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1.
Article in Chinese | WPRIM | ID: wpr-977826

ABSTRACT

@#Objective To observe the effect of Xiaoyingqiangjitang on the ultrastructure of motor end-plate of skeletal muscle in rats with hyperthyroid myopathy, and changes of acetylcholin esterase (AchE).Methods The 36 healthy female Wistar rats were randomly divided into the normal control group (n=6), and model group, Chinese medicine treated group and saline control group (all n=10). All animals in the model group, Chinese medicine treated group and saline control group were treated with group given L-thyroxine intraperitoneal injection for 42 days to establish the animal model of hyperthyroid myopathy. The animals of the Chinese medicine treated group were treated with Xiaoyngqiangjitang for 30 days after L-thyroxine intraperitoneal injection. The enzyme activity of AchE and ultrastructure of motor end-plate were observed by light and electron microscopes.Results The enzyme activity and content in the group of hyperthyroid myopathy was decreased, the reaction products of AchE located in synapse became weaker and distributed heterogeneously, the junction infolding of motor end-plate became smaller and shorter, the mitochondria in axon terminal became vacuolated. After given Chinese medicine, the enzyme activity and content increased, the junction folding, the mitochondria showed normal ultrastructural appearance.Conclusion Xiaoyingqiangjitang can improve the function of skeletal muscle in hyperthyroid myopathy by recovering the enzyme activity of AchE and ultrastructures of motor end-plate.

2.
Arq. bras. cardiol ; Arq. bras. cardiol;65(1): 17-22, Jul. 1995. ilus, tab
Article in Portuguese | LILACS | ID: lil-319675

ABSTRACT

PURPOSE--To investigate the sensitivity of the muscarinic receptors to acetylcholine (Ach) and to vagal stimulation in rats during the acute and the chronic phases of myocardial infarction (MI). METHODS--Male albino rats were submitted to ligature of the descending anterior branches of the left coronary artery to produce MI. Control rats (Con) were submitted to a sham surgery. The animals were studied 1-3 days (acute phase) or 30 days (chronic phase) after surgery. Under anesthesia (ketamine+xylazine) the right vagus nerve was isolated at the neck and stimulated with suprathreshold pulses (2ms, 1-64Hz). Atrial and ventricular rates were measured in the ECG recording. Dose-response curve to Ach (5-80 micrograms) was studied in the isolated hearts perfused according to the Langendorftechnique. Atrial and ventricular rates were evaluated through the surface electrogram recording. The left ventricular pressure was measured with an intraventricular balloon. RESULTS--Basal heart rate in the anesthetized animals was similar in Con and MI rats. The vagal stimulation produced a frequency dependent reduction of the heart rate. This reduction was less intense in the MI groups to stimulation rates of 32 and 64Hz. It was not observed any difference in the sensitivity of sinus and AV nodes to exogenous Ach in infarcted hearts. The reduction of the systolic pressure obtained after Ach administration to the hearts paced artificially (3.3Hz) was similar in MI and Con hearts. CONCLUSION--MI hearts were less sensitive to vagal stimulation than Con hearts. Since the in vitro effects of Ach remained unchanged after infarction, these results suggest an impairment of the cardiac neuroeffector vagal synapse. This may contribute to a less efficient control of the heart rate by the parasympathetic pathway in infarcted individuals.


Objetivo − Determinar a sensibilidade dos receptores muscarínicos à acetilcolina (Ach) e ao estímulo vagal em ratos nas fases aguda e crônica do infarto do miocárdio (IM). Métodos −Ratos albinos machos submetidos à ligadura dos ramos descendentes anteriores da artéria coronária esquerda para produção do IM. Os ratos controles (Con) foram submetidos a cirurgia fictícia. Grupos de animais foram estudados 1-3 (fase aguda) ou 30 dias (fase crônica) após a cirurgia. Sob anestesia (ketamina + xilazina), o nervo vago direito era isolado na altura do pescoço e estimulado com pulsos supralimiares (2ms) nas freqüências de 1 a 64Hz. A redução das freqüências atrial e ventricular foi analisada pelo registro contínuo do ECG. A sensibilidade dos marcapassos sinusal e AV à Ach (5-80µg) foi estudada em corações isolados, perfundidos pela técnica de Langendorf, registrando-se o eletrograma de superfície e a pressão ventricular desenvolvida em sístoles isovolúmicas. Resultados − A freqüência cardíaca (FC) basal sob anestesia foi similar nos animais Con e IM. A estimulação vagal produziu redução progressiva da freqüência sinusal em todos os grupos. Nos animais com IM, entretanto, a redução de FC foi significantemente menor (p<0,05) na estimulação de 32 e 64Hz. Não se detectou nenhuma diferença na sensibilidade dos nódulos cardíacos ao efeito da Ach in vitro. Além disso, a redução da pressão desenvolvida pelo ventrículo esquerdo, sob efeito de Ach nos corações estimulados artificialmente (3,3Hz), foi similar nos corações Con e IM. Conclusão − Os corações com IM foram sensíveis à descarga vagal. Uma vez que não se detectou alteração ao nível dos receptores muscaríneos pós-juncionais, estes dados sugerem existir alteração da sinapse neuro-efetora vagal cardíaca. Isso poderia contribuir para reduzir a participação do controle vagal sobre a FC após o infarto


Subject(s)
Animals , Male , Rats , Vagus Nerve , Myocardial Infarction/physiopathology , Vagus Nerve , Acetylcholine , Electric Stimulation , Hemodynamics/drug effects , Rats, Inbred Strains
3.
Article in Chinese | WPRIM | ID: wpr-550057

ABSTRACT

The experiments of rabbit mydriasis & isolated cat ciliare muscle paralysis of atropine Methobromide (AMB) have demonstrated that : AMB has much larger mydriasis effect. It effects faster than Atropine Sulfate, Homatropine & Tropinexamide in acetylcholin -induced ciliare muscle contraction. The combined-force of AMB on ciliare muscle is less than Atropine & Homatropine, but a little larger than Tropinexamide. There fore AMB is a rapid & short-time mydriasis agent & ciliare muscle paralysis agent.

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