That gallamine causes tachycardia during general anesthesia is well known, but the efficacy of its anticholinergic action or an adrenergic beta blocking action remains to be determined. Twelve patients were subjected to this study, in which under halothane anesthesia small doses of propranolol. an adrenergic beta-blocker, was administered. In all cases bradycardia resulted and the greatest decrease was noted five minutes after intravenous injection of propranolol(0. 5 1. 0mg). At the height of bradycardia, gallamine 80 mg was administered intravenously. In all cases gallamine produced a significant increase of heart rate over the level before the injection of propranolol, but not so much as without propranolol pretreatment. But fifth minute values after propranolol expressed as 100 per cent, (per cent change in heart rate after propranolol followed by gallamine,) and after gallamine were similar effectively. This study suggested that gallamine-induced tachycardia is modified, but its anticholinergic action is not impaired by propranolol, and that gallamine-induced tachycardia is caused by anticholiaergic action of gallamine.
Anesthesia* ; Anesthesia, General ; Bradycardia ; Gallamine Triethiodide ; Halothane* ; Heart Rate ; Humans ; Injections, Intravenous ; Propranolol* ; Tachycardia*

In human volunteers, 0.25mg of atropine was given in divided doses(0.1mg and 0.15mg) with an interval of 15 minutes and 50 minutes When atropine was given with an interval of 15 minutes, the first dose (0.1mg) produced bardycardia and the second does caused slight increase of pulse rate which did not exceed the original rate. When atropine was given with an interval of 50 minutes, the first dose (0.1mg) produced bradycardia and the second dose marked increase of pulse rate which exceeded the original rate.
Atropine* ; Bradycardia ; Healthy Volunteers ; Heart Rate*

BACKGROUND: Recent evidences suggest that anesthetic action within the spinal cord is important in suppressing somatic responses to painful stimuli. Intrathecal endothelin-1 (ET-1) is known to have antinociceptive effect. The purpose of this experiment was to determine whether intrathecal ET-1 may influence the minimum alveolar concentration (MAC) of isoflurane in rats and access the role of the spinal cord as the sites of anesthetic action in blocking somatic responsiveness. METHODS: In Sprague-Dawley rats fitted with an indwelling intrathecal catheter, we determined the MAC of isoflurane using a tail-clamp technique as a painful stimulus, combined with end-tidal anesthetic sampling. In experiment 1, the control MAC was determined and changes of control MAC were observed after intrathecal ET-1 (4x10-2 nmol, 4x10-3 nmol) administration. In experiment 2, we observed the effects of L or N type Ca++ channel blocker such as verapamil (50 g) or W-conotoxin (0.5 g) on the MAC after measurement of the control MAC. In experiment 3, after measurement of the control MAC, ET-1 (10-2 nmol) was administered intrathecally and the MAC was determined again. Next, intrathecal verapamil (50 g) or W-conotoxin (0.5 g) was injected. After that, the MAC was determined again. RESULTS: In experiment 1, ET-1 decreased the MAC of isoflurane and its effect was sustained over 2 hours. In experiment 2, the MAC, determined following administration of verapamil or W-conotoxin, was not different from that of the control. In experiment 3, the MAC was decreased after ET-1 administration and then increased following injection of verapamil or W-conotoxin. CONCLUSIONS: These results suggested that ET-1, in relation to calcium, might play an important role in determining the MAC of isoflurane in the spinal cord.
Animals ; Calcium ; Catheters ; Endothelin-1* ; Isoflurane* ; Rats* ; Rats, Sprague-Dawley ; Spinal Cord ; Verapamil

A 17 year old girl underwent a surgery of spine fusion for a tuberculous cervical spine (C(4~5) ) under halothane-02 anesthesia. On the 1st postoperative day, sudden high fever(39.7 degrees C) with chillness and leukocytosis with eosinophilia were noted. On the following day, generalized jaundice, right hypochondralgia and slight hepatomegaly with marked impairment of liver function tests were noted. HB antigens were negative and there was no transfusion history of blood or blood products. About 2 months after operation, she was discharged with symptomatic improvement and almost normal laboratory data.
Anesthesia* ; Drug-Induced Liver Injury* ; Eosinophilia ; Female ; Halothane* ; Hepatomegaly ; Humans ; Jaundice ; Leukocytosis ; Liver Function Tests ; Spine

Succinylcholine has been reported to cause elevation of intraocular pressure(IOP.) IOP measurements, following single and mixed intravenous administration of succinylcholine and pancuronium, given immediately after thiopental, were made in 40 surgical patients, to assess the effect of pacuronium on the succinylcholine induced increase in IOP. The major findings of this study were as follows; 1) Tbiopental showed significant lowering effect on IOP. 2) A single intravenous injection of succinylcholine(1mg/kg) caused a slight rise of lOP. 3) A single intravenous injection of pancuronium(4mg) caused a slight decrease of IOP. 4) A mixed intravenous injection of succinylcholine and pancuronium increased the IOP more significantly than succinylcholine alone, This also means that pancuronium do not inhibit succinylcholine induced increase In IOP. 5) Tracheal intubation caused a rise of IOP significantly.
Administration, Intravenous* ; Humans ; Injections, Intravenous ; Intraocular Pressure* ; Intubation ; Pancuronium* ; Succinylcholine* ; Thiopental

Effect of succinyleholine on the intra-ocular pressure was assessed in 29 surgical patients. After pretreatment of thiopental in a dose to induce the loss of eye-lid reflex the intra- ocular pressure was measured following intravenous administrdtion of succinylcholine. The following were the results. 1) Thiopental showed a significant lowering effect on the intra-ocular pressure. 2) A small dose(0.5mg/kg) of succinylcholine, given immediately after thiopental restored the intra-ocular pressure to the preanesthetic level. 3) A large dose(1.0~2.0mg/kg) of succinylcholine, administered immediately after thiopental, sustained the intra-ocular pressure below the preanesthetic leve. 4) Teacheal intubation caused a rise of the intra-ocular pressure above the preanesthetic level, more significantly than that of succinyleholine. 5) Suecinylcholine, in a large dose, showed a depressing effect on elevation of the intraocular pressure induced by tracheal intubation.
Humans ; Intraocular Pressure ; Intubation ; Reflex ; Succinylcholine* ; Thiopental

No abstract available.
Anesthesia* ; Neurosurgery*

The decreasing effect on the heart rate of propranolol, a beta-adrenergic blocker, is well known. This effect of propranolol was studied in conscious and anesthetized men. Propranolol in small doses (0.5 mg and l.0 mg) was given intravenously to fifteen conscious and ten halothane anesthetized men. The heart rate showed definite decrease in all cases, the effect being more pronounced in the halothane anesthetized group than in the conscious group. The bradycardia action mechanism of propranolol is different from that of small doses of the belladona alkaloids.
Alkaloids ; Anesthesia* ; Bradycardia ; Halothane* ; Heart Rate* ; Heart* ; Humans ; Male ; Propranolol*

In order to observe the effect on cardiovascular depression due to ether, halothane or penthrane anesthesia with pretreatment of propranolol (1mg) , change in the blood pressure and pulse rate were measured after intravenous administration of atropine(0.5mg), ephedrine(20mg) or aramine(2mg) to healthy volunteers. The results were as follos, 1) In conscious patients, intravenous administration of propranolol(1mg) caused a statistically significant decrease in pulse rate but no significant change in the blood pressure. 2) The atropine group showed that blood pressure increased by 33/23(p<0.01), 15/13(p<0.01) and 3/4(NS) mmHg, and pulse rate also increased by 20(p<0.01), 24(p<0.05), 11(p<0.05) per min. respectively during ether, halothane and penthrane anesthesia. 3) The ephedrine group showed that blood pressure decreased by 5/0(NS) during ether anesthesia, and increased by 27/17(p<0.01) and 30/15(p<0.01) mmHg during halothane and penthrane anesthesia respectively. Pulse rate decreased by 7(p<0.05) per min. during ether anesthesia but showed no significant change during halothane and Penthrane anesthesia. 4) The aramine group showed that blood pressure increased by 70/34(p<0.01), 29/19(p<0.01) and 28/19Ip<0.001) mmHg during ether, halothane and Penthrane anesthesia respectively. Pulse rate increased by 7(NS) per min. during ether anesthesia and decreased by 8(p<0.05) per min. during halothane and Penthrane anesthesia respectively. 5) The above results have shown that atropine caused effective correction of the cardiovascular depression induced by ether, halothane and Penthrane anesthesia with pretreatment of propranolol. Ephedrine showed futher depression and aramine effected elevation of the blood pressure.
Administration, Intravenous ; Anesthesia* ; Atropine ; Blood Pressure ; Depression ; Ephedrine ; Ether* ; Halothane* ; Healthy Volunteers ; Heart Rate* ; Humans ; Metaraminol ; Methoxyflurane* ; Propranolol*

It is well known that a small dose of atropine produces a significant decrease in the heart rate in normal human volunteers. The authors administered a small dose of atropine intravenously to thirteen halothane anesthetized and sixteen comatose patients, and compared its effect on the heart rate in both groups. The results are as follows: 1) In the halothane anesthetized patients, atropine(0.25mg) produced a significant increase in the heart rate. 2) In the comatose patients, atropine(0.25mg) also produced an increase in the heart rate, but the increase was less significant than that in the anesthetized patient. 3) Under halothane anesthesia and in the comatose state, the absence of bradycardia after atropine may suggest the fact that the sympathetic ganglion is already depressed in both states.
Anesthesia ; Atropine* ; Bradycardia ; Coma ; Ganglia, Sympathetic ; Halothane ; Healthy Volunteers ; Heart Rate* ; Heart* ; Humans