{"title":"l - name治疗小鼠的动态心血管活动","authors":"Jong Y. Lee, S. Azar","doi":"10.2174/1876526201104010023","DOIUrl":null,"url":null,"abstract":"Objective: High blood pressure (BP) is a dominant risk factor in cardiovascular diseases. An experimental model of nitric oxide synthase (NOS) inhibitor induced hypertension was developed to study some etiologic mechanisms in cardiovascular parameters. Methods: Cardiovascular rhythm characteristics were documented in mice following the N-omega-nitro-L-arginine- methyl-ester (L-NAME)-treatment (Rx). Radio-telemetered BP, heart rate (HR), and locomotor activity (LA) were measured every 4 min for 5 days before and for 14 days after Rx. Data was converted into an hourly average and analyzed by the linear least square rhythmometry. Results: L-NAME-Rx increased systolic BP (SBP) significantly without significant changes in diastolic BP and markedly reduced HR: SBP (mm Hg) 143.4 ± 0.6 versus 148.9 ± 0.4, P <0.0001; HR (beat/min): 552.13 ± 2.7 vs. 481 ± 1.8, P <0.0001, with markedly depleted amplitude. SBP variations were mainly during the night time, while HR variations were almost every time-point comparison throughout the 24-h span. Although the overall LA was not significantly changed with L-NAME-Rx, time-point depleted LA was noted, especially when the light was off at 18:00 hour through midnight (P <0.0001), while an opposite result was observed at noon with significantly increased LA in this nocturnal animal (P <0.005), with markedly decreased amplitude (P <0.01). Interestingly, we observe reduced HR with L-NAME-Rx contradicted to other reports. Conclusion: The results suggest that the NOS blockade may impair cardiovascular autonomic adaptations and arterial baroreflex integration, resulting in an increased vascular tone during the systole, but not an end diastole in the relaxed cardiac autonomic tonus.","PeriodicalId":38918,"journal":{"name":"Open Hypertension Journal","volume":"4 1","pages":"23-32"},"PeriodicalIF":0.0000,"publicationDate":"2011-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"1","resultStr":"{\"title\":\"Ambulatory Cardiovascular Activities in L-NAME-Treated Mice\",\"authors\":\"Jong Y. Lee, S. Azar\",\"doi\":\"10.2174/1876526201104010023\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Objective: High blood pressure (BP) is a dominant risk factor in cardiovascular diseases. An experimental model of nitric oxide synthase (NOS) inhibitor induced hypertension was developed to study some etiologic mechanisms in cardiovascular parameters. Methods: Cardiovascular rhythm characteristics were documented in mice following the N-omega-nitro-L-arginine- methyl-ester (L-NAME)-treatment (Rx). Radio-telemetered BP, heart rate (HR), and locomotor activity (LA) were measured every 4 min for 5 days before and for 14 days after Rx. Data was converted into an hourly average and analyzed by the linear least square rhythmometry. Results: L-NAME-Rx increased systolic BP (SBP) significantly without significant changes in diastolic BP and markedly reduced HR: SBP (mm Hg) 143.4 ± 0.6 versus 148.9 ± 0.4, P <0.0001; HR (beat/min): 552.13 ± 2.7 vs. 481 ± 1.8, P <0.0001, with markedly depleted amplitude. SBP variations were mainly during the night time, while HR variations were almost every time-point comparison throughout the 24-h span. Although the overall LA was not significantly changed with L-NAME-Rx, time-point depleted LA was noted, especially when the light was off at 18:00 hour through midnight (P <0.0001), while an opposite result was observed at noon with significantly increased LA in this nocturnal animal (P <0.005), with markedly decreased amplitude (P <0.01). Interestingly, we observe reduced HR with L-NAME-Rx contradicted to other reports. Conclusion: The results suggest that the NOS blockade may impair cardiovascular autonomic adaptations and arterial baroreflex integration, resulting in an increased vascular tone during the systole, but not an end diastole in the relaxed cardiac autonomic tonus.\",\"PeriodicalId\":38918,\"journal\":{\"name\":\"Open Hypertension Journal\",\"volume\":\"4 1\",\"pages\":\"23-32\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2011-11-04\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"1\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Open Hypertension Journal\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.2174/1876526201104010023\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Open Hypertension Journal","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2174/1876526201104010023","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 1
摘要
目的:高血压(BP)是心血管疾病的主要危险因素。建立一氧化氮合酶(NOS)抑制剂诱导高血压的实验模型,探讨其心血管参数的发病机制。方法:用n -omega-硝基- l-精氨酸-甲基酯(L-NAME)治疗(Rx)后记录小鼠的心血管节律特征。在服药前5天和服药后14天,每隔4分钟测一次血压、心率(HR)和运动活动(LA)。数据被转换成每小时的平均值,并用线性最小二乘节律法进行分析。结果:L-NAME-Rx可显著提高收缩压(SBP),但舒张压无明显变化,并可显著降低HR:收缩压(mm Hg) 143.4±0.6 vs 148.9±0.4,P <0.0001;HR(心跳/分钟):552.13±2.7 vs. 481±1.8,P <0.0001,幅度明显降低。收缩压变化主要发生在夜间,而心率变化几乎发生在整个24小时跨度的每个时间点。虽然L-NAME-Rx对整体LA的影响不显著,但时间点上的LA明显减少,尤其是在18:00至午夜熄灯时(P <0.0001),而在中午,这种夜行动物的LA显著增加(P <0.005),幅度明显降低(P <0.01)。有趣的是,我们观察到L-NAME-Rx降低了HR,这与其他报告相矛盾。结论:NOS阻断可能损害心血管自主神经适应和动脉压力反射整合,导致收缩期血管张力增加,而舒张末期血管张力松弛。
Ambulatory Cardiovascular Activities in L-NAME-Treated Mice
Objective: High blood pressure (BP) is a dominant risk factor in cardiovascular diseases. An experimental model of nitric oxide synthase (NOS) inhibitor induced hypertension was developed to study some etiologic mechanisms in cardiovascular parameters. Methods: Cardiovascular rhythm characteristics were documented in mice following the N-omega-nitro-L-arginine- methyl-ester (L-NAME)-treatment (Rx). Radio-telemetered BP, heart rate (HR), and locomotor activity (LA) were measured every 4 min for 5 days before and for 14 days after Rx. Data was converted into an hourly average and analyzed by the linear least square rhythmometry. Results: L-NAME-Rx increased systolic BP (SBP) significantly without significant changes in diastolic BP and markedly reduced HR: SBP (mm Hg) 143.4 ± 0.6 versus 148.9 ± 0.4, P <0.0001; HR (beat/min): 552.13 ± 2.7 vs. 481 ± 1.8, P <0.0001, with markedly depleted amplitude. SBP variations were mainly during the night time, while HR variations were almost every time-point comparison throughout the 24-h span. Although the overall LA was not significantly changed with L-NAME-Rx, time-point depleted LA was noted, especially when the light was off at 18:00 hour through midnight (P <0.0001), while an opposite result was observed at noon with significantly increased LA in this nocturnal animal (P <0.005), with markedly decreased amplitude (P <0.01). Interestingly, we observe reduced HR with L-NAME-Rx contradicted to other reports. Conclusion: The results suggest that the NOS blockade may impair cardiovascular autonomic adaptations and arterial baroreflex integration, resulting in an increased vascular tone during the systole, but not an end diastole in the relaxed cardiac autonomic tonus.