Aim Baroreflex dysfunction is associated with a higher rate of sudden death after myocardial infarction （MI）. Ketanserin enhances baroreflex function in rats. The present work was designed to examine whether ketan- ...Aim Baroreflex dysfunction is associated with a higher rate of sudden death after myocardial infarction （MI）. Ketanserin enhances baroreflex function in rats. The present work was designed to examine whether ketan- serin improves the post-MI cardiac function and to explore the possible mechanism involved. Methods Spontane- ously hypertensive rats （SHR） were treated with ketanserin （0.3 mg · kg^-1 · d^-l）. Two weeks later, blood pres- sure and baroreflex function were measured, followed by a ligation of the left coronary artery. The expressions of ve- sicular acetylcholine transporter （VAChT） and α7 nicotinic acetylcholine receptor （α7-nAChR） in ischemic myo- cardium, angiogenesis, cardiac function, and left ventricular （LV） remodeling were evaluated subsequently. Re- sults Ketanserin significantly improved baroreflex sensitivity （0.62 ± 0. 21 vs. 0.34 ± 0. 12 ms/mmHg, P 〈 0.01 ） and vagal tonic activity （ heart rate changes in response to atropine, 54.8 ± 16.2 vs. 37.6 ± 13.4 b. p. m. , P 〈 0.01 ） without affecting the blood pressure or basic heart rate in SHR. Treatment of SHR with ketanserin promi- nently improved cardiac function and alleviated LV remodeling, as reflected by increases in the ejection fraction, fractional shortening, and LV systolic pressure as well as decreases in LV internal diameter and LV relative weight. The capillary density, vascular endothelial growth factor expression, and blood flow in the ischemic myocardium were significantly higher in the ketanserin-treated group. In addition, ketanserin markedly increased the expression of VAChT and α7-nAChR in ischemic myocardium. Conclusion Ketanserin improved post-MI cardiac function and angiogenesis in ischemic myocardium. The findings provide a mechanistic basis for restoring baroreflex function using ketanserin in the treatment of MI.展开更多
OBJECTIVE Microglia M1/M2 po⁃larization play pro-inflammatory and anti-inflam⁃matory roles,respectively,which is involved in memory decline.There is a close relationship between impaired baroreflex function and memory...OBJECTIVE Microglia M1/M2 po⁃larization play pro-inflammatory and anti-inflam⁃matory roles,respectively,which is involved in memory decline.There is a close relationship between impaired baroreflex function and memory impairment.The present study was designed to investigate whether arterial baroreflex deficiency induced by sinoaortic denervation(SAD)affected inflammation through modulation of M1/M2 polar⁃ization leading to the aggravation of learning and memory disorders in rats.METHODS Adult male SD rats were divided into four groups:the sham control,the SAD,the sham+scopolamine,the SAD+scopolamine.In another experiment,there were also four groups:the sham control,the SAD,the SAD+scopolamine and the SAD+scopolamine+ketanserin.All rats were examined for various behaviors using Morris water maze test,new object recognition test,and light dark shuttle test and Y maze test 4 weeks after sham or SAD surgery.CD16,CD206,IL-10,IL-6,IL-1βand TNF-αfrom hippocampus using Western blotting,immunofluorescence and turbidimetry.RESULTS Compared with the sham+scopol⁃amine,the SAD+scopolamine rats showed the reduced crossing times in Morris water maze test,the longer residence time in dark box during light dark shuttle test,and the decreased alterna⁃tion ratio in Y maze test.The level of CD206,IL-10,T-AOC and GSH was decreased,whereas CD16,IL-6,TNF-α,MDA was increased in the hippocampus of SAD+scopolamine rats.Addi⁃tionally,all the above changes were improved in the SAD+scopolamine+ketanserin rats when compared with the SAD+scopolamine.CONCLU⁃SION Arterial baroreflex dysfunction aggravates learning and memory disorders in rats,which may be related to the polarization of microglia.展开更多
OBJECTIVE Platelets play a major role in mediating inflammatory response.The present work was designed to investigate whether arterial baroreflex impairment induced by sinoaortic denervation(SAD)affect platelet activa...OBJECTIVE Platelets play a major role in mediating inflammatory response.The present work was designed to investigate whether arterial baroreflex impairment induced by sinoaortic denervation(SAD)affect platelet activation,leading to the exacerbation of cerebral cortex and hippocampus inflammation in rats.METHODS Adult male SD rats were divided into four groups:the sham control,the sinoaortic denervation(SAD),the sham+LPS,the SAD+LPS.In another experiment,there were also four groups:the sham control,the SAD,the SAD+LPS and the SAD+LPS+asprin.Four weeks after sham or SAD surgery,all rats were examined for the level of CD41,CD45,IL-1βand PF-4 in the cerebral cortex and hippocampus using immunofluorescence and ELISA.Blood platelet and leukocyte count,platelet microaggre⁃gation,expression of CD154 and CD62P on platelet surface and platelet-leukocyte aggregate level was detected by flow cytometry.RESULTS Compared with sham+LPS group,the in SAD+LPS group rats exhibited the high level of CD41,CD45,IL-1βand PF-4 in the cerebral cortex and hippocampus.Leukocyte count,platelet microag⁃gregation,expression of CD154 and CD62P on platelet surface and platelet-leukocyte aggregate level was increased,while blood platelet count was decreased in the SAD+LPS.Moreover,all the above changes were improved in the SAD+LPS+asprin group when compared with the SAD+LPS group.CONCLUSION Arterial baroreflex dysfunction exacerbates inflammation in the rat cerebral cortex and hippocampus,which is likely mediated by platelet.展开更多
文摘Aim Baroreflex dysfunction is associated with a higher rate of sudden death after myocardial infarction （MI）. Ketanserin enhances baroreflex function in rats. The present work was designed to examine whether ketan- serin improves the post-MI cardiac function and to explore the possible mechanism involved. Methods Spontane- ously hypertensive rats （SHR） were treated with ketanserin （0.3 mg · kg^-1 · d^-l）. Two weeks later, blood pres- sure and baroreflex function were measured, followed by a ligation of the left coronary artery. The expressions of ve- sicular acetylcholine transporter （VAChT） and α7 nicotinic acetylcholine receptor （α7-nAChR） in ischemic myo- cardium, angiogenesis, cardiac function, and left ventricular （LV） remodeling were evaluated subsequently. Re- sults Ketanserin significantly improved baroreflex sensitivity （0.62 ± 0. 21 vs. 0.34 ± 0. 12 ms/mmHg, P 〈 0.01 ） and vagal tonic activity （ heart rate changes in response to atropine, 54.8 ± 16.2 vs. 37.6 ± 13.4 b. p. m. , P 〈 0.01 ） without affecting the blood pressure or basic heart rate in SHR. Treatment of SHR with ketanserin promi- nently improved cardiac function and alleviated LV remodeling, as reflected by increases in the ejection fraction, fractional shortening, and LV systolic pressure as well as decreases in LV internal diameter and LV relative weight. The capillary density, vascular endothelial growth factor expression, and blood flow in the ischemic myocardium were significantly higher in the ketanserin-treated group. In addition, ketanserin markedly increased the expression of VAChT and α7-nAChR in ischemic myocardium. Conclusion Ketanserin improved post-MI cardiac function and angiogenesis in ischemic myocardium. The findings provide a mechanistic basis for restoring baroreflex function using ketanserin in the treatment of MI.
基金Natural Science Foundation of Shandong Province(ZR2017MH048)。
文摘OBJECTIVE Microglia M1/M2 po⁃larization play pro-inflammatory and anti-inflam⁃matory roles,respectively,which is involved in memory decline.There is a close relationship between impaired baroreflex function and memory impairment.The present study was designed to investigate whether arterial baroreflex deficiency induced by sinoaortic denervation(SAD)affected inflammation through modulation of M1/M2 polar⁃ization leading to the aggravation of learning and memory disorders in rats.METHODS Adult male SD rats were divided into four groups:the sham control,the SAD,the sham+scopolamine,the SAD+scopolamine.In another experiment,there were also four groups:the sham control,the SAD,the SAD+scopolamine and the SAD+scopolamine+ketanserin.All rats were examined for various behaviors using Morris water maze test,new object recognition test,and light dark shuttle test and Y maze test 4 weeks after sham or SAD surgery.CD16,CD206,IL-10,IL-6,IL-1βand TNF-αfrom hippocampus using Western blotting,immunofluorescence and turbidimetry.RESULTS Compared with the sham+scopol⁃amine,the SAD+scopolamine rats showed the reduced crossing times in Morris water maze test,the longer residence time in dark box during light dark shuttle test,and the decreased alterna⁃tion ratio in Y maze test.The level of CD206,IL-10,T-AOC and GSH was decreased,whereas CD16,IL-6,TNF-α,MDA was increased in the hippocampus of SAD+scopolamine rats.Addi⁃tionally,all the above changes were improved in the SAD+scopolamine+ketanserin rats when compared with the SAD+scopolamine.CONCLU⁃SION Arterial baroreflex dysfunction aggravates learning and memory disorders in rats,which may be related to the polarization of microglia.
基金Natural Science Foundation of Shandong Province(ZR2017MH048)。
文摘OBJECTIVE Platelets play a major role in mediating inflammatory response.The present work was designed to investigate whether arterial baroreflex impairment induced by sinoaortic denervation(SAD)affect platelet activation,leading to the exacerbation of cerebral cortex and hippocampus inflammation in rats.METHODS Adult male SD rats were divided into four groups:the sham control,the sinoaortic denervation(SAD),the sham+LPS,the SAD+LPS.In another experiment,there were also four groups:the sham control,the SAD,the SAD+LPS and the SAD+LPS+asprin.Four weeks after sham or SAD surgery,all rats were examined for the level of CD41,CD45,IL-1βand PF-4 in the cerebral cortex and hippocampus using immunofluorescence and ELISA.Blood platelet and leukocyte count,platelet microaggre⁃gation,expression of CD154 and CD62P on platelet surface and platelet-leukocyte aggregate level was detected by flow cytometry.RESULTS Compared with sham+LPS group,the in SAD+LPS group rats exhibited the high level of CD41,CD45,IL-1βand PF-4 in the cerebral cortex and hippocampus.Leukocyte count,platelet microag⁃gregation,expression of CD154 and CD62P on platelet surface and platelet-leukocyte aggregate level was increased,while blood platelet count was decreased in the SAD+LPS.Moreover,all the above changes were improved in the SAD+LPS+asprin group when compared with the SAD+LPS group.CONCLUSION Arterial baroreflex dysfunction exacerbates inflammation in the rat cerebral cortex and hippocampus,which is likely mediated by platelet.
