{"title":"Intermittent coronary sinus occlusion: hemodynamic and anti-ischemic effects","authors":"A. Guerci, R. Beyar","doi":"10.1109/IEMBS.1988.94400","DOIUrl":null,"url":null,"abstract":"To determine the anti-ischemic mechanism of intermittent occlusion of the coronary sinus (ICSO), the authors measured coronary arterial and sinus pressure and coronary arterial oxygen saturation before and after coronary artery litigation, with and without ICSO. In dogs, ICSO produced a systolic pressure gradient between the coronary artery and coronary sinus of -20+or-9 mm Hg (higher venous pressure, p<0.001) and a reduction in the oxygen of 20+or-13% (p<0.005). In parallel studied the authors constructed a mathematical model of known physiology to test the possibility of venoarterial flow. Predicted and experimental data were similar, indicating a reversal of flow at the microcirculatory level of ischemic regions during ISCO. These data indicate that alternating arteriovenous and venoarterial flow over the ischemic territory is the anti-ischemic mechanism of ICSO.<<ETX>>","PeriodicalId":227170,"journal":{"name":"Proceedings of the Annual International Conference of the IEEE Engineering in Medicine and Biology Society","volume":"276 1","pages":"0"},"PeriodicalIF":0.0000,"publicationDate":"1988-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Proceedings of the Annual International Conference of the IEEE Engineering in Medicine and Biology Society","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1109/IEMBS.1988.94400","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
To determine the anti-ischemic mechanism of intermittent occlusion of the coronary sinus (ICSO), the authors measured coronary arterial and sinus pressure and coronary arterial oxygen saturation before and after coronary artery litigation, with and without ICSO. In dogs, ICSO produced a systolic pressure gradient between the coronary artery and coronary sinus of -20+or-9 mm Hg (higher venous pressure, p<0.001) and a reduction in the oxygen of 20+or-13% (p<0.005). In parallel studied the authors constructed a mathematical model of known physiology to test the possibility of venoarterial flow. Predicted and experimental data were similar, indicating a reversal of flow at the microcirculatory level of ischemic regions during ISCO. These data indicate that alternating arteriovenous and venoarterial flow over the ischemic territory is the anti-ischemic mechanism of ICSO.<>