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)

Guinea pig papillary muscles were used to study the activation of myocardial contractions under depolarizing conditions. Depolarization promoted by TKBa (normal Tyrode solution containing KCl and BaCl2) and TKAdr (normal Tyrode solution containing KCl and adrenaline) inactivates the fast Na current and under these conditions only slow responses are available to activate contractions. Since the slow response is sensitive to changes in rate and rhythm, we searched for mechanical correlates using isometrically contracting preparations to study the force-frequency relationship as well as rest potentiation. We also investigated if contractions are dependent only on the slow response or if the complete action potential plays a special role in the activation of contractions. We conclude that the slow response is the main mechanism for the activation of myocardial contraction, because complete mechanical activation was observed under depolarizing conditions. However, the electrical behavior of the slow response is reflected in the mechanical behavior of the depolarized preparations. At high rates, disturbances of excitation occur in depolarized cells and contractions appear to be bigeminal or with 2:1 block. Furthermore, after long pauses, post-rest contractions are depressed and increase progressively with repetitive stimulation, probably due to changes in the latency and threshold of the slow response. The complete action potential also plays a role in the activation of myocardial contractions which is necessary for the resting potentiation phenomena and also to avoid the larger depression of the rest contractions that can be seen in depolarized muscles when the pause is prolonged. This behavior seems to be related to the decrease of intracellular Na concentration produced by the inhibition of the fast inward Na-current.
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PMID:Characteristics of myocardial contractions activated under depolarizing conditions. 359 10

Tetrachloroethylene (1,1,2,2-tetrachloroethene) is a widely used organic solvent capable of producing adverse renal, hepatic, and central nervous system effects. The cardiac effects of tetrachloroethylene, thus far unexplored, were studied in several species. To standardize the dosimetry, tetrachloroethylene was prepared for intravenous injection in solutions of Tween 80, which had no demonstrable cardiotoxicity. In rabbits under urethane and in cats and dogs under pentobarbital, tetrachloroethylene increased the vulnerability of the ventricles to epinephrine-induced extra-systoles, bigeminal rhythms, and tachycardia. The mean threshold doses of tetrachloroethylene were 10 mg/kg in rabbits, 24 mg/kg in cats, and 13 mg/kg in dogs. In rabbits this threshold dose for cardiac arrhythmias correspond to blood levels between 2.2 and 3.6 microgram/ml. Animals demonstrating a reflex bradycardia to vasopressor doses of epinephrine were relatively resistant to the arrhythmogenic action of tetrachloroethylene. Ventricular arrhythmias occurred in less than 30% of the animals after tetrachloroethylene alone. In cats higher doses of tetrachloroethylene (40 mg/kg) produced acute pulmonary edema. Tetrachloroethylene (30-40 mg/kg) decreased left intraventricular dP/dt (max) in dogs, without significantly increasing left intraventricular end-diastolic pressure, although there was a transient decrease in arterial blood pressure that accompanied the early phase of myocardial depression. These results are being used as the basis for studies of the chronic effects of tetrachloroethylene on cardiac performance.
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PMID:Cardiopulmonary toxicity of tetrachloroethylene. 713 86