Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The protective effect of (+/-)-(R*)-2,6-dimethyl-4-(m-nitrophenyl)-1, 4-dihydropyridine-3,5-dicarboxylic acid (R*)-1-benzyl-3-piperidinyl ester, methyl ester hydrochloride (benidipine hydrochloride, KW-3049) on ischemic myocardium was examined comparing with that of nifedipine in anesthetized dogs subjected to a brief (10 min) coronary artery occlusion and reperfusion (2h). Occlusion of left anterior descending coronary artery elicited elevation of ST-segment and T-wave of epicardial ECG in the ischemic area. Regional myocardial contractile force in this area was depressed throughout the reperfusion period as well as during coronary occlusion period. LV max dp/dt, stroke volume and cardiac output tended to be reduced. In the dogs pretreated with 10 micrograms/kg of KW-3049 (i.v.) and 50 micrograms/kg of nifedipine (i.v.), both of which lowered the blood pressure to the same extent, elevation of ST-segment and T-wave was inhibited, and the prevention of irreversible depression of regional myocardial contraction observed at reperfusion periods was slightly more prominent in KW-3049 administration group. Stroke volume and cardiac output in both KW-3049 and nifedipine administration groups were maintained at higher levels than those in control group throughout coronary occlusion and the following reperfusion periods. LV max dp/dt of KW-3049 administration group was kept higher than that of the control group, while the value of the nifedipine administration group changed as that of the control group. These results demonstrate that KW-3049 as well as nifedipine exert protective effects on ischemic myocardium induced by coronary occlusion and reperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Beneficial effects of the new calcium antagonist benidipine hydrochloride on myocardial dysfunction following coronary occlusion and reperfusion in anesthetized dogs. 321 47

Regardless of the factor assumed responsible for precipitation of myocardial ischemia - varying from coronary occlusion in acute myocardial infarction to increased oxygen demand in exertional angina pectoris and reduced myocardial oxygen supply due to plaque rupture or changes in vasomotor tone in unstable angina - its incurrence may or may not be associated with pain. In the vast majority of cases, silent myocardial ischemia is observed in patients with established symptomatic coronary artery disease. Interindividual comparisons have not enabled reliable differentiation between those with painful and those with silent ischemia based on the anatomic extent of coronary artery disease, left ventricular function or previous myocardial infarction. Similarly, functional parameters such as exercise capacity, exercise duration, time to onset of ST-segment depression during exercise as well as heart rate and blood pressure both at rest and during exercise have failed to reveal differences between the symptomatic and the asymptomatic patients. Intraindividual differences have also been noted, but not consistently corroborated, and postulated as responsible for the fact that ischemia in a given patient alternates in its presence with and without pain. Since most patients with silent ischemia either have, or at some time in the past have experienced, painful ischemia, the integrity of the appropriate nervous system function can be assumed to be intact and neurocardiologic factors seem most likely to account for apparent discrepancies in pain perception. Prior to precipitation of pain, myocardial ischemia must elicit an adequate stimulus. According to some investigators, the adequate stimulus is that associated with a duration of the ischemic episode of at least three minutes and with increase in left ventricular filling pressure of more than 7 mm Hg. This threshold, consequently, represents a prerequisite but not invariably sufficient criteria for the occurrence of pain. The next step in the sequence of pain is generation of an action potential, that is, transduction by means of chemical or mechanical stimuli. During this process, a latency of 20 to 40 seconds is incurred such that the appearance of pain usually has its onset after derangement of relaxation and contraction, increased filling pressure and the observation of ECG changes. Through conduction, the information is forwarded to the central nervous system after coding of the details with regard to intensity. The intensity, in turn, is determined by the number of receptors (free nerve endings) in the field activated by the ischemic event.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Pathophysiology of painful and silent myocardial ischemia]. 332 3

A patient had repetitive ventricular fibrillation preceded by alternating ST segment depression and elevation. The ECG changes were confined to the precordial leads only, reflecting subendocardial and transmural ischemia, respectively. It is speculated that the patient exhibited consecutive episodes of subtotal and total coronary occlusion, both episodes being critical enough to induce lethal arrhythmias.
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PMID:Repetitive ventricular fibrillation preceded by both ST segment depression and elevation during acute myocardial ischemia. 278 22

Sympathetic innervation of the normal and acutely ischemic myocardium and the effects of regional myocardial sympathetic denervation of the ischemic area on the evolving electrical changes during coronary occlusion were assessed in pigs anesthetized with pentobarbital sodium. The histofluorescence of the adrenergic nerve fibers (glyoxylic acid reaction), which in the normal myocardium were distributed in a diffuse network, decreased slightly after 45 min of occlusion of the left anterior descending (LAD) coronary artery and nearly disappeared after 2 h of ischemia. Topical application of phenol (carbolic acid, 88%) to the coronary arterial wall produced a transmural loss of catecholamine histofluorescence in the distal myocardium supplied by the phenol-treated arterial segment. Mapping of the epicardial direct current (DC) electrograms in sympathetically denervated and in nondenervated sections of the same ischemic area, using three rows of seven cotton-wick electrodes, was performed in eight pigs and validated in eight other nondenervated pigs. During 45 min of LAD occlusion, the denervated area, with respect to the nondenervated region, showed a greater decline in T-Q segment depression after 20 min of ischemia (P less than 0.0001), a lesser degree of S-T segment elevation throughout the study (P less than 0.0001), a delayed development of monophasic potentials (P less than 0.05), a minor degree of S-T segment alternans (P less than 0.0001), and a less marked, but still present, period of transient electrical recovery. Thus acute regional myocardial sympathectomy reduces the magnitude of the local electrical manifestations of acute myocardial ischemia in the in situ pig heart. Also in this model, sympathetic fibers appeared to lose the catecholamine histofluorescence after 2 h of acute ischemia.
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PMID:Effects of regional denervation on epicardial DC electrograms during coronary occlusion in pigs. 360 60

To determine whether the admission electrocardiogram can identify left circumflex or right coronary artery occlusion as the cause of an inferior acute myocardial infarction (AMI), findings from electrocardiography and coronary angiography performed within 12 hours of each other were retrospectively assessed in 41 consecutive patients with inferior AMI. All patients had ST-segment elevation in 1 or more inferior leads (II, III or aVF). Of the 12 patients with circumflex coronary artery occlusion, 10 (83%) had ST-segment elevation in 1 or more lateral leads (aVL, V5 or V6) without ST-segment depression in lead I. Similar electrocardiographic findings were noted in only 1 of 29 patients (4%) with right coronary occlusion (p less than 0.001). ST-segment depression in precordial leads V1-V3 was equally prevalent in both groups. Thus, the presence of both ST-segment elevation in 2 or more inferior leads and ST-segment elevation in 1 or more lateral leads with an isoelectric or elevated ST segment in lead I identified circumflex coronary occlusion with a sensitivity of 83%, specificity of 96%, positive predictive accuracy of 91% and negative predictive accuracy of 93%. When these criteria were prospectively applied to an additional cohort of 19 consecutive patients with inferior AMI (5 with left circumflex and 14 with right coronary artery occlusion), presence of left circumflex coronary artery occlusion was predicted with a sensitivity of 80%, specificity of 93%, positive predictive accuracy of 100% and negative predictive accuracy of 93%. Thus, the admission 12-lead electrocardiogram can assist in differentiating left circumflex from right coronary artery occlusion in patients with inferior AMI.
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PMID:Electrocardiographic differentiation of occlusion of the left circumflex versus the right coronary artery as a cause of inferior acute myocardial infarction. 363 Sep 27

Proton NMR methods can monitor mobile lipids (e.g., fatty acids and glycerides) in intact tissue. Lipids play a major role in cardiac energy production, and elevated levels of myocardial lipids have been reported following an ischemic insult. The present study examines the potential of high-resolution 1H NMR spectroscopy to monitor lipid alterations 24 h following coronary occlusion in dogs, and to correlate these finds with regional myocardial blood flow (RMBF) measured by radiolabeled microspheres. The dogs were killed, and samples of excised myocardium were studied by high-resolution 1H NMR spectroscopic analysis using solvent suppression in combination with the Hahn spin-echo pulse sequence. Mobile lipids levels in myocardium with moderate blood flow reduction (28.6 +/- 7, integral values, arbitrary units; flow 5-50% of control) were significantly elevated compared to the mobile lipid levels in control myocardium (5.3 +/- 8, P less than 0.001) and in myocardium with severe flow reduction (7.2 +/- 10, P less than 0.001; flow less than 5% of control). The mobile lipids in myocardium with severe flow reduction were not elevated significantly relative to control tissue. As anticipated, depression in the level of creatine paralleled the microsphere determined degree of ischemia, i.e., compared to control (9.0 +/- 3); creatine levels were moderately decreased with flows 5-50% of control (5.5 +/- 4, P less than 0.001) and markedly decreased with flows less than 5% of control (1.0 +/- 2, P less than 0.001). This study suggests that high-resolution 1H NMR spectroscopy may be used to evaluate alterations in myocardial lipid levels following an ischemic insult.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Proton NMR spectroscopy in myocardial ischemic insult. 365 93

Transient coronary occlusion (15 minutes) does not result in irreversible myocardial injury but is associated with a depression of contractile function sustained for several hours to days ("stunned myocardium"). The defect in the contractile process responsible for this phenomenon has been suggested to be causally related to a reduced energetic state, altered excitation or excitation-contraction coupling, or damaged contractile filaments. The purpose of this study was to attempt to exclude one or more of these hypotheses by evaluating the contractile reserve of reperfused myocardium. Regional subendocardial segment function was measured (sonomicrometry) in a control region and in an area (treatment region) perfused by a carotid artery to anterior descending coronary artery bypass in 13 chloralose-anesthetized dogs. Dose-response curves were constructed from changes in segment shortening (%SS) in response to intracoronary calcium infusion before ischemia and following 5 or 15 minutes of occlusion and reperfusion (30 minutes). Calcium infusion before ischemia resulted in dose-dependent increases in %SS in the treatment area to a maximum value of 36.6% from a preinfusion value of 25.5% (p less than 0.01), in the absence of changes in control region shortening (23.7%). After 15 minutes of occlusion and reperfusion, treatment area %SS had fallen to a depressed but stable level (46% of preischemic values; p less than 0.01). Subsequent calcium infusion at the same doses as in the preischemic trial produced increases in treatment segment function with return of shortening to control levels at an intermediate dose. At the highest dose, %SS was 35.4%, which was not different from the maximal value found in the preischemic trial. Alterations in heart rate and left ventricular systolic and diastolic pressures during calcium infusion were minor and similar before and after ischemia. Calcium-induced increases in regional segment shortening above control levels (113% of control) in reperfused myocardium were sustained with continuous infusion (30 minutes) without deleterious effects on subsequent function. These results demonstrate that stunned myocardium in this model retains a normal contractile reserve in response to calcium, suggesting that the mechanism responsible for postischemic contractile dysfunction involves calcium.
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PMID:Reversibly injured, postischemic canine myocardium retains normal contractile reserve. 367 40

To determine the contribution of transsarcolemmal calcium flux to abnormal diastolic function produced by brief periods of flow-limiting ischemia and reperfusion, we evaluated early and late diastolic function during transient coronary occlusion and reperfusion before and during administration of intravenous nifedipine (NIF) (10 +/- 1 microgram/kg/min) in nine preinstrumented conscious dogs. We also assessed the effects of nitroprusside (NTP) (2 +/- 0.2 micrograms/kg/min) during an identical period of ischemia and reperfusion to independently assess the consequences of altered loading alone on diastolic function. To minimize the effects of temporal dysynchrony and altered ventricular loading conditions on isovolumetric relaxation, we developed a conscious dog preparation of reversible transient (30 to 60 sec) bilateral coronary occlusion (BCO). BCO was characterized by significant systolic depression: maximum (+)dP/dt decreased (from 2617 +/- 600 to 1981 +/- 565 mm Hg/sec, p less than .05), left ventricular transverse dimension shortening diminished (from 20 +/- 5 to 9 +/- 5%, p less than .05), and the left ventricle dilated (42.4 +/- 6.4 to 43.8 +/- 6.3 mm, p less than .05). Concomitantly the time constants of isovolumetric relaxation prolonged (from 22 +/- 3 to 28 +/- 4 msec, p less than .05) and minimal diastolic left ventricular pressure increased (from -3 +/- 6 to 6 +/-6 mm Hg, p less than .05). The passive diastolic pressure-dimension relationship shifted upward and to the right and was associated with increased chamber stiffness (from 0.50 +/- 0.26 to 1.03 +/- 0.53 mm Hg/mm, p less than .05) and increased left ventricular end-diastolic pressure (from 7 +/- 7 to 19 +/- 7 mm Hg, p less than .05). Reperfusion immediately after BCO was characterized by prompt restoration of systolic contractile performance [maximum (+)dP/dt 3220 +/- 530 mm Hg/sec] but persistently abnormal early and late diastolic function (time constant of isovolumetric relaxation 30 +/- 6 msec, left ventricular end-diastolic pressure 20 +/- 7 mm Hg). The effects of drug administration on ventricular function during BCO were then evaluated under matched loading conditions. NTP improved time constant of isovolumetric relaxation (20 +/- 8 vs 28 +/- 4 msec, p less than .05) and minimal diastolic left ventricular pressure (2 +/- 5 vs 6 +/- mm Hg, p less than .05) during BCO, but NIF did not (time constant of isovolumetric relaxation 27 +/- 6 msec, minimal diastolic left ventricular pressure 7 +/- 5 mm Hg).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of nifedipine on diastolic function during brief periods of flow-limiting ischemia in the conscious dog. 367 62

Left ventricular function and systemic regional blood flow (radioactive microspheres, 15 +/- 5 mu) were studied 1, 3, 10 or 42 days after left coronary occlusion in conscious rats. One day after coronary occlusion, vascular resistance in the skeletal muscle and cutaneous beds increased while stroke work and left ventricular systolic pressure were depressed. Regional blood flow and hemodynamic data were similar for sham and infarction groups at 3 and 10 days after surgery, except for left ventricular end-diastolic pressure, which was significantly increased in rats with infarction (sham versus infarct: 11.5 +/- 1.0 versus 18.4 +/- 3.2 at day 3 and 12.2 +/- 1.4 versus 19.9 +/- 3.2 at day 10) (p less than 0.05). At 42 days after myocardial infarction, manifest heart failure occurred as documented by decreased cardiac output and left ventricular systolic pressure and elevated left ventricular end-diastolic pressure and vascular resistance in the cutaneous, skeletal muscle and renal beds. In a separate group of animals with moderate (33.2 +/- 2% of left ventricle) and large infarctions (45 +/- 1.3% of left ventricle), regional blood flow was compared with the sham group. Rats with a large infarct demonstrated significant (p less than 0.05) reduction in flow to kidney, gut and liver. In rats with a medium sized infarct, only renal blood flow was significantly reduced. It is concluded that in this model of myocardial infarction, early cardiocirculatory depression is followed by a partially compensated state with increased left ventricular end-diastolic pressure and subsequent systemic and regional vasoconstriction which, in turn, may contribute to late deterioration of heart failure.
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PMID:Regional vascular adjustments during recovery from myocardial infarction in rats. 371 8

By measuring ECG ST segment deviation and regional mechanical dysfunction, we assessed the effects of an alteration in afterload pressure on regional myocardial ischemia due to a partial coronary occlusion of the left circumflex coronary artery (CFX). Eight isolated, perfused and paced dog hearts were loaded with an artificial arterial system which simulated the aortic input impedance of the dog arterial tree. Afterload pressure was altered by stepwise changes in peripheral resistance (Rp), while left ventricular end-diastolic pressure (LVEDP) and heart rate were kept constant. Coronary perfusion pressure (CPP) was kept equal to mean aortic pressure (AoP). ECG and myocardial systolic segment shortening (SS) were measured in both areas perfused by the CFX and the left anterior descending coronary artery (LAD). In the presence of CFX stenosis, mean AoP decreased from 96 +/- 7 to 46 +/- 7 mmHg following a decrease in Rp and cardiac output increased progressively from 465 +/- 30 to 1055 +/- 100 ml/min. In this situation, CFX coronary blood flow decreased from 75 +/- 2 to 28 +/- 6 ml/100 g/min. Epicardial ECG in the ischemic region showed two types of ST segment deviation after CFX stenosis: ST segment elevation and ST segment depression. Moreover, following afterload reduction, these individual ECG ST segment changes showed further deviations. The levels of mean AoP, below which further ST segment deviations significantly occurred, were as follows: 71 +/- 6 mmHg in ST segment elevation cases and 52 +/- 7 mmHg in ST segment depression cases. Myocardial systolic segment shortening in the ischemic region also significantly decreased following CFX stenosis (91 +/- 8% of pre-ischemic control, p less than 0.05). Then, during afterload reduction, SS in the CFX area appeared to be bimodal and it definitely decreased when mean AoP was 46 +/- 7 mmHg. To enhance the sensitivity of detection of further mechanical dysfunction throughout afterload reduction following regional myocardial ischemia, we calculated percentage values of the SS in the CFX area to the SS in the LAD area at each Rp. By this normalization, mechanical dysfunction was found when mean AoP was below 67 +/- 5 mmHg. These results suggest that reduction in afterload pressure below a certain level aggravated the regional ischemia, despite an increase in cardiac output, and to detect this change in the ischemic region during afterload reduction, ECG ST segment deviation seems to be a useful indicator.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The changes in ECG ST segment and mechanical function of regional ischemic myocardium during afterload reduction in isolated dog hearts with coronary stenosis. 373 58


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