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

Previous studies have shown a close temporal relationship between lipid abnormalities and membrane dysfunction in ischemia and that phospholipase-inhibiting drugs limit such derangements. Amiodarone is a potent phospholipase inhibitor, but its potential or that of any other inhibitor to simultaneously attenuate lipid abnormalities and electrophysiological changes in the very early phase of ischemia has never been studied. We therefore investigated simultaneously such changes in early ischemia. In isolated porcine hearts perfused with or without pure amiodarone solutions, electrophysiologic changes before and during 20 min of LAD occlusion were recorded using unipolar electrodes and Franz contact electrode catheters, and full thickness myocardial biopsies obtained for lipid analyses. In untreated hearts (n = 5), occlusion of LAD resulted in the rapid onset of TQ depression/ST elevation within 1 min and plateauing at 10 min. There were mean increases of 33% and 50% in lysophosphatidylcholine and 33% and 70% in lysophosphatidylethanolamine levels at 5-7 min and 20 min of ischemia, respectively. Non-esterified fatty acid (NEFA) content did not change significantly during the first 5-7 min, but increased by 75% after 20 min of LAD occlusion. In treated hearts (n = 5) there was a 37% increase in sinus cycle length after amiodarone administration (503 +/- 85 vs 689 +/- 115 ms, P < 0.01) but no significant change in ventricular effective refractory period (202 +/- 22 vs 204 +/- 21 ms), action potential duration (215 +/- 11 vs 217 +/- 7 ms), or amplitude (31 +/- 6 vs 28 +/- 3 mV) was observed. Also, amiodarone treatment did not alter total phospholipid content, lysophospholipids and NEFA levels of non-ischemic hearts. However, there was significant attenuation (P < 0.01) of the onset of the TQ/ST shift and preservation of action potential amplitude (P < 0.02) during the first 5-7 min of LAD occlusion with concomitant suppression of the increase in both lysophospholipids (hydrolysis products of membrane phospholipids by endogenous phospholipases) and NEFA levels observed after 5-7 and 20 min of ischemia. The results suggest that amiodarone can delay the onset and limit the extent of electrophysiologic change in early myocardial ischemia in temporal association with suppression of myocardial phospholipase activities.
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PMID:Phospholipase inhibition and the electrophysiology of acute ischemia: studies with amiodarone. 828 71

Although calcium channel blockers may preserve function in ischemic myocardium, they may also produce myocardial depression and dysfunction in the presence of decreased coronary flow. This study was designed to examine the issue of possible protection afforded by diltiazem against ischemia-induced myocardial dysfunction during propofol anesthesia. In eight anesthetized and ventilated dogs, regional myocardial (ultrasonic crystals in both left anterior descending [LAD] and left circumflex [LC] perfusion areas) and global ventricular function were evaluated during progressively severe degrees of myocardial ischemia (LAD constriction) before and after intravenous diltiazem (150 micrograms/kg). As coronary flow decreased, heart rate increased, and arterial and coronary perfusion pressures, left ventricular dP/dt, and cardiac output decreased. Systemic vascular resistance was unaffected. Diltiazem without coronary constriction increased heart rate, and decreased diastolic arterial pressures, left ventricular (LV) end-diastolic, coronary perfusion pressures, LV dP/dt max, LAD coronary blood flow, stroke volume, and cardiac output. At all levels of coronary constriction following diltiazem, there were decreases in systolic and diastolic arterial pressures, stroke volume, cardiac output, LV dP/dt, and coronary perfusion pressure. Heart rate increased at critical coronary constriction, and then remained constant relative to the prediltiazem state. The regional muscle effects of the reductions in coronary flow in the LAD perfusion territory included decreased systolic shortening and increased postsystolic shortening before and after diltiazem. Diltiazem did not alter the magnitude of the alterations in systolic or postsystolic shortening brought about by coronary constriction. No changes occurred in the LC area.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Diltiazem and regional left ventricular function during graded coronary constriction and propofol anesthesia in the dog. 830 61

The influence of intracoronary enoximone at a dose of 0.075 mg/ kg/10 min on global and regional wall motion and myocardial perfusion (Group I, n = 10) as well as on diastolic LV function (Group II, n = 8) during pacing-induced ischemia was investigated in 18 patients with significant LAD stenoses. The hemodynamic parameters were determined by left heart catheterization, the systolic and diastolic left ventricular function by echocardiography including Doppler technique, and myocardial perfusion analysis was done after intracoronary application of contrast medium. Enoximone did not change either heart rate (79 +/- 9 vs 80 +/- 9 min-1) or blood pressure (LVSP: 159 +/- 7 vs 162 +/- 5 mm Hg) at rest. In the postpacing ischemic period after enoximone, LVEDP fell from a mean of 28.9 to 18.4 mm Hg (p < 0.001), dp/dtmax increased from 1050 to 1369 mm Hg/s (p < 0.001) and regional EF from 47% to 58% (p < 0.01), while global EF remained unchanged (45% vs 47%). ST-segment depression was reduced significantly from 2.3 to 1.5 mm (p < 0.01). Enoximone induced an increase in myocardial perfusion by 129% (p < 0.001) in the stenosis-dependent myocardial areas with shortening of the wash-out half-life time of the echo contrast medium from a mean of 14 s to 5 s (p < 0.001). The isovolumetric relaxation was shortened by 13% (p < 0.05), the E wave by 5%, and dp/dtmin increased by 17% (p < 0.01). In summary, intracoronary application of enoximone led to an improvement in both systolic and diastolic LV function without concomitant peripheral effect due to regression of myocardial ischemia.
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PMID:[Acute effects of enoximone after intracoronary administration on hemodynamics, myocardial perfusion and regional wall motion]. 906 48

In this prospective study, we examined the diagnostic accuracy of exercise-induced left QRS axis deviation as a marker of LAD coronary artery stenosis. The mean frontal QRS axis of 66 consecutive patients with chest pain and exercise-induced ST segment depression referred for diagnostic coronary angiography was analyzed and related to the angiographic findings. An exercise-induced leftward QRS axis deviation was found in 9/40 patients with and 0/26 patients without obstructive (> or = 70%) LAD disease (sensitivity 23%, specificity 100%, p = 0.025). In 7 of the 9 patients with left axis deviation, the lesion was proximal to and in 2 in the region of the first septal perforator. Inclusion of patients with 0 degrees exercise-induced QRS axis deviation provided a more sensitive but less specific marker of LAD disease [sensitivity 53% (21/40), specificity 81% (21/26), p = 0.015]. The findings were similar in patients with single and with multivessel coronary artery disease. Grouping all patients in the present prospective and two previous retrospective studies (n = 165), the sensitivity was 29% and specificity 100% (p < 0.0001). Exercise-induced left QRS axis deviation was a highly specific marker of LAD coronary artery stenosis.
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PMID:Accuracy of exercise-induced left axis QRS deviation as a specific marker of left anterior descending coronary artery disease. 964 78

Patients with penetrating cardiac injury usually present with cardiac tamponade and shock upon hospital arrival. However, absence of hemodynamic depression does not exclude a potentially fatal injury of the heart. This article reports on a patient who developed neither hemodynamic depression nor ECG changes for several hours, despite two left ventricular lacerations with puncture of the LAD. Echocardiography is advocated as the diagnostic tool of choice, and it is emphasized that no penetrating objects should be removed from the wound before surgical access to the heart is established, as this may result in the sudden development of cardiac tamponade.
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PMID:Absence of hemodynamic and ECG changes in a patient with traumatic left ventricular injury and puncture of the left anterior descending branch. 1114 9

The efficacy of Withania somnifera (Ws) to limit myocardial injury after ischemia and reperfusion was explored and compared to that of Vit E, a reference standard known to reduce mortality and infarct size due to myocardial infarction. Wistar rats (150-200 g) were divided into six groups and received orally saline (sham, control group), Ws-50/kg (Ws control and treated group) and Vit E-100 mg/kg (Vit E control and treated group) respectively for 1 month. On the 31st day, rats of the control, Vit E and Ws treated groups were anesthetized and subjected to 45 min occlusion of the LAD coronary artery followed by 60 min reperfusion. Hemodynamic parameters: systolic, diastolic and mean arterial pressure (SAP, DAP, MAP), heart rate (HR), left ventricular end diastolic pressure (LVEDP), left ventricular peak (+)LVdP/dt and (-)LVdP/dt were monitored. Hearts were removed and processed for histopathological and biochemical studies: Myocardial enzyme viz, creatin phosphokinase (CPK), and antioxidant parameters: malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSHPx) were estimated. Postischemic reperfusion produced significant cardiac necrosis, depression of left ventricular functions (MAP, LVEDP, (+) and (-)LVdP/dt) and a significant fall in GSH (p < 0.01), SOD, CAT (p < 0.05), LDH and CPK (p < 0.01) as well as an increase in MDA level (p < 0.05) in the control group rats as compared to sham group. The changes in levels of protein and GPx was however, not significant. Ws and Vit E favorably modulated most of the hemodynamic, biochemical and histopathological parameters though no significant restoration in GSH, MAP (with Vit E) were observed. Ws on chronic administration markedly augmented antioxidants (GSH, GSHPx, SOD, CAT) while Vit E did not stimulate the synthesis of endogenous antioxidants compared to sham. Results indicate that Ws significantly reduced myocardial injury and emphasize the beneficial action of Ws as a cardioprotective agent.
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PMID:Cardioprotection from ischemia and reperfusion injury by Withania somnifera: a hemodynamic, biochemical and histopathological assessment. 1522 84

The present study was undertaken to evaluate the cardioprotective potential of Curcuma longa (Turmeric) in the ischemia-reperfusion (I/R) model of myocardial infarction (MI). Wistar rats were divided into three groups and received saline orally (sham, control I/R group) and Curcuma longa 100 mg/kg (CL-100 treated group) respectively for one month. On the 31st day, rats of the control I/R and Cl treated groups were subjected to 45 min of occlusion of the LAD coronary artery and were thereafter reperfused for 1 h. I/R resulted in significant cardiac necrosis, depression in left ventricular function, decline in antioxidant status and elevation in lipid perodixation in the control I/R group as compared to sham control. Myocardial infarction produced after I/R was significantly reduced in the Cl treated group. Cl treatment resulted in restoration of the myocardial antioxidant status and altered hemodynamic parameters as compared to control I/R. Furthermore, I/R-induced lipid peroxidation was significantly inhibited by Cl treatment. The beneficial cardioprotective effects also translated into the functional recovery of the heart. Cardioprotective effect of Cl likely results from the suppression of oxidative stress and correlates with the improved ventricular function. Histopathological examination further confirmed the protective effects of Cl on the heart.
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PMID:Protective effects of Curcuma longa on ischemia-reperfusion induced myocardial injuries and their mechanisms. 1526 70

The efficacy of lycopene to limit myocardial injury after ischemia and reperfusion was explored in the present study. Adult male albino Wistar rats were divided into three experimental groups and orally received olive oil as vehicle (sham and control I-R) or lycopene 1 mg/kg dissolved in olive oil (lycopene treated group) respectively for 31 days. On the 31st day, animals of the control I-R and lycopene treated groups were subjected to 45 min of occlusion of the LAD coronary artery and were thereafter reperfused for 1 h. The ischemia-reperfusion injury resulted in significant cardiac necrosis, depression in hemodynamics, decline in antioxidant status and rise in lipid peroxidation product levels in the control I-R group as compared to sham control. In histopathological examinations myocardial damage produced after I-R was significantly prevented in the lycopene treated group. Lycopene treatment resulted in preservation of the myocardial antioxidant status and altered hemodynamic parameters as compared to control I-R group. Furthermore, I-R-induced lipid peroxidation was significantly inhibited in the lycopene treated group. These beneficial cardioprotective effects also translated into the functional recovery of the heart. The beneficial effect of lycopene likely results from the suppression of oxidative stress, which results in the reduction of myocardial injury.
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PMID:Cardioprotective effect of lycopene in the experimental model of myocardial ischemia-reperfusion injury. 1660 21

Penetrating chest trauma involving the heart is usually known with a high mortality rate. Neither the absence of hemodynamic depression nor ECG changes exclude a potential fatal injury to the heart. We report on the diagnosis and definitive treatment of a stab wound injury with transected coronary artery, concomittant ventricular penetration, and pulmonary injury.A 37-year-old female was admitted to our emergency room with multiple left-sided gashes (cheek, neck, upper extremity) and a single stab wound in the left thorax. At the scene of the accident the patient's hemodynamic condition was stable with no signs of shock or shortness of breath. Auscultation revealed regular respiratory sound on both lung sides. Hospital transfer by ground was uneventful. Chest X-ray showed left pleural effusion with no signs of pneumothorax. ECG demonstrated regular sinus rhythm without repolarization changes or low voltage. Transthoracic echocardiography revealed pericardial effusion with a swinging heart. The patient was electively intubated in the emergency room and transferred to the operating room for pericardial paracentesis. Median sternotomy was necessary due to extensive bleeding in the drain. Examination of the heart showed a laceration of the left coronary artery (LAD), left ventricle, and upper lobe of the left lung. Cardiopulmonary bypass was instituted and the LAD was ligated proximal to the penetration. The left internal thoracic artery was used for coronary revascularization of the LAD. Postoperative ECG and creatine kinase evaluations excluded myocardial ischemia. The patient was discharged from hospital at POD 10 fully recovered. Transthoracic echocardiography in the emergency room is the diagnostic tool of choice to exclude/confirm a potential cardiac injury. In the case of pericardial effusion, paracentesis sometimes followed by thoracotomy should be performed. The importance of rapid diagnosis and intervention should be emphasized to reduce mortality due to cardiac tamponade or acute myocardial infarction as illustrated by this case.
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PMID:[Transthoracic echocardiography as a diagnostic tool in patients with thoracic stab wounds: early ultrasonographic evaluation in the emergency room]. 1770 Nov 51

With the MEM test (Field) one can establish a cellular immune reaction because the sensitized lymphocytes release the macrophage slowing factor (MSF) upon interaction with the appropriate antigen. A macrophage migration inhibition was detected in some neurological diseases with destruction of the parenchyma. The modification MEM-LAD (linoleic acid depression) test made further differentiation possible in the 146 neurological patients and normals. The reduction of macrophage mobility inhibition was 94.7+/-4.7% in multiple sclerosis (MS) cases as compared with that of normals of 55.1+/-3.7% and of other neurological diseases of 47.8+/-7.1%. There were no significant differences due to the course and duration of the disease or to immunosuppressive therapy. The pathogenically important results in relatives of MS patients with values between the MS and normal group (78.5+/-0.7%) in mothers suggested a familial (genetic) disposition. The same value was found in a monozygotic twin of an MS patient. The results in the children studied showed that besides the endogenic metabolic component the aetiopathogenically important exogenic factors can operate early in life. In correlation with the principle of the MEM-LAD test the suppressive action of linoleic acid can result in a further therapeutic concept.
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PMID:[The macrophage electrophoretic mobility LAD test - a diagnostic method for multiple sclerosis.]. 2056 72


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