1.The intervention effect of tanshinone on electrophysiological abnormality of hypertrophic myocardium
Zhouhua WANG ; Zhi ZHANG ; Qiangsheng LIANG ; Liping SUN ; Cuntai ZHENG
Chinese Journal of Emergency Medicine 2008;17(10):1039-1044
Objective To study the intervention effect of tanshinone on electrophysiological abnormality of hypertrophic cardicoyte in order to illuminate the underlying mechanism of tanshinone in preventing the arrhythmia induced by myocardial hypertrophy. Method Twenty-week-rid SD rats (200~250 g) were divided into 4 groups (8 in each group) randomly. Of 4 groups, rats of three groups were operated on by a procedure of 'one kidney one clamp' to make renal artery constriction. The rest group served as sham operation group (control group). When the blood pressure increased,rats of operation groups were divided into tanshinone group, captopril group and hyper-trophic group. The effects of tanshinoe and captopril were observed and compared on the action potential duration (APD),L-type calcium current (ICa, L) and transient outward potassium current (Ito) density in cellular membrane of hypertrophic myocardium by using patch clamp and intra-cellular calcium survey technique. Results The blood pressure in operation groups was obviously higher than that in sham-operation group (P<0.01), but there was no difference between operation groups (P>0.05). The ratio of ventricle weight to body weight (VW/BW) was much higher in hypertrophic group than in control group (P<0.01), and it significantly decreased after interven-tion with tanshinone or captopril (P<0.01). Compared with hypertrophic group, tanshinone markedly shortened the prolongation of action potential duration (P<0.01), decreased membrane capacity and peak amplitude of ICa,L(P<0.01), but had no effect on the density of ICa,L. Tanshinone also significantly increased Ito current density and peak amplitude, which were completely different from hypertrophic group (P<0.05). There were similar results foundin captopril intervention. Conclusions Tanshinone could reduce calcium influx and resume the activity of ho ion channels, and thus shorten the first phase and the plateau phase of repolarization and decrease the prolongation of APD in hypertrophic cadiocyte. So tanshinone can prevent the onset of arrhythmia attributed to the myocardial hypertrophy.
2.Application and prospect of reconstructing bladder micturition reflex in neurogenic bladder after spinal cord injury
Lifen ZHAN ; Kun AI ; Xuejiu ZENG ; Rouyun LIANG ; Qiangsheng DING ; Hong ZHANG
Chinese Journal of Tissue Engineering Research 2024;28(18):2925-2931
BACKGROUND:The dysfunction of bladder function caused by spinal cord injury is a difficult point in clinical treatment and a hot spot in research.Repairing the injured spinal cord and remodeling the bladder micturition reflex pathway are the fundamental treatment methods. OBJECTIVE:To summarize the reconstruction of the bladder innervation pathway after spinal cord transection injury and its related influencing factors. METHODS:The relevant literature concerning the reconstruction of bladder micturition reflex,neurogenic bladder and urinary reflex and spinal cord repair was retrieved on CNKI,WanFang Data,PubMed and Web of Science.Chinese and English search terms were"neurogenic bladder;spinal cord injury;micturition reflex;spinal cord repair". RESULTS AND CONCLUSION:In the process of reconstructing the bladder micturition reflex,there are many factors involved,including the repair and reconstruction of the injured spinal cord,the remodeling of micturition center,the changes of bladder tissue and substances and hormones in and out of the body.In this process,there are mainly the following problems:(1)As a complex process,there are many sites involved in the reconstruction of the micturition reflex,so the main sites of action can be selected for in-depth study,so as to break through the doubts existing in the reconstruction of the micturition reflex pathway.(2)The mechanism of the normal micturition reflex is complex.After spinal cord transection injury,whether the central nucleus mass controlling or participating in the micturition reflex is compensated and the corresponding compensatory mechanism needs to be further investigated.(3)Information communication between the center and the bladder is interrupted after spinal cord transection injury.Whether there is a direct information connection between the center and the bladder remains to be further investigated.(4)The relationship between reconstructing micturition reflex and body fluid after spinal cord transection injury needs further study.In the reconstruction of the bladder micturition reflex,the key treatment is to promote spinal cord repair,nerve reflex reconstruction,substance metabolism and bladder tissue structure adjustment through intervention.Chinese medicine and Western medicine have their methods.
3.Electroacupuncture improves morphological structure of the detrusor muscle and bladder function in rats with spinal cord injury
Ziyuan JIAO ; Yue ZHUO ; Roujun LIANG ; Qiangsheng DING ; Xuejiu ZENG ; Ming XU ; Hong ZHANG
Chinese Journal of Tissue Engineering Research 2024;28(28):4484-4490
BACKGROUND:Numerous clinical and basic studies have shown that electroacupuncture can improve the function of neurogenic bladder after suprasacral spinal cord injury. OBJECTIVE:To observe the effects of electroacupuncture on bladder function and connective tissue growth factor expression in rats with suprasacral spinal cord injury. METHODS:Forty-eight female Sprague-Dawley rats were randomly divided into four groups(n=12 per group):the blank group did not receive any treatment;the sham-operated group only exposed the T8 subvertebral spinal cord;in the model group established,a T8 subvertebral spinal cord transection injury model was established;in the electroacupuncture group,the T8 subvertebral spinal cord transection injury model was established,and electroacupuncture intervention at Ciliao(BL32),Zhongji(RN03)and Sanyinjiao(SP06)was given at 19 days after modeling,20 minutes once a day,for 10 continuous days.After the intervention,the relevant indicators were detected. RESULTS AND CONCLUSION:Urodynamics:Compared with the blank group,the leakage point pressure,maximum bladder capacity and maximum bladder pressure of rats in the model group increased(P<0.05).Compared with the model group,the leakage point pressure,maximum bladder capacity and maximum bladder pressure of rats in the electroacupuncture group decreased(P<0.05).Hematoxylin-eosin staining:Compared with the blank group,the bladder epithelial cells in the model group were arranged in a disordered manner,the lamina propria was destroyed,the detrusor muscle bundles were hypertrophied,the muscle fibers were arranged in a disordered manner,and the tissue edema was obvious.Compared with the model group,the bladder epithelial cells in the electroacupuncture group were arranged in a regular and orderly manner,and the degree of bladder fibrosis and tissue edema was relatively reduced.Masson staining:The degree of bladder detrusor muscle fibrosis was severe in the model group and it was lighter in the electroacupuncture group than in the model group.Transmission electron microscopy:Mitochondria in the bladder tissue in the model group were swollen and vacuolated,the morphology of the detrusor muscle was twisted and distorted,and the muscle gap was widened.Compared with the model group,mitochondria in the electroacupuncture group had a slightly clearer contour and were less vacuolated,and the muscle gap was narrowed.Western blot detection:The protein expression of connective tissue growth factor in the detrusor muscle of the bladder was elevated in the model group compared with the blank group(P<0.05).Compared with the model group,the protein expression of connective tissue growth factor in the bladder detrusor muscle was decreased in the electroacupuncture group(P<0.05).To conclude,electroacupuncture at Ciliao(BL32),Zhongji(RN03)and Sanyinjiao(SP06)acupoints can improve the morphology,structure and function of the bladder in rats with suprasacral spinal cord injury,and the mechanism of action may be related to the down-regulation of connective tissue growth factor protein expression in the detrusor muscle.