I sopropylmine vanillinate (IV) given iv 5 , 10 mg/kg in anesthe tized rats produced a dose-dependent decrease in mean arterial pressure and a concomitant decrease in heart rate.In pithed rats IV was unable to shift the phenylephrine doserespon-se curve to the right, but prazosine caused 53-fold shift.No direct effect of vasodilation was shown by IV on rabbit aorta strips .The concentration-response curve of isoprenaline in isolated rat right atrium was competitively inhibited by IV and propranolol. pA2 value was 4.0 for IV and 8.2 for propranolol. In addition, 'IV depressed contractility & heart rate of isolated rat atria.These results suggest that the hypotensive action of IV may be related to the decrease of HR, inhibition of contractility and slight blocking of B-adrenergic receptor. However the mechanism underlying the hypotensive effect of IV is to be further studied.

Benzyltetrahydropalmatine ( BTHP ) which is a derivative of tet-rahydropalmatine, induced concentration-dependent decreases of the APA & dV/dt max and prolongation of conduction delay (CD) in toad sciatic neural action potential while it has little effect on APD.Bloocking action of Na+ -channel was measured with the dose required to produce 50% diminution of the value of APA, ie,EC50. EC50 of BTHP was 2.8 folds less than that of lidocaine and 11.9 folds more than that of quinidine, reflecting blocking action of Na+ -channel by BTHP, lidocaine, quinidine respectively.

IQ86034 (5.3).In addition, the blocking action of 4 isoquinoline derivatives on ?1 and ?2 adrenoceptors was similar to that of benzoquinolizine derivatives.

AIM　To investigate the effect of 4-aminopyridine (4-AP) on ion channels of myocytes. METHODS　L-type calcium channel and sodium channel currents were recorded in guinea pig single ventricular myocyte using whole-cell patch-clamp techniques. RESULTS　4-AP, 0.1, 0.5 and 1.0 mmol*L-1 were shown to inhibit L-type calcium channel currents (ICa,L) and sodium channel currents (INa) concentration-dependently. The percentage of inhibition were (11.6±1.7)%, (37.5±8.3)% and (54.5±6.9)% (P<0.01) respectively for ICa,L, and (22.1±14.3)% (P<0.05), (39.4±8.8)% and (62.3±6.8)% (P<0.01) respectively for INa. 4-AP 0.5 mmol*L-1 shifted the I-V curves of ICa,L and INa upwardly. CONCLUSION　4-AP blocked L-type calcium channel and sodium channels in guinea-pig ventricular myocytes concentration-dependently.

Objective To investigate the mechanism of electro-acupuncture (EA) at different frequency in improving synaptic plasticity injury in Alzheimer's disease(AD) rats, and to provide the theoretical basis for the clinical application of electro-acupuncture for the treatment of AD. Methods Ninety Wistar rats were randomly divided into normal group, model group, sham-operation group, and 2 Hz, 30 Hz, 50 Hz acupuncture groups, 15 rats in each group. AD rat model was established by injection of amyloid β1-42 (Aβ1-42) into the lateral ventricle. The rats in EA groups were treated with EA on Baihui and Shenshu acupoints at different frequencies (2, 30, 50 Hz). Learning and memory ability and space exploration ability of rats in each group were measured by Morris water maze test. The synaptic ultrastructure of hippocampus was observed by transmission electron microscopy. Nerve fibers were stained using Golgi techniques. The protein and phosphorylation levels of glycogen synthase kinase 3 beta (GSK-3β) in the brain tissues were detected by Western blotting method. Results(1) Compared with the normal group, the average escape latency time in the model group was significantly prolonged (P < 0.05), and the number of platform crossing was significantly reduced (P < 0.05), indicating that AD model had been established successfully. The average escape latency of rats in EA groups was significantly shortened and the frequency of platform crossing was increased as compared with those of the model group (P < 0.05). (2) The synaptic morphology of the hippocampus showed that the anterior membrane, posterior membrane and the interspace of the synapses in the model group were blurred, and the membrane structures of synapses were incomplete and dissolved. But the synaptic ultrastructures of the 3 EA groups were improved.(3) In the model group, the neurofibrillary tangles were found in the brain tissue, while the neurofibrillary tangles were relieved and the nerve fibers became clear in EA groups.(4) The levels of GSK-3β and GSK-3β(pTyr216) in the model group were significantly higher than those in the normal group (P < 0.05), whearas the GSK-3β(pSer9) level was significantly down-regulated (P < 0.05). In the EA groups, the levels of GSK-3βand GSK-3β(pTyr216) were down-regulated, while GSK-3β(pSer9) level was increased with the frequency of EA, and there was significant difference compared with the model group (P<0.05). (5) Compared with 2 Hz and 30 Hz EA groups, the number of plateau crossing, the average escape latency and the protein and phosphorylation levels of GSK-3β in 50 Hz EA group were significantly improved (P < 0.05). The improvement of synaptic morphology and neurofibrillary tangles of 50 Hz EA group was superior to that of the other 2 EA groups. Conclusion EA at different frequency can improve the learning and memory ability of AD rats, and the effect of 50 Hz is stronger. The therapeutic effect might be achieved by regulating the expression level of GSK-3βprotein and phosphorylation levels, which can improve synaptic plasticity damage of AD rats.

The effects of Arecoline (Are) on calcium mobilization were investigated. In isolated single ventricular myocyte of guinea pig, patch clamp whole cell recording techniques were used to record the current of L-type calcium channel and cytosolic Ca2+ level ([Ca2+]i) labeled with fluorescence probe Fluo-3/AM was measured under a laser scanning confocal microscope. Results revealed that Are (3-100 mumol/L) could inhibit L-type calcium current in a concentration-dependent manner and the value of IC50 was 33.73 mumol/L (n = 5). In the absence of extracellular calcium, the resting levels of [Ca2+]i was not affected by Are (n = 6, P > 0.05), but pretreatment with Are (30 mumol/L) could significantly inhibit the [Ca2+]i elevation induced by caffeine (10 mmol/L, n = 6, P < 0.01). It was concluded that Are could inhibit not only calcium influx through L-type calcium channel but also calcium release from sarcoplasmic reticulum.
Animals ; Arecoline ; pharmacology ; Biological Transport, Active ; Caffeine ; pharmacology ; Calcium ; metabolism ; Calcium Channels, L-Type ; drug effects ; metabolism ; Cell Separation ; Cholinergic Agonists ; pharmacology ; Guinea Pigs ; Heart Ventricles ; cytology ; Myocytes, Cardiac ; cytology ; metabolism ; Patch-Clamp Techniques ; Sarcoplasmic Reticulum ; metabolism

ObjectiveTo evaluate the effects of high intensity interval training (HIIT) on patients with type 2 diabetes mellitus (T2DM). MethodsFrom May to October, 2021, twelve patients with T2DM were recruited with internet. An HIIT exercise intervention based on WHO Guidelines on Physical Activity and Sedentary Behaviour and World Health Organization Family of International Classifications (WHO-FICs) was constructed. They received aerobic combined with resistance training in a multi-combination HIIT using whole-body exercise, 30 to 35 minutes a time, three times a week, for eight weeks. Before and after intervention, their blood glucose levels, lipid levels, pancreatic fat content and body composition were measured. ResultsOne cased was dropped. After intervention, the fasting glucose, 2-hour postprandial glucose, hemoglobin A1c, fasting serum insulin, insulin resistance index, serum total cholesterol, serum triglycerides, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, pancreatic fat content, body weight, body mass index, and body fat percentage improved (t > 2.258, P < 0.05). ConclusionHIIT exercise intervention based on the Guidelines and WHO-FICs could improve the related functions of patients with T2DM, such as blood glucose levels, blood lipid levels, pancreatic fat content and body composition, and reduce the consumption of hypoglycemic drugs.