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Biomedical subjects

K Amaha

Publications and source records attributed to K Amaha.

At least 127 records · Page 7Linked to original sources
PubMed1982

Chronotropic effects of succinylcholine and succinylmonocholine on the sinoatrial node.

The mechanism of bradycardia caused by the administration of succinylcholine has not been fully elucidated. Accordingly, the effects of succinylcholine and succinylmonocholine on the sinoatrial node were studied in 35 mongrel dogs. The sinus node artery was selectively perfused with autologous blood from a femoral artery at a constant pressure of 100 mmHg, and 30 to 1,000 micrograms of succinylcholine or succinylmonocholine was administered directly into the artery. Succinylcholine caused a transient (63-600 s) dose-related positive chronotropic effect. The heart rate was increased to 14.4 +/- 2.1% (mean +/- SE) above the control value after the administration of 1,000 micrograms of succinylcholine. This positive chronotropic effect was inhibited by pretreatment with pindolol or reserpine. By contrast, succinylmonocholine produced a transient (30-248 s) dose-related negative chronotropic effect. The heart rate was decreased to 17.5 +/- 1.4% below the control value after administration of 1,000 micrograms of succinylmonocholine. The negative chronotropic effect was blocked partially by atropine. It was concluded that the positive chronotropic effect of succinylcholine may be mediated through beta-adrenergic receptor stimulation by catecholamine released from the adrenergic nerve endings in the sinoatrial node, and that the negative chronotropic effect of succinylmonocholine may be the result of excitation of cholinergic receptors in the sinus node. However, a direct effect of succinylmonocholine on the sinus node could not be ruled out.

Animals↗
PubMed1981

Ventilatory response to CO2 in patients after long-term ventilation for acute respiratory failure secondary to chronic obstructive lung disease.

Ventilatory response to CO2 was examined in 6 patients with severe chronic obstructive lung disease (COLD) shortly after discontinuance of long-term ventilation for acute respiratory failure (ARF). Ventilatory response to CO2 was extremely low in all patients 6-10 h after discontinuance from ventilator. Our month later, however, CO2 response curves shifted to the left and in 3 patients there was improvement which was seen in the slope of response curve. In patients who had mechanical ventilation for ARF from COLD, abnormally low responses to CO2 probably contribute to the difficulty in weaning from mechanical ventilation. The presence of reduced CO2 responsiveness should be considered in these circumstances.

Aged↗
PubMed1980

Inotropic effects of non-depolarizing muscle relaxants in isolated canine heart muscle.

The inotropic effects of five non-depolarizing muscle relaxants were examined using an isolated canine heart muscle preparation. Except for fazadinium, all drugs were studied in their commercially available forms. d-Tubocurarine chloride (dTc) and metocurine iodide (MTC) produced dose-dependent decreases in isometric force (F) and the maximum velocity of force development (dF/dt) at concentrations greater than 22.5 x 10(-3) g/L for dTc and greater than 15.0 x 10(-3) g/L for MTC, concentrations which are 3 and 6 times higher than estimated clinical serum concentrations, respectively. Myocardial depression was about 3 times less with MTC than with dTc at equipotent concentrations. The degree of depression in F and dF/dt produced by MTC was almost identical with that produced by phenol, a preservative of MTC, indicating that MTC-induced myocardial depression may be due to the effect of the preservative. Pancuronium bromide (PC) produced a dose-dependent increase in F and dF/dt and decrease in the time to peak force. PC-induced changes in F, dF/dt, and time to peak force were inhibited by administration of propranolol 10(-6) M. The results indicate that PC possesses a positive inotropic effect mediated by beta-adrenergic stimulation. Alcuronium chloride did not change F or dF/dt at concentrations from 5.0 x 10(-3) to 60.0 x 10(-3) g/L. Frazadinium bromide increased F and dF/ dt slightly at a low concentration (1.875 x 10(-2) g/L), but further increases in its concentration returned the values of F and dF/dt to control levels. F and dF/dt were not altered in vitro by concentrations of relaxants that would be anticipated in plasma in vivo in patients given clinically effective doses of 0.3 mg/kg of dTc, 0.1 mg/kg of MTC or PC, 0.2 mg/kg of alcuronium chloride, or 0.75 mg/kg of fazadinium bromide.

Alcuronium↗