{"title":"健康受试者对低血糖刺激自主心血管和呼吸反应的瞬时时间过程","authors":"S. Carrasco-Sosa, A. Guillén-Mandujano","doi":"10.23919/CinC49843.2019.9005662","DOIUrl":null,"url":null,"abstract":"In 13 healthy subjects we assessed the effect of hypoglycemia (HG) provoked by insulin on: R-R intervals (RR), systolic pressure (SP), diastolic pressure (DP), pulse pressure (PP), respiratory frequency (RF) and tidal volume (V<inf>T</inf>) 5-min time series; the instantaneous time courses of their low-frequency (LF<inf>RR</inf>, LF<inf>SP</inf>, LF<inf>DP</inf>, LF<inf>PP</inf>), high-frequency (HF<inf>RR</inf>, HF<inf>Res</inf>) powers and their respective central frequencies (cfLF<inf>RR</inf>, cfLF<inf>SP</inf>, cfLF<inf>DP</inf>, cfLF<inf>PP</inf>), computed by a time-frequency distribution; instantaneous baroreflex (BRS) and respiratory sinus arrhythmia sensitivities (RSAS), obtained by alpha index, and their coherences (cBRS and cRSAS) by cross time-frequency analysis. Peak HG (2.7±0.3 mmol/l) induced: 1) decreases (p<0.03) in five 1-min epoch means (EM) of HF<inf>RR</inf>, LF<inf>RR</inf>, BRS and RSAS dynamics, three EM of CFLFPP and cBRS, two EM of CFLFRR and CFLFSP; 2) increases (p<0.02) in five EM of SP, DP, PP, V<inf>T</inf> and RF, three EM of HF<inf>Res</inf>, two EM of LF<inf>SP</inf> and LF<inf>DP</inf>, one EM of LF<inf>PP</inf>; 3) no change in <inf>CF</inf>LF<inf>DP</inf>, RR and cRSAS. In healthy subjects, insulin-provoked HG elicits changes in the fluctuating time courses of all measures studied, integrating a counterregulatory response of autonomic control mechanisms and vagal depression associated with sympathetic, cardiovascular and respiratory activation.","PeriodicalId":6697,"journal":{"name":"2019 Computing in Cardiology (CinC)","volume":"14 1","pages":"Page 1-Page 4"},"PeriodicalIF":0.0000,"publicationDate":"2019-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Instantaneous Time Course of the Autonomic Cardiovascular and Respiratory Response of Healthy Subjects to Hypoglycemic Stimulus\",\"authors\":\"S. Carrasco-Sosa, A. Guillén-Mandujano\",\"doi\":\"10.23919/CinC49843.2019.9005662\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"In 13 healthy subjects we assessed the effect of hypoglycemia (HG) provoked by insulin on: R-R intervals (RR), systolic pressure (SP), diastolic pressure (DP), pulse pressure (PP), respiratory frequency (RF) and tidal volume (V<inf>T</inf>) 5-min time series; the instantaneous time courses of their low-frequency (LF<inf>RR</inf>, LF<inf>SP</inf>, LF<inf>DP</inf>, LF<inf>PP</inf>), high-frequency (HF<inf>RR</inf>, HF<inf>Res</inf>) powers and their respective central frequencies (cfLF<inf>RR</inf>, cfLF<inf>SP</inf>, cfLF<inf>DP</inf>, cfLF<inf>PP</inf>), computed by a time-frequency distribution; instantaneous baroreflex (BRS) and respiratory sinus arrhythmia sensitivities (RSAS), obtained by alpha index, and their coherences (cBRS and cRSAS) by cross time-frequency analysis. Peak HG (2.7±0.3 mmol/l) induced: 1) decreases (p<0.03) in five 1-min epoch means (EM) of HF<inf>RR</inf>, LF<inf>RR</inf>, BRS and RSAS dynamics, three EM of CFLFPP and cBRS, two EM of CFLFRR and CFLFSP; 2) increases (p<0.02) in five EM of SP, DP, PP, V<inf>T</inf> and RF, three EM of HF<inf>Res</inf>, two EM of LF<inf>SP</inf> and LF<inf>DP</inf>, one EM of LF<inf>PP</inf>; 3) no change in <inf>CF</inf>LF<inf>DP</inf>, RR and cRSAS. In healthy subjects, insulin-provoked HG elicits changes in the fluctuating time courses of all measures studied, integrating a counterregulatory response of autonomic control mechanisms and vagal depression associated with sympathetic, cardiovascular and respiratory activation.\",\"PeriodicalId\":6697,\"journal\":{\"name\":\"2019 Computing in Cardiology (CinC)\",\"volume\":\"14 1\",\"pages\":\"Page 1-Page 4\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2019-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"2019 Computing in Cardiology (CinC)\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.23919/CinC49843.2019.9005662\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"2019 Computing in Cardiology (CinC)","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.23919/CinC49843.2019.9005662","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Instantaneous Time Course of the Autonomic Cardiovascular and Respiratory Response of Healthy Subjects to Hypoglycemic Stimulus
In 13 healthy subjects we assessed the effect of hypoglycemia (HG) provoked by insulin on: R-R intervals (RR), systolic pressure (SP), diastolic pressure (DP), pulse pressure (PP), respiratory frequency (RF) and tidal volume (VT) 5-min time series; the instantaneous time courses of their low-frequency (LFRR, LFSP, LFDP, LFPP), high-frequency (HFRR, HFRes) powers and their respective central frequencies (cfLFRR, cfLFSP, cfLFDP, cfLFPP), computed by a time-frequency distribution; instantaneous baroreflex (BRS) and respiratory sinus arrhythmia sensitivities (RSAS), obtained by alpha index, and their coherences (cBRS and cRSAS) by cross time-frequency analysis. Peak HG (2.7±0.3 mmol/l) induced: 1) decreases (p<0.03) in five 1-min epoch means (EM) of HFRR, LFRR, BRS and RSAS dynamics, three EM of CFLFPP and cBRS, two EM of CFLFRR and CFLFSP; 2) increases (p<0.02) in five EM of SP, DP, PP, VT and RF, three EM of HFRes, two EM of LFSP and LFDP, one EM of LFPP; 3) no change in CFLFDP, RR and cRSAS. In healthy subjects, insulin-provoked HG elicits changes in the fluctuating time courses of all measures studied, integrating a counterregulatory response of autonomic control mechanisms and vagal depression associated with sympathetic, cardiovascular and respiratory activation.