Search PubMed⌕ Search

Biomedical subjects

S Denda

Publications and source records attributed to S Denda.

24 records · Page 2Linked to original sources

Pretreatment with d-tubocurarine, vecuronium, and pancuronium attenuates succinylcholine-induced increases in plasma norepinephrine concentrations in humans.

We studied in patients the effect of d-tubocurarine, which has sympathetic ganglion blocking action, on succinylcholine-induced increases in plasma levels of catecholamines, and compared it with the effects of vecuronium and pancuronium, which have little sympathetic ganglion blocking action. Thirty-two patients were divided into five groups: seven were given 3 mL saline; seven received 1 mg/kg succinylcholine; and six, seven, and five patients were given 0.08 mg/kg d-tubocurarine, 0.01 mg/kg vecuronium, and 0.01 mg/kg pancuronium, respectively, all of which were injected 5 min before 1 mg/kg succinylcholine. Succinylcholine alone significantly increased plasma norepinephrine concentrations, systolic blood pressure, and heart rate from 187 +/- 39 pg/mL (mean +/- SEM), 93 +/- 2 mm Hg, and 77 +/- 4 beats/min to 429 +/- 61 pg/mL, 120 +/- 7 mm Hg, and 102 +/- 6 beats/min, respectively, with onset of fasciculations. Pretreatment with d-tubocurarine, vecuronium, and pancuronium significantly and equally attenuated both the fasciculations and the cardiovascular responses to succinylcholine. These results suggest that the sympathetic ganglion blocking action of neuromuscular relaxants when given before succinylcholine is not an important factor in attenuation of succinylcholine-induced increases in plasma levels of catecholamines.

Adult↗

[Anesthetic management of pheochromocytoma by continuous intravenous injection of prostaglandin E1].

We had five cases of surgical removal of pheochromocytoma by continuous intravenous injection of prostaglandin E1. During anesthesia, we used Swan-Ganz catheter for circulatory monitoring and measured plasma catecholamines. When PGE1 dose was increased from 0.05 to 0.1 and 0.15 microgram.kg-1.min-1, total systemic vascular resistance and mean arterial pressure were decreased but heart rate and cardiac output were not significantly altered from the preanesthetic values. Plasma catecholamines were also similar to the preanesthetic values. Therefore, the results suggest that the mechanism of suppression of hypertension by PGE1 is by affecting vascular beds directly rather than by diminishing catecholamine excretion from sympathetic nerve and adrenal medulla. During manipulation of pheochromocytoma, mean arterial blood pressure increased extremely. Although PGE1 was injected at a rate of 0.3 to 0.5 microgram.kg-1.min-1 in some cases, we could not suppress the elevation of blood pressure. PGE1 alone could not normalize blood pressure and heart rate, and other cardiovascular agents were necessary.

Adolescent↗

Effects of isoflurane on spinal inhibitory potentials.

The effects of isoflurane on segmental spinal cord potentials and heterosegmental slow positive potentials in response to fore- and hindpaw stimulation were studied in the rat. The heterosegmental slow positive potential and late (second) component of the slow positive wave (P2) of segmental spinal cord potential, thought to be primary afferent depolarization, an agent of presynaptic inhibition activated by a feedback loop via supraspinal structures, were greatly suppressed by the anesthetic. In contrast the negative wave (N1) of segmental spinal cord potential, believed to be synchronized activity of dorsal horn neurons, was only minimally affected. No differential effects of isoflurane on spinal cord potentials activated by fore- and hindpaws were found. Thus, the inhibitory activities of the spinal cord, particularly those produced by a feedback loop via supraspinal structures, are suggested to be highly vulnerable to isoflurane.

Animals↗

[Anesthesia for pectus excavatum].

The incidence of arrhythmia, postoperative complication and pulmonary oxygenation (PaO2) were studied in 48 patients with pectus excavatum scheduled for the Ravitch operation under halothane-nitrous oxide-oxygen (GOF) and enflurane-nitrous oxide-oxygen (GOE) anesthesia. Preoperative abnormalities of ECG were observed in 36 of 18 cases. Main abnormalities were incomplete right bundle branch block, left atrium enlargement, and sinus arrhythmia. Ventricular arrhythmia was observed in 4 of 12 cases during GOF anesthesia, whereas no arrhythmia was observed during GOE anesthesia. In postoperative chest X-ray, pulmonary atelectasis (60%), pleural effusion (48%), and pneumothorax (8%) were observed. The results suggest that GOE is more advantageous for pectus excavatum operation than GOF. Postoperative pulmonary surveillance is important for pectus excavatum operation.

Adolescent↗

Tolerance to N2O-induced alterations in somatosensory evoked potentials.

The effect of nitrous oxide (N2O) on somatosensory evoked potentials from the cortical (CEP) and spinal cord (SCP) regions in response to forepaw stimulation was studied in ketamine-anesthetized and mechanically ventilated rats. The CEP was recorded from the skull over the contralateral somatosensory area; the SCP was recorded from the supraspinous ligament at C57-6 and L1-2 levels of the spine. Rats were exposed to 70% N2O for 5 h, whereupon N2O was withdrawn for 2 h. Thereafter, the rats were re-exposed to N2O for 10 min. The N13-P21 component of the CEP, the slow positive wave (P2) of the segmental SCP, and the heterosegmental positive cord dorsum potential (HSP) were significantly suppressed by N2O, while the large negative (N1) component of the segmental SCP remained unchanged. A partial recovery of the CEP and HSP was observed during the 5 h of N2O anesthesia, while significant recovery of the P2 component of the SCP was not observed. The withdrawal from N2O following 5 h exposure caused an augmentation of the CEP (When compared to the control values). Re-exposure of rats to N2O again caused the suppression of these potentials as in the initial exposure. The results suggest that the phenomenon of tolerance to N2O in terms of evoked potentials develops within 5 h in the brain but not in the spinal cord.

Journal Article↗