Search

To clarify the role of autonomic nervous function in motion sickness, the effect of agents that act on the autonomic nervous system on the motion stimuli-induced emesis was studied in two strains of Suncus murinus (Jic:SUN-Her and Jic:SUN-Ler) with congenitally different sensitivity to veratrine sulfate. We demonstrated significant differences between the two strains in sensitivity to motion stimuli. Isoproterenol (2.5 mg kg(-1), s.c.) significantly prolonged the latency to the first emetic episode induced by motion stimuli and significantly decreased the number of emetic episodes in Jic:SUN-Her suncus. Hexamethoium (2.0 mg kg(-1), s.c.) tended to shorten the latency in Jic:SUN-Ler. Acetylcholine (1.2 mg kg(-1), s.c.) enhanced the emetic response in Jic:SUN-Ler, but atropine (4.0 mg kg(-1), s.c.) suppressed motion stimuli-induced emetic response in Jic:SUN-Her. These results suggest that the predominance of parasympathetic nervous activity is relevant to the enhancement of motion stimuli-induced emetic response, whereas the predominance of sympathetic nervous activity suppresses motion stimuli-induced emetic response. Norepinephrine (0.8 mg kg(-1), s.c.) enhanced motion stimuli-induced emesis contrary to isoproterenol in Jic:SUN-Ler although both drugs are adrenergic agents. However, atropine pretreatment (4.0 mg kg(-1), s.c.) inhibits norepinephrine-induced emetic response. It was considered that norepinephrine-induced emetic response might be dependent on a secondary increase of parasympathetic nervous activity due to bororeflex. Moreover, the different emetic response in Jic:SUN-Her and Jic:SUN-Ler suncus to motion stimuli and drug administration mentioned above indicated that different participation of autonomic nervous activity and/or afferent information from the baroreceptor in the emetic response may exist between these animal groups.

Study Objectives: To evaluate the effects of unilateral stellate ganglion blockade on left ventricular function., Design: Prospective cohort of patients with chronic regional pain syndrome type I and II of the upper extremity requiring therapeutic stellate ganglion blockade., Setting: University-affiliated hospital., Patients: Fifteen adult ASA physical status I and II patients with the diagnosis of chronic regional pain syndrome type I and II of the arm were studied. Right stellate ganglion block was performed in nine subjects and a left in six., Interventions: Stellate ganglion block was performed with 10 mL of 1% plain Xylocaine. Transthoracic echocardiograms were performed immediately prior and 30 min following the block., Measurements: Heart rate and blood pressure were monitored at regular intervals. Global systolic function was determined by calculating ejection fraction. Regional systolic motion was evaluated on the short axis and four-chamber views using the American Society of Echocardiography criteria. Diastolic function was assessed with pulsed-wave Doppler of the left ventricular outflow tract and the mitral valve. Data collected included isovolumic relaxation time and early and atrial velocity patterns., Main Results: A successful stellate ganglion block was achieved in all patients. Blood pressure and heart rate were not significantly different during data collection. Patients who underwent a right stellate ganglion block showed no significant differences in systolic or diastolic function. Following a left stellate ganglion block, global and regional systolic function remained unchanged. Isovolumic relaxation time was increased but did not reach statistical significance (80 +/- 13 ms to 88 +/- 9 ms; p = 0.09). Left ventricular end-diastolic (LVEDV) and end-systolic volumes (LVESV) were significantly increased (LVEDV from 73 +/- 9 mL to 100 +/- 9 mL, p < 0.02; LVESV from 31 +/- 4 mL to 37 +/- 4 mL, p < 0.03)., Conclusions: In patients without cardiovascular disease, unilateral denervation of the left ventricle after stellate ganglion block produces no clinical deleterious effects on left ventricular function.

Purpose: Infrarenal aortic cross-clamping performed during vascular reconstructive procedures is often accompanied by systemic supraclamp hypertension. Much of the disease and death that attend aortic cross-clamping centers around hypertension. Many different strategies have been developed to attenuate intraoperative hypertension, and a host of pharmacologic agents are regularly used to lessen the heart-related, cerebral, and systemic effects of clamp-induced hypertension. This study was performed to evaluate two such strategies; the intravenous administration of either trimethaphan camsylate or nitroprusside., Methods: We used a highly controllable and reproducible model of aortic cross-clamping in which we have previously shown the hypertension associated with clamping to be an active process mediated by means of a reflex arc. Ten dogs, five treated with nitroprusside (NP group) and five treated with trimethaphan camsylate (TC group), underwent 90 minutes of aortic cross-clamping. During this 90-minute period each group received 30 minutes of antihypertensive therapy., Results: Control mean arterial pressure +/- SEM was 80 +/- 5 mm Hg for both groups and increased to 140 +/- 5 mm Hg with clamp application. With antihypertensive treatment the elevation in mean arterial pressure produced by cross-clamping was reduced to preclamp levels in the TC group and only partially (52%) in the NP group, despite very high doses of nitroprusside. Cardiac output (CO) increased in the NP group by 115% and decreased by 36% in the TC group. This increase in CO translates into a large (101%) increase in cardiac minute work for the NP group., Conclusions: The attenuation of clamp-induced hypertension by nitroprusside is associated with a dramatic increase in CO and cardiac work whereas the use of trimethaphan camsylate is not. The use of this ganglionic blocker may be more appropriate in this setting.

Patients suffering from the long QT syndrome (LQTS) are threatened by sudden arrhythmic cardiac death. This case report describes a new therapeutic approach to ventricular tachyarrhythmias refractory to oral pharmacological treatment (propranolol + phenytoin) using a drug-reservoir-pump system for the pharmacologic blockage of the left stellate ganglion.

Atropine, in combination with 1 of 6 other drugs, was tested in mice for the ability to prevent death by an otherwise lethal dose of the cholinesterase inhibitor, physostigmine. The atropine dose (4 mg/kg, i.p.) was kept constant, while the dose of the other drug in the pair was tested in 5 geometrically spaced doses, ranging down to 1/16 of the maximum dose (which caused no gross behavioral signs). Atropine alone saved 20% of the mice. The combination of atropine and benactyzine saved 100% of the mice at all 5 doses of benactyzine; similar complete protection was afforded by the combination of atropine and the largest dose of an oxime, TMB4 (15 mg/kg). Over 80% survivals were achieved with the larger doses of atropine combinations involving hexamethonium, mecamylamine, and diazepam. No enhanced protection occurred with atropine combinations with the oxime, 2-PAM. The toxicity of the effective combinations, when used in high doses without physostigmine challenge, revealed that deaths occurred over a narrow range of doses of all combinations except atropine/diazepam. An additive toxic effect of atropine was suggested with its combinations with TMB4, mecamylamine, and diazepam, whereas no additive toxicity occurred with combinations involving hexamethonium or benactyzine (i.e., the LD50 of the combinations was about the same as for hexamethonium or benzactyzine alone). The combinations with the best therapeutic safety ratio were with diazepam (no deaths at a dose 10 times that which saved 100% of mice) and benactyzine (no deaths at a more than 50-fold dose).

As the physiology of deliberate hypotension has been unravelled, and as each new pharmacological agent has become available which either depresses or blocks peripheral vascular tone, depresses myocardial performance, or interferes with the conducting tissues within the myocardium, its possible incorporation into the armamentarium of the anaesthetist who offers induced hypotension has been considered. The result has been a sequence of variations in technique of characteristically recognizable vintage. No matter how the condition of induced hypotension is produced, there is usually vasodilatation, and the characteristic disturbance in physiology is of a loss of postural reactivity in the cardiovascular system. Important lessons have been learned concerning the management of shock states. Though it is difficult to evaluate the morbidity of deliberate induced hypotension, and terms such as "physiological trespass" have been used by its antagonists, it would appear that a well-considered and skilfully managed controlled hypotension is no more of a physiological trespass than anaesthesia, nor indeed than the trespass of the surgeon's knife itself.