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Biomedical subjects

K Tsuchida

Publications and source records attributed to K Tsuchida.

At least 199 records · Page 11Linked to original sources
PubMed1986

Double orifice mitral valve associated with endocardial cushion defect.

Duplication of the mitral valve is a rare congenital cardiac anomaly. We encountered a case of duplication of the mitral valve associated with a partial form of endocardial cushion defect in a 6-year-old girl. The mitral orifice was separated by a fibrous tissue and each orifice provided papillary muscle and complete subvalvular mechanisms except for the cleft region. The fibrous tissue also provided a subvalvular apparatus. The cleft was repaired without complication. The short axis view of the two-dimensional echocardiogram demonstrated two separate holes in the mitral valve, which constituted the most obvious diagnostic sign prior to surgery.

Child↗
PubMed1986

Effects of a K ionophore, lonomycin A, on the action potential in canine cardiac Purkinje fibers.

Effects of a K ionophore, lonomycin A (K+:Na+ = 6:1), on the action potential and contractile force in canine cardiac Purkinje fibers were examined. Lonomycin A increased the developed and resting tensions. The agent shortened the action potential, decreased the plateau height and suppressed the automaticity. In addition, lonomycin A also shortened the duration of the slow action potential response, and it shortened the action potential duration to about the same extent in the presence and absence of tetrodotoxin. In quiescent Purkinje fibers, lonomycin A decreased K content in both 1.8 mM Ca Tyrode's solution (contracture observed) and 0.18 mM Ca Tyrode's solution (contracture not observed). These results suggest that lonomycin A-induced changes in the action potential configuration of Purkinje fibers is mainly due to the increase in K conductance, and the increase is induced irrespective of the degree of the increased [Ca2+]i.

Action Potentials↗
PubMed1986

Degradation of myocardial structural proteins in myocardial infarcted dogs is reduced by Ep459, a cysteine proteinase inhibitor.

The purpose of this study is to clarify whether cysteine proteinases play an important role in the degradation of myocardial proteins in the infarcted tissue. We studied the effects of a cysteine proteinase inhibitor, Ep459, on degradation of cardiac structural proteins caused by ischemia due to coronary artery ligation for 24 h. Proteolytic effects of purified cysteine proteinases on isolated cardiac tissue were also examined. Using sodium dodecyl sulfate-polyacrylamide gel electrophoresis, degradation of cardiac structural proteins, particularly of myosin heavy chain, alpha-actinin and troponin-I was observed in the infarcted tissue. Treatment with Ep459 significantly reduced protein degradation and total activity of cathepsins B and L in the infarcted tissue, compared with the findings in the untreated group. The electrophoretic pattern of the infarcted myocardium was similar to that of myofibrillar proteins degraded by cathepsins B and L. These results suggest that cysteine proteinases, particularly cathepsins B and L, are involved in degradation of myofibrillar proteins in myocardial infarction.

Animals↗
PubMed1986

Effects of midodrine on blood flow in dog vascular beds.

Effects of alpha-(2,5-dimethoxyphenyl)-beta-glycinamide-ethanol hydrochloride (midodrine, ST-1085) on blood flow in different vascular beds were examined in anesthetized dogs. Intravenously administered midodrine at doses of 0.3 and 0.6 mg/kg induced a transient increase followed by a long-lasting decrease in femoral arterial blood flow. Renal arterial blood flow exhibited an initial decrease followed by returning toward the control level, and thereafter decreased again. Vertebral, common carotid, superior mesenteric and coronary arterial blood flow, and cardiac output gradually decreased. Midodrine did not have any effects on cerebral tissue blood flow. The changes were more remarkable at a dose of 0.6 mg/kg than at 0.3 mg/kg. Each arterial blood flow change was statistically analyzed 20, 30 and 60 min after the administration of 0.6 mg/kg of midodrine. The decrease of coronary arterial blood flow by the treatment with midodrine was significantly smaller than those of superior mesenteric and femoral arterial blood flow at 20 and 30 min after midodrine administration. The decrease of renal arterial blood flow was significantly smaller than those of superior mesenteric arterial blood flow at 20 and 30 min, and femoral arterial blood flow at 20, 30 and 60 min after the administration. The decrease of vertebral arterial blood flow was also smaller than that of femoral arterial blood flow at 20, 30 and 60 min after the administration.

Adrenergic alpha-Agonists↗
PubMed1986

Effects of midodrine on experimentally-induced postural hypotension in dogs.

Effects of alpha-(2,5-dimethoxyphenyl)-beta-glycinamide-ethanol hydrochloride (midodrine, ST-1085) on experimental postural hypotension was examined in hexamethonium (20 mg/kg s.c.)-treated anesthetized dogs. The dogs were tilted 30 degrees to a head-up position. A 30 degree-tilt caused a significant decrease in blood pressure. Midodrine, 0.3 mg/kg, attenuated the decrease in blood pressure induced by the tilt significantly at 10 and 30 min after administration of the drug. The heart rate increased following the tilt, but the degree of the increase was rather small. Cerebral tissue blood flow significantly decreased by the tilt. Midodrine, 0.3 mg/kg, significantly attenuated the decrease in cerebral tissue blood flow induced by the tilt at 10 and 30 min. Vertebral arterial blood flow significantly decreased by the tilt. Midodrine reduced the decrease in vertebral arterial blood flow induced by the tilt significantly at 10 and 30 min. Cardiac output also decreased significantly by the tilt. Midodrine attenuated the decrease in cardiac output significantly at 10 min. Femoral arterial blood flow decreased significantly by the tilt. Midodrine tended to reduce the decrease in femoral arterial blood flow induced by the tilt at 30 min. Therefore, midodrine via vasoconstriction seems to be useful for the decrease in blood flows due to the postural hypotension.

Adrenergic alpha-Agonists↗
PubMed1985

Effects of propranolol on infarct size and the impaired hemodynamics in experimental myocardial infarcted dogs.

We studied the effects of propranolol on infarct size and hemodynamic impairment induced by 24 h-coronary ligation. The myocardial infarction produced by the left circumflex coronary artery ligation was more consistent than that induced by the left anterior descending coronary artery ligation, suggesting that the former is a more appropriate experimental model for pharmacological evaluations. Oral treatment with propranolol, 3-30 mg/kg, reduced infarct size and reduced the elevated left ventricular end-diastolic pressure, which was shown to be most closely related with infarct size, in dogs with circumflex coronary artery ligation extending over 24 h. In conclusion, our results indicate that propranolol protects against the enlargement of infarct size and improves the impaired hemodynamics observed in myocardial infarcted dogs with occlusions extending over 24 h, as well as in dogs with less than 24 h-occlusions reported by numerous investigators.

Administration, Oral↗
PubMed1985

Cardiovascular effects of an ionophorous antibiotic, lonomycin A, in anesthetized dogs.

An intracoronary administration of ionomycin A, a K-selective ionophore, produced coronary vasodilation in the presence of pindolol in anesthetized dogs. Coronary vasodilation induced by ionomycin A, KCI and nifedipine was inhibited by pretreatment with an intracoronary injection of ouabain. This result suggests that lonomycin A-induced coronary vasodilation may be partly due to a stimulation of Na+, K+-ATPase as well as KCI and/or a decrease in Ca2+ influx as well as nifedipine.

Animals↗