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Biomedical subjects

M Kawada

Publications and source records attributed to M Kawada.

At least 145 records · Page 8Linked to original sources
PubMed1986

Infundibular septum and coronary anatomy in Jatene operation.

Displacement of the infundibular septum and coronary anatomy was studied in 40 patients with variable transposition of the great arteries who underwent the Jatene operation between August, 1982, and May, The perioperative mortality was 12.5%. Fourteen of the 16 patients (87.5%) with intact ventricular septum (Group I), eight of the 12 patients (67%) with aligned infundibular septum and perimembranous trabecular defect (Group II-A), and four of the 12 patients (33%) with anteriorly displaced infundibular septum, malaligned defect, overriding of the pulmonary valve, and severe pulmonary hypertension (Group hypertension (Group II-B) has Shaher type 1 coronary anatomy. In this type of coronary anatomy, the left coronary artery courses in front of the pulmonary artery. However, two patients (12.5%) from Group I, four (33%) from Group II-A, and eight (67%) from Group II-B had various unusual coronary patterns, such as Shaher types 2,3,4,7, and 9. All patients had a left or circumflex coronary artery coursing behind the pulmonary artery. These data suggest that the displacement of the infundibular septum not only determines the type of the defect and hemodynamics, but also often relates to the coronary anatomy Removal of a whole, scallop-shaped sinus of Valsalva and minimal dissection of the coronary artery are preferable, particularly for translocation of such unusual coronary anatomy.

Child, Preschool↗
PubMed1985

Nicardipine releases sustained coronary arterial constriction induced by acetylcholine in the rhesus monkey.

In five rhesus monkeys (Macaca mulatta) the vascular bed of the left anterior descending coronary artery (LAD) was perfused at constant pressure with autologous blood. Nicardipine (1-30 micrograms), a dihydropyridine calcium antagonist when injected into the LAD, increased LAD flow without producing significant changes in other cardiohemodynamic variables. With continuous infusions of acetylcholine into the LAD, the flow decreased by about 34% of the basal value. Under these conditions, intra-LAD nicardipine produced an increase in LAD flow almost to the same extent as in the control. The effects of nicardipine were qualitatively similar to those of other calcium antagonists observed in previous experiments and indicate that nicardipine would be useful as an antianginal drug.

Acetylcholine↗
PubMed1985

Assessment of left ventricular function before and after Fontan's operation for the correction of tricuspid atresia. Changes in left ventricular function determined by left ventricular volume change.

Functional change in the left ventricle was studied in the light of changes in the left ventricular (LV) volume preload before and after Fontan's operation. Six cases with tricuspid atresia (TA) were studied, and they had either types Ib or IIb. The preoperative LV end-diastolic volume index (LVEDVI) was 123 +/- 44 ml/m2, which corresponds to 166% +/- 45% of normal values. This suggests that in TA the preload of the LV volume is increased because of its peculiar hemodynamic situation. After Fontan's operation, the LVEDV decreased by 24.6% to 119.6 +/- 87.7 ml (P = 0.01), which corresponds to 120% +/- 50.9% of normal values. Presenting a striking contrast to the decrease in LVEDV, the postoperative reduction in LV end-systolic volume (LVESV) was approximately 8%. Preoperative and postoperative values for LVESV were 67.1 +/- 50.8 ml and 62 +/- 45.6 ml, thus, the systolic volume was decreased. Because of the small change in LVESV, the ejection fraction (EF) of the left ventricle significantly decreased from 0.61 +/- 0.1 preoperatively to 0.48 +/- 0.1 postoperatively. The cardiac index (CI) remained in the range of 1.9-2.5 l/min/m2 with a mean of 2.2 +/- 0.2 l/min/m2 at 1 month after operation. But, later, improvement in EF was observed in one case, in which the CI increased from 2.5 to 3.2 l/min/m2.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1984

Glucocorticoid receptor in chick embryonic epidermis. Inhibition by progesterone of both the binding of glucocorticoid to the receptor and glucocorticoid-induced keratinization.

Our previous study showed that hydrocortisone (10(-8) M) induced epidermal alpha-type keratinization in 13-day-old chick embryonic tarsometatarsal skin cultured in a chemically defined medium. In this study, we show that typical glucocorticoid receptor is present in epidermal cells of chick embryonic cultured skin and that alpha-type keratinization of epidermal cells is completely prevented by the coexistence of a 100-fold excess concentration of progesterone with glucocorticoid. The physiologic importance of the receptor is suggested by some correlation between the ability of progesterone to block both the differentiation-induction and the binding of active glucocorticoid to the receptor.

Acyltransferases↗
PubMed1984

Mode and mechanism of action of 3,4-dihydro-6-[4-(3,4-dimethoxybenzoyl)-1-piperazinyl]-2(1H)- quinolinone (OPC-8212), a novel positive inotropic drug, on the dog heart.

Mode and mechanism of action of 3,4-dihydro-6-[4-(3,4- dimethoxybenzoyl )-1-piperazinyl]-2(1H)- qu inolinone ( OPC -8212) were investigated exclusively on dogs both in vivo and in vitro. When assessed by intra-arterial administration in isolated, blood-perfused papillary muscle, sinoatrial node and atrioventricular (AV) node preparations, OPC -8212 produced a positive inotropic effect scarcely causing either positive or negative chronotropic and coronary vasodilator effects. AV nodal conduction was slightly facilitated with OPC -8212, whereas ventricular automaticity was rather suppressed. No arrhythmias were produced. Thus, OPC -8212 is highly specific for force. In heart-lung preparations OPC -8212 improved cardiac function depressed with pentobarbital, and caused bradycardia. In trabecular muscles of the right ventricle (hereafter simply called ventricular muscles) OPC -8212 produced a concentration-dependent positive inotropic effect in the presence of the beta 1-adrenoceptor antagonist, atenolol. This indicates that the positive inotropic effect of OPC -8212 is not mediated through a beta-adrenoceptor mechanism. In ventricular muscles OPC -8212 increased plateau potentials of normal action potentials in the presence of atenolol. In K+-depolarized ventricular muscles OPC -8212 increased overshoot potentials and durations of slow response action potentials in the presence of atenolol. These suggest an increase in the slow inward current to underlie the positive inotropic effect of OPC -8212. In ventricular muscles OPC -8212 shortened total duration of contraction and time to peak tension in the presence of atenolol. In ventricular muscles OPC -8212 increased force of contraction and intracellular concentrations of cyclic AMP in a parallel way in time course in the presence of atenolol.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Selectivity of alinidine, a bradycardic agent, for SA nodal automaticity versus other cardiac activities in isolated, blood-perfused dog-heart preparations.

Selectivity of alinidine for SA nodal automaticity vs. other cardiac activities was investigated using isolated, blood-perfused SA node, AV node and papillary muscle preparations of the dog. The drug was administered intra-arterially. In SA node preparations alinidine (1 microgram-1 mg) produced a dose-dependent decrease of sinus rate down to about 74% of the basal value at 1 mg, but no atrial standstill. In AV node preparations alinidine, injected into the posterior septal artery (PSA) which supplies the AV node, prolonged AV conduction time up to about 124% of the basal value but only in large doses (30 micrograms-1 mg). In the same preparations, when injected into the anterior septal artery, which supplies structures from the His bundle down to the ventricular septum (the intraventricular conduction system), alinidine in large doses (300 micrograms-1 mg) also prolonged AV conduction time nearly to the same extent as when injected into the PSA. In both cases neither second- nor third-degree AV block occurred. In paced papillary muscle preparations alinidine reduced the force of contraction down to about 64% of the basal value but in large doses (100 micrograms-1 mg). In spontaneously beating papillary muscle preparations alinidine reduced the rate of ventricular automaticity down to about 78% of the basal value but in large doses (100 micrograms-1 mg). Alinidine (100 micrograms-1 mg) produced a transient increase in blood flow in these preparations but not in SA node preparations. The cardiac effects of alinidine were longer-lasting than its vascular effect and the reduction of sinus rate was particularly long-lasting. The order of selectivity of alinidine determined from the above results is as follows: SA nodal automaticity much greater than ventricular automaticity greater than intraventricular conduction divided by AV nodal conduction divided by cardiac muscle contraction divided by coronary blood flow. Such a cardiovascular profile of alinidine is different from that of AQ-A 39, another bradycardic agent, which is nearly equi-effective on both SA nodal and ventricular automaticity.

Animals↗
PubMed1984

Cardiovascular actions of the dihydropyridine calcium antagonist nimodipine in the dog.

When injected i.v. into anaesthetized, open-chest dogs, isopropyl (2-methoxyethyl)-1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3, 5-pyridinedicarboxylate (nimodipine, Bay e 9736) (0.3-10 micrograms/kg) produced an increase in coronary sinus outflow and decreases in mean arterial blood pressure, coronary resistance, arterio-venous oxygen difference and heart rate in a dose-dependent manner, but virtually no change in myocardial oxygen consumption. At 3 micrograms/kg i.v. of the drug coronary resistance fell nearly to half the pre-drug value, coronary sinus outflow nearly doubled and heart rate decreased by about 10 beats/min. Myocardial oxygen consumption was slightly reduced at 30 micrograms/kg i.v. and atrioventricular (AV) conduction time was slightly increased at 10 and 30 micrograms/kg i.v. of the drugs. When the coronary vascular and cardiac effects of nimodipine were assessed in isolated, blood-perfused dog heart preparations, i.e., sinoatrial node, AV node and papillary muscle preparations, by intra-arterial administration, the following was revealed. In nearly twice the dose doubling coronary arterial blood flow, nimodipine produced a 15% decrease in sinus rate and a 15% increase in AV conduction time. However, in reducing the force of contraction of the papillary muscle by half the pre-drug value was needed nearly 17 times the dose of nimodipine doubling coronary arterial blood flow. Suppression of AV conduction by large doses of nimodipine was evident only when it was injected into the artery supplying the AV node but not into the artery supplying the His-Purkinje-ventricular system.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗