reduced ischemic zone fractional area change from 33.0 +/- 14.9 to 12.2 +/- 9.5% (p less than 0.01). This depression was promptly reversed to 33.6 +/- 12.2% when retroperfusion was resumed. Segmental wall thickening followed a similar trend.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Synchronized coronary venous retroperfusion: prompt improvement of left ventricular function in experimental myocardial ischemia. 397 63

After permanent coronary artery occlusion, the extent of two-dimensional echocardiographically detected dyskinesis correlates well with infarct size. Reperfusion after coronary artery occlusion decreases infarct size; however, contractile function of myocardium salvaged in this way may remain depressed for several weeks. The purpose of this study was to explore the relationship between echocardiographically detected dyskinesis and infarct size in reperfused myocardium. We hypothesized that after transient coronary artery occlusion, the relationship between dyskinesis and infarct size would be altered because of the prolonged depression of contractile function after reperfusion so that dyskinesis would not predict infarct size. We also wanted to explore two related questions: (1) Does inotropic stimulation of reperfused myocardium result in improved systolic function in segments that are dysfunctional but not necrotic? (2) Does the relationship between infarct size and coronary risk region, which is linear in myocardium subjected to permanent coronary occlusion, remain linear in myocardium subjected to a sequence of occlusion and reperfusion? Thirty-seven sedated dogs with preplaced circumflex occluders underwent 1 or 2 hr of coronary artery occlusion, then 2 or 10 days of reperfusion. The percentage of the left ventricle that was dyskinetic was estimated from short-axis two-dimensional echocardiograms at the chordal and papillary muscle level obtained at control, after 1 or 2 hr of occlusion, after 20 min of reperfusion, and after 2 or 10 days of reperfusion. At 2 or 10 days of reperfusion, echocardiograms were also obtained during infusion of dobutamine. Area at risk was determined from postmortem barium-gelatin angiography and infarct size was determined at pathologic examination. We found a significant linear correlation between infarct size and risk region size in reperfused myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Echocardiographically detected dyskinesis, myocardial infarct size, and coronary risk region relationships in reperfused canine myocardium. 399 17

Prior studies have shown that tachycardia results in ST segment depression in dogs with chronic, gradual coronary occlusion. This response was compared with that produced by acute, total occlusion of the left anterior descending artery. Ten dogs served as controls; in another 10 dogs, an ameroid constrictor was implanted about the left anterior descending artery. This artery was acutely ligated in a third set of 10 animals, and in a final set of 10, the distal left anterior descending coronary vasculature was embolized by latex injection. Tachycardia was produced by atrial pacing from rates of 90 to 250 beats/min using implanted atrial electrodes. Electrocardiographic signals registered from 84 torso electrodes were used to construct body surface isopotential maps during the ST segment. In normal dogs, pacing increased repolarization potentials without shifts in spatial features. New and abnormal anterior negativity, correlating with significant ST depression, appeared at rates of 170 beats/min or faster in dogs with ameroid constriction. However, in both groups with acute occlusion that produced transmural myocardial infarction, tachycardia resulted in increases in anterior ST elevation and reciprocal ST depression. Specific findings demonstrated the lead dependency of the response to tachycardia and the greater than normal increase in potential magnitudes after infarction than in control cases. The similarity of the response with acute occlusion and with embolization suggested that the response to tachycardia after infarction was not dependent on coronary collateral function but may represent a direct electrophysiologic effect of rate. Thus, these acute occlusion models simulate exercise-induced ST segment elevation as it may be seen clinically.
 ...
PMID:Effects of experimental myocardial infarction on the ST segment response to tachycardia. 403 Dec 79

Myocardial contrast echocardiography can define in vivo the area at risk for necrosis after coronary occlusion. However, if this technique is to be used, it cannot be intrinsically toxic to the heart or other critical organs. To determine the functional and pathologic effects of contrast echocardiography, six intracoronary, six intrarenal and six intracarotid artery injections of 2 to 6 cc of a commonly employed contrast agent (agitated Renografin-saline solution) were performed in five dogs. A sixth dog served as a sham to assess any deleterious effects of the model preparation. Two-dimensional echocardiographic images and electrocardiograms were recorded during intracoronary injections, and heart rate, blood pressure, left ventricular end-diastolic pressure and rate of rise of left ventricular pressure (dP/dt) were continuously monitored. At 24 hours, echocardiographic and hemodynamic measurements were repeated, the dogs were killed and the heart, brain and kidneys were removed and prepared for light microscopic examination. Quantitative analysis of left ventricular wall motion was performed on control, peak contrast, post-contrast and 24 hour studies. With each intracoronary injection, there were transient decreases in blood pressure (p = 0.05 versus control) and increases in left ventricular end-diastolic pressure (p = 0.04 versus control). These were associated with depression of wall motion in contrast-enhanced regions (p = 0.01 versus control) and ST-T segment changes on the electrocardiogram. No significant change in heart rate or left ventricular dP/dt was noted. All variables normalized with the clearance of the contrast effect and remained normal to 24 hours. Light microscopic examination revealed no myocardial or cerebral changes attributable to the contrast agent injections.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Functional and pathologic effects of multiple echocardiographic contrast injections on the myocardium, brain and kidney. 403 Dec 82

The topographical and physiopathological aspects of the danger of extension of infarction of the myocardium are defined with the aid of data collected by electrocardiogram and coronarography in 50 patients. The danger of extension in situ, observed in 64% of the cases, is the most frequent and complicates particularly the progression of anterior infarcts. In fact, it is located in the same area as the initial infarct in 91% of the cases for anterior infarcts and in 40% of the cases for inferior infarcts. It is expressed by an elevation of the ST segment in 84% of the cases and corresponds to a monotruncular attack in 63% of the cases. The downstream bed of the vessel destined for the infarcted area and threatened secondarily remains permeable in the anterograde sense. Apart from infarcts, the danger of extension is less frequent, found in 36% of the cases, and complicates preferentially the progression of inferior infarcts. It finds expression in a depression of the ST segment in 77% of the cases and the coronary attack is always pluritruncular. The mortality in one month is 35% of 17 patients treated medically and 3% of 33 patients who have been equipped with a shunt or angioplasty. In situ the danger of extension denotes the presence of cellular islets, which are still healthy, in the region of an infarcted myocardial zone, the viability of which may be threatened secondarily by a phenomenon of coronary occlusion, which is intermittent and repeated. Except for an infarct, the danger of extension implies the diffusion of an atheromatous effect. The good results of surgical treatment or dilatation argues in favour of an early coronarographic exploration.
 ...
PMID:[Topographic aspects of threatened extension of transmural myocardial infarction. Electrocardiographic and coronarographic data]. 408 71

The effects of both intracoronary and intravenous administration of nitroglycerin on transmural distribution of blood flow in the left ventricle after partial coronary artery occlusion was investigated using two independent methods. In 16 open chest, anesthetized dogs, tubing supplying the cannulated left coronary artery was partially occluded. Strain gauges sutured paralled to superficial and deep fibers of the myocardium separately recorded the contractile force of each layer. With occlusion set so that depression of the deep contractile force was imminent. 12 mug intracoronary nitroglycerin in seven dogs depressed only the deep contractile force without changing systemic hemodynamics. Intravenous administration of 180 mug nitroglycerin in nine dogs resulted in a decrease of deep contractile force and aortic pressure often associated with an increase in superficial contractile force. Distribution of myocardial blood flow during peak coronary flow after intracoronary administration of nitroglycerin or during a decrease in aortic pressure after intravenous nitroglycerin administration was determined by the tissue uptake of an intracoronary bolus of rubidium-(80). This was compared with the uptake of potassium-(42) injected before nitroglycerin. Intravenous or intracoronary administration of nitroglycerin caused a significant reduction in subendocardial blood flow with a decrease in the subendocardial/subepicardial ratio of isotope. These experiments suggest that under conditions of acute partial coronary occlusion, the autoregulatory response results in more fully dilated subendocardial vessels causing them to be less responsive to nitroglycerin. Nitroglycerin may then reduce the vascular resistance in the subepicardial more than the subendocardial vessels, resulting in a "steal" of blood flow from deep to superficial myocardium.
 ...
PMID:Nitroglycerin and heterogeneity of myocardial blood flow. Reduced subendocardial blood flow and ventricular contractile force. 463 92

The influence of the administration of pharmacologic doses of hydrocortisone on the extent and severity of acute myocardial ischemic injury and on subsequent necrosis after acute coronary occlusion was investigated in 28 dogs. In order to study acute myocardial injury, repeated epicardial electrocardiograms were recorded from 10 to 15 sites on the anterior surface of the left ventricle. Average ST segment elevation (ST) and the number of sites in which ST segment elevation exceeded 2 mV (NST), indices of the magnitude and extent of myocardial injury, respectively, were analyzed at 30 and 60 min after coronary occlusion. In the control group ST and NST did not change significantly in this time interval while in the treated group, which received 50 mg/kg hydrocortisone just after the 30 min recording, ST fell from 3.5+/-0.8 to 1.1+/-0.4 mV (P<0.01) and NST was reduced from 6.7+/-1.1 to 1.4+/-0.8 (P<0.01). In order to study the influence of hydrocortisone on necrosis, epicardial ST segment elevation 15 min after coronary occlusion was compared to myocardial creatine phosphokinase activity (CPK) and histologic appearance 24 h later in each site. In a control group (14 dogs) a relationship was established between ST segment elevation at 15 min (in millivolts) and CPK activity (in international units per milligram of protein) 24 h later: log CPK = -0.0611ST + 1.26 (N = 102 specimens, r = -0.79). In the treated groups, hydrocortisone (50 mg/kg i.v.) was given either at 30 min after occlusion (seven dogs) or at 6 h after occlusion (six dogs). Both groups received supplementary doses of hydrocortisone (25 mg/kg) 12 h after occlusion. The two treated groups exhibited less CPK depression than that expected from ST segment elevation at each site, with slopes of the regression lines which were significantly less steep: log CPK = -0.0288ST + 1.26 (N = 48, r = -0.71) and log CPK = -0.0321ST + 1.31 (N = 48, r = -0.76) in the (1/2) h and 6 h groups, respectively. Histologically, sites with ST segment elevations of less than 2 mV at 15 min after occlusion exhibited normal appearance 24 h later. Sites with ST segment elevations (> 2 mV) in the control group showed histologic changes compatible with early myocardial infarction in 96% of specimens, while this occurred only in 61% and 63% of specimens, respectively, in the treated groups, showing that over one third of the sites were protected from undergoing necrosis due to the intervening hydrocortisone treatment. Thus pharmacological doses of hydrocortisone prevent myocardial cells from progressing to ischemic necrosis even when administration is initiated 6 h after coronary occlusion.
 ...
PMID:Reduction of experimental myocardial infarct size by corticosteroid administration. 468 84


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>