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Biomedical subjects

H Komai

Publications and source records attributed to H Komai.

At least 73 records · Page 4Linked to original sources
PubMed1985

Negative inotropic effect of etomidate in rabbit papillary muscle.

The effect of etomidate on the developed force of isometrically contracting rabbit papillary muscles in modified Krebs-Henseleit bicarbonate medium was evaluated under various stimulation conditions to gain insight into the mechanism underlying the negative inotropic effect of this anesthetic. Myocardial depressant effects of etomidate (2 and 4 mg/L) on steady-state contractions at low stimulation frequencies (0.1-0.5 Hz) were more pronounced than the effects on either steady-state contraction at high stimulation frequencies (1.0-2.0 Hz) or the effects on post-rest potentiated state contractions. Increases in the concentration of extracellular Ca2+ from an initial level of 2.5 mM to 3.4-4.0 mM reversed the effect of 2 mg/L of etomidate, whereas an increase to 4.6-5.0 mM was required to reverse the effect of 4 mg/L of etomidate. The dependence of post-rest potentiation on the duration of the preceding rest period was virtually unaffected by etomidate. These results suggest that etomidate inhibits the influx of extracellular Ca2+ but has little effect on the availability of intracellular Ca2+ required for the activation of myocardial contractile activity. Because the concentrations of etomidate required to produce negative inotropic responses in the present study are substantially greater than those likely to be achieved under clinical conditions, the present results also suggest that negative inotropism is unlikely in patients with normal hearts.

Animals↗
PubMed1984

Inotropic effect of amrinone in rabbit papillary muscle: reversal of the myocardial depressant effect of halothane.

In rabbit papillary muscles, the pronounced inotropic effect of amrinone (0.4-0.8 mg/mL) observed at low stimulation frequencies (0.1-0.5 Hz) diminished as the frequency was increased to 1.0-2.0 Hz. Reversal of the negative inotropic effect of halothane (1%) by amrinone (0.8 mg/mL) was similarly dependent on stimulation frequency. The contractile response to paired-pulse stimulation in the presence of amrinone (0.8 mg/mL) was summation rather than postextrasystolic potentiation. Amrinone (0.8 mg/mL) was not effective in reversing the negative inotropic effect of halothane (1%) on potentiated state contraction generated by paired-pulse stimulation. These results suggest that amrinone increases the influx of extracellular Ca2+ across the sarcolemma but not the availability of cellular Ca2+ which accumulates, most likely in sarcoplasmic reticulum, under the condition of potentiation.

Aminopyridines↗
PubMed1984

Differences in the myocardial depressant action of thiopental and halothane.

The negative inotropic effects of thiopental (10-30 mg/L) and halothane (0.5-1.5%) were compared in rabbit papillary muscles under various stimulation conditions to gain insight into the action of these anesthetics on the availability of Ca2+ for the activation of myocardial contractile activity. The negative inotropic effect of thiopental was more pronounced at short (0.5 sec) than at long (1 sec) beat-to-beat intervals under steady-state conditions, and thiopental's effect on potentiated state contractions was less than that on steady-state contractions. For all variables studied, the effect of halothane was opposite that of thiopental. These results suggest that thiopental reduces the influx of extracellular Ca2+ and the amount of Ca2+ in sarcolemmal sites and slows the transport of intracellular Ca2+ within the sarcoplasmic reticulum from sites of uptake to sites of release without markedly diminishing the amount of intracellular Ca2+. Halothane does not appreciably affect the transport but does diminish the amount of Ca2+ within the sarcoplasmic reticulum that is available for the activation of myocardial contractile activity.

Animals↗
PubMed1982

Effect of halothane on rested-state and potentiated-state contractions in rabbit papillary muscle: relationship to negative inotropic action.

The effect of halothane on the availability of different sources of activator calcium for myocardial contraction was evaluated in relationship to the negative inotropic effect on the anesthetic. This was studied in rabbit papillary muscle under various stimulation conditions that are known to vary the importance of one or another of two sources of Ca2+ for production of contraction. The rested-state contraction is known to depend primarily on the transsarcolemmal influx of Ca2+ for its activation whereas the potentiated-state contraction is dependent largely on Ca2+ released from intracellular stores. In the presence of 0.6% halothane (gas phase) the rested-state and potentiated-state contractions were depressed (mean +/- SEM) 38% +/- 5% (n = 15) and 32% +/- 3% (n = 7), respectively (no statistically significant difference). Halothane accelerated the decay of the potentiated state, indicating that it stimulates the loss of Ca2+ from internal stores. Halothane also acted to slow the time course of force increase following restimulation of rested muscles, indicating that it inhibits the filling of internal stores. These observations suggest that the negative inotropic effect of halothane is caused by a combination of quantitatively similar effects of the anesthetic on the transsarcolemmal and intracellular sources of activator Ca2+.

Animals↗
PubMed1981

Effects of bupivacaine and lidocaine on AV conduction in the isolated rat heart: modification by hyperkalemia.

The intrinsic cardiotoxicities of bupivacaine and lidocaine were examined in the isolated, perfused rat heart. The perfusates contained no protein and were equilibrated with a gas mixture of 95 per cent O2 and 5 per cent CO2. Autonomic activity, competitive binding, and postseizure hypoxia and acidosis were absent in this experimental model. The effects of the two local anesthetics were evaluated at normokalemia (5.9 mEq/l) and hyperkalemia (9.0 mEq/l). For normokalemia, the ratio of the potency of bupivacaine to that of lidocaine was 14 for slowing ventricular rate to 50 per cent of control, 6 for slowing atrial rate to 50 per cent of control, and 17 for doubling of the PR interval. The action of bupivacaine to slow ventricular rate was due to an inhibitory effect on both AV conduction and atrial rate. For lidocaine, ventricular slowing was mediated mainly by an inhibition of atrial rate with decreased AV conduction playing a minor role. Hyperkalemia of 9.0 mEq/l had little effect on heart rate or AV conduction in the absence of bupivacaine or lidocaine. It did, however, greatly potentiate the effect of both local anesthetics to slow ventricular rate. For bupivacaine, ventricular slowing to 50 per cent of control during hyperkalemia was accomplished almost entirely via an inhibition of AV conduction, while for lidocaine it occurred because of inhibition of both AV conduction and atrial rate. Regardless of the mechanism, hyperkalemia of this degree increased the ventricular slowing effect of both bupivacaine and lidocaine.

Animals↗
PubMed1980

Comparison of Ca2+, Sr2+, and Mn2+ fluxes in mitochondria of the perfused rat heart.

The amount of readily exchangeable Ca2+ in mitochondria of an isolated working rat heart is less than 10 ng-ions/g heart. We therefore conclude that either no Ca2+ enters mitochondria or that the Ca+ which does enter is removed continuously. Using Sr2+ and Mn2+, we obtained evidence that the mitochondrial Na+-Ca2+ exchanger was indeed operational in releasing metal from mitochondria of the heart. When Ca2+ in the perfusate was replaced by Sr2+, we found that a significant amount of Sr2+ (approximately 100 ng-ions/g heart) entered mitochondria. When the heart then was returned to a Ca2+-containing perfusate, over 80% of the Sr2+ was washed out of mitochondria within 30 seconds. When low levels of Mn2+ were added to the perfusate, we found that Mn2+ accumulated in mitochondria irreversibly. This is evidence for the operation of the Na+-Ca2+ exchanger because Na+ was found to release Ca2+ and Sr2+ but not Mn2+ from isolated rat heart mitochondria. Our estimates indicate that when the Na+-Ca2+ exchanger is maximally operative, as in the Sr2+-perfused heart, the flux of Sr2+ through mitochondria is at most 10% of the total flux needed for the activation of contraction. The low level of Ca2+ in the mitochondria of Ca2+-perfused hearts suggests a much smaller flux of Ca2+ through the mitochondria in this case. We therefore conclude that mitochondria play little if any role in the beat-to-beat regulation of normal Ca2+ fluxes in the rat heart.

Animals↗
PubMed1976

Targets of gazing and eye contact during interviews: effect on Japanese nonverbal behavior.

The gaze direction of both the subject and his interviewer were varied independently, such that either looked at the other's eyes or at the other's knees in a 2 X 2 design. A repeated measures design was used with nonverbal vehaviors of Japanese manes as dependent variables. When the interviewers gazed at the subjects' eyes, the response latencies of the subjects were shortened and their torso movements were reduced. Results from other studies of Japanese nonverbal behavior suggest that this pattern of response indicated greater subject invlovement in the interaction. The magnitude of these effects was unchanged whether the subject was reciprocating the interviewer's gaze and making eye contact or looking at the interviewer's knees. It was thus reasoned that effects produced by eye contact in other research may have resulted from subjects' knowledge that they were being gazed at and not from the unique properties of eye contact. When the subjects gazed at the interviewer's eyes, the hand self-manipulations of the subjects increased, reflecting the upsetting effects of monitoring the interviewer's face during interaction. The consequences of gazing at another's eyes thus appear to be different from having one's eyes gazed at by another.

Adult↗