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)

Effects of calcium antagonists on the ST alternans and associated mechanical alternans during acute coronary occlusion were examined in anesthetized dogs. The heart rate was fixed by atrial pacing. The intravenous administration of 0.2 mg/kg verapamil attenuated the ST alternans as did 0.5 mg/kg diltiazem. Although these drugs significantly attenuated TQ depression during occlusion, the attenuation was observed after a longer period of occlusion and when the degree of TQ depression was comparable to that during the control occlusion. Nifedipine, 0.03 mg/kg, slightly attenuated the ST alternans, but 0.5 mg/kg dipyridamole had no effect. These results support the idea that slow inward currents are involved in the ST alternans. On the other hand, the mechanical alternans was attenuated in six of 11 dogs. It is probable that factors other than the electrical alternans may also contribute to the mechanical alternans.
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PMID:Effects of calcium antagonists on the electrical alternans of the ST segment and on associated mechanical alternans during acute coronary occlusion in dogs. 687 77

Attempts were made to demonstrate release of vasoactive substances from the heart during coronary occlusion (for 60 min) and reperfusion (for 60 min), and to clarify the pathophysiological significance of them. Vasoactive substances were detected by superfusion of rabbit aortic and dog coronary arterial strips with great coronary venous blood. Plasma thromboxane (TX) B2 was radioimmunologically assayed. Gradually developing, sustained contraction of both vascular strips was noted during coronary occlusion and reperfusion, while a transient contraction in rabbit aortic and relaxation in dog coronary arterial strips were seen immediately after reperfusion. The TXB2 released into the great coronary venous blood significantly increased during occlusion and reperfusion. Indomethacin treatment of the dog abolished the sustained contraction of both vascular strips and TXB2 release. The transient contraction of rabbit aorta after reperfusion was inhibited by phenoxybenzamine. Reactive hyperaemia following a 60 min occlusion was significantly depressed, as compared with that following 30 s to 30 min occlusion, and the depression was alleviated by indomethacin and imidazole. These results suggest that catecholamine(s) and TXA2 are released during coronary occlusion and reperfusion, and that the latter might be responsible for the coronary circulatory failure during reperfusion of irreversibly damaged myocardium.
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PMID:Coronary circulatory failure and thromboxane A2 release during coronary occlusion and reperfusion in anaesthetised dogs. 707 70

1 The effects of Ca2+ -antagonists on the relationships between alternate changes in the ST-T complex in the epicardial electrogram, ST-T alternans, and associated excitation-conduction abnormalities during coronary occlusion were examined in anaesthetized dogs. 2 Epicardial unipolar electrograms, bipolar electrograms (BPEG) and monophasic action potentials (MAP) were recorded with unipolar, composite and suction electrodes, respectively. 3 ST-T alternans was associated with serious conduction delay. During the period of ST-T alternans, the amplitude of MAP changed alternately and the negative deflection of the ST-T complex was associated with a larger MAP. A depression of the TQ level and decrease in the resting potential of MAP were marked. 4 Verapamil (0.2 mg/kg) and diltiazem (0.5 mg/kg) inhibited ST-T alternans, conduction abnormalities, TQ depression and changes in MAP. However, after these drugs, the TQ depression and the decrease in the resting potential were evident after a longer period of occlusion at a time when ST-T alternans, conduction abnormalities and alternate changes in MAP were still inhibited. Dipyridamole (0.5 mg/kg) had no effect on either ST-T alternans or the conduction abnormalities. 5 Verapamil and diltiazem inhibited ST-T alternans and the associated excitation and conduction abnormalities. The effects of these two drugs cannot be explained on the basis of attenuation of the decrease in the resting potential.
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PMID:Effects of calcium antagonists on the alternation of the ST-T complex and associated conduction abnormalities during coronary occlusion in dogs. 731 86

The 2,6-dimethylanilide of quinuclidine-3-carboxylic acid hydrochloride (EO-122), a new structural analog of lidocaine, has been shown to possess potent antiarrhythmic activity in experimentally induced arrhythmias in animals. Restoration of normal sinus rhythm and suppression of ouabain-induced arrhythmia in cats and dogs, and of coronary occlusion-induced arrhythmia in dogs, followed a single IV injection of 1--3 mg/kg, with an onset of 2 minutes and a duration of 20--240 minutes. Occlusion-induced arrhythmia was likewise suppressed after an oral dose of 10--20 mg/kg, with an onset of 11--65 minutes and a duration of 25--120 minutes. Under similar conditions, lidocaine was either totally ineffective or of ultra-short duration. The bioavailability of EO0122 by the oral route exceeded 80% of the oral dose. Therapeutic blood concentrations were in the range 0.5--7 microgram/ml. At about 5 microgram/ml there was a slight depression of cardiac function in the anesthetized cat, but not in the conscious dog. In cats, complete A-V block occurred at concentrations of 60--70 microgram/ml. The IV LD50 in mice was 22 mg/kg, and in rabbits 8.5 mg/kg. No overt signs of neurotoxicity could be observed at any dose of EO-122. The pharmacokinetic profile of the drug fits a two-compartment open model, with t1/2 congruent to 150 min and Vd (SS) congruent to 1.5 l/kg.
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PMID:A preclinical study of EO-122, a new lidocaine-like antiarrhythmic drug. 741 54

To test the hypothesis that right ventricular (RV) involvement may affect precordial T wave polarity, the relationship of T wave polarity in lead V1 to right coronary pathoanatomy was examined in 61 patients with first inferoposterior wall acute myocardial infarction (AMI) due to right coronary occlusion within 5 hours of symptom onset. One hundred healthy subjects served as normal controls. The patients were divided into two major groups based on the site of right coronary occlusion: group A (n = 34) with proximal occlusion and group B (n = 27) with distal occlusion. Each major group was classified into two subgroups according to the direction of the ST segment shift in lead V1. Group A was divided into subgroups A1 (27 patients with isoelectric or ST segment elevation) and A2 (7 patients with ST segment depression), and group B into subgroups B1 (8 patients with isoelectric or ST segment elevation) and B2 (19 patients with ST segment depression). The incidence of upright T wave in lead V1 (> or = 0.15 mV) was higher in the patients with proximal right coronary occlusion (70.6%) than in the controls (27%) (p < 0.001) or the patients with distal right coronary occlusion (18.5%) (p < 0.001). Upright T wave occurred most frequently in subgroup A1 (89%) (p < 0.001 vs controls), and least in subgroup B2 (6%) (p < 0.05 vs controls). T wave polarity agreed with the direction of the ST segment shift in 40 of 61 AMI patients (66%) and disagreed in only one patient (2%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Relation of T wave polarity in precordial V1 lead to right coronary pathoanatomy in inferoposterior wall acute myocardial infarction]. 815 27

Myocardial ischemia interrupts neurotransmission and causes the depression of norepinephrine release. However, the effects of sympathetic nerve stimulation on neurotransmission and norepinephrine release in post-ischemic myocardium are not well defined. We measured regional myocardial length and norepinephrine (NE) release during sympathetic nerve stimulation in anesthetized dogs. Dogs were divided into 2 groups: Group 1 (n = 14); sympathetic nerve stimulation, Group 2 (n = 9); pre-treatment with alpha-blockade yohimbine hydrochloride (0.2 mg/kg) followed by sympathetic nerve stimulation. The left anterior descending artery was occluded for 15 min. Sympathetic nerve stimulation was performed before coronary occlusion and after reperfusion. In group 1, the decrease in systolic shortening in the ischemic region persisted for more than 60 min. Although sympathetic nerve stimulation caused an increase in systolic shortening, it was lower than the pre-ischemic value. NE release from the post-ischemic myocardium remained decreased for 60 min. The decrease in the post-ischemic myocardial response to sympathetic nerve stimulation was associated with diminished NE release. When the cardiac sympathetic nerve was denervated with an epicardial phenol application, NE release decreased even further. In group 2, NE release did not decrease following reperfusion. These results suggest that sympathetic nerve conduction is not completely impaired in post-ischemic myocardium and that pre-synaptic alpha -2 receptors might play an important role in diminished NE release.
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PMID:Response of post-ischemic myocardium to sympathetic stimulation--relation to local norepinephrine release. 823 Jun 78

Experiments on open-chest anaesthetized cats were made to test derivatives of crown ethers, such as benzylase-15-crown-5 and dibenzylase-15-crown-5 for their effects on myocardial ischemia and the functional status of a myocardial ischemic focus in temporary coronary occlusion during coronary spasm induced by dihydroergotamine and during coronary microthrombosis caused by ADP. When intravenously administered in doses of 0.5-15 mg/kg, the tested agents were found to enhance myocardial tolerance to ischemia, depressed ST segment in ischemia induced by coronary occlusion and administration of ATP, and prevented ST-segment depression during coronary spasm.
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PMID:[The anti-ischemic properties of crown ether derivatives]. 831 1

It has recently been shown that ischemia in collateral-dependent myocardium may develop at a very variable threshold in anginal patients; accordingly, the aim of this study was to assess whether nifedipine and diltiazem can increase blood flow to collateralized myocardium in man. Nine patients with complete coronary occlusion filled by collaterals, with no other coronary stenosis, normal left ventricular function, and reproducibly positive exercise tests were studied. They underwent exercise tests off therapy and after acute randomized administration of nifedipine (10 mg sublingually), diltiazem (120 mg orally), and nitroglycerin (0.5 mg sublingually), the latter a drug known to increase blood flow to collateralized myocardium. Following nifedipine, time to 1 mm ST segment depression increased significantly (from 430 +/- 176 to 576 +/- 205 seconds, p < 0.01), while heart rate and rate-pressure product remained unchanged (115 +/- 16 vs 121 +/- 17 beats/min and 199 +/- 29 vs 204 +/- 44 beats/min.mm Hg.10(2), respectively, p = NS for both). Similarly, diltiazem significantly increased time to ischemic threshold from baseline to 638 +/- 125 seconds (p < 0.01), but did not change heart rate and rate-pressure product at 1 mm ST segment depression. Submaximal rate-pressure products were significantly lowered by both nifedipine and diltiazem. Nitroglycerin not only significantly improved time to ischemic threshold (from baseline to 666 +/- 76 seconds, p < 0.01), but also increased heart rate (from baseline to 137 +/- 16 beats/min, p < 0.01) and rate-pressure product (from baseline to 242 +/- 48 beats/min.mm Hg.10(2), p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ischemia in collateral-dependent myocardium: effects of nifedipine and diltiazem in man. 832 95

To assess the significance of ST segment shift during the acute phase of non-Q myocardial infarction we studied the clinic echocardiographic, ergometric and coronarographic findings of 46 patients with a first non-Q wave myocardial infarction. The study population was subdivided in 2 subgroups on the basis of acute electrocardiographic change (Group I with ST elevation, Group II with ST depression). Patients with ST elevation had little myocardial infarction with enzymatic (early CPK peak) and coronarographic (low prevalence of coronary occlusion) signs of early spontaneous fibrinolysis. The second group had more diffuse myocardial infraction, higher prevalence of multivessel coronary disease and positive stress test. The ECG changes in this subgroup an probably due to subendocardial necrosis for the presence of collateral flow. The worse intrahospital prognosis of patients with ST segment depression may be related to cardiac function and age.
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PMID:[A non-Q wave myocardial infarct with an up or down shift of the ST segment in the acute phase: the clinical, echocardiographic, ergometric and coronary angiographic correlates]. 832 71

Three patients showed ST elevation on precordial electrocardiogram and ST depression on intracoronary electrocardiogram during angioplasty of the left anterior descending coronary arteries (LAD). While none of the patients had spontaneously visible collaterals, all showed transient recruitable collaterals to the LAD. No evident collaterals into the diagonal branches were observed. Possibly, if the intracoronary electrocardiogram represents the potential changes of the epicardial surface in the vicinity of the guidewire tip, then endocardial ischemia may have developed even though epicardial ischemia was not observed, due to relatively sufficient blood flow through the recruitable collaterals to the LAD. ST elevation on the precordial electrocardiogram may have represented epicardial and endocardial ischemia of the diagonal branches, where the recruitable collaterals could not protect against transmural ischemia. These phenomena suggests that the recruitable collaterals are functionally limited during acute coronary occlusion, even though the collaterals are well developed.
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PMID:Functional limitation of recruitable collaterals in human subjects--ST segment deviation on intracoronary electrocardiogram during transient coronary occlusion induced by balloon inflation. 835 97


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