A. Kaya, Alev Arat-Özkan, Özge Köner, H. Balcı, O. Abacı, T. Gürmen, S. Kucukoğlu, Z. Yiğit
{"title":"冠心病患者急性运动对一氧化氮的反应","authors":"A. Kaya, Alev Arat-Özkan, Özge Köner, H. Balcı, O. Abacı, T. Gürmen, S. Kucukoğlu, Z. Yiğit","doi":"10.18478/IUFSJB.73777","DOIUrl":null,"url":null,"abstract":"Nitric oxide (NO) has been identified as a vasodilatory substance released from the endothelium which decreases in the presence of atherosclerosis. This study aimed to evaluate the systemic NO response to acute exercise in untrained diabetic and nondiabetic patients with atherosclerotic coronary artery disease (CAD). This is a prospective, clinical study consisting of three groups. Group A (n=50) consisted of nondiabetic CAD patients,group B (n=20) consisting of diabetic, CAD patients and group C (n=20) of healthy controls. All patients underwent a standard symptom limited treadmill exercise test according to the modified Bruce protocol after 24 hours low nitrite/ nitrate diet. End products of nitric oxide metabolism (NOx) were determined as the half life of NO is very short. Basal serum NOx levels of both diabetics (24±8.4μmol/L,p<0.0001)and nondiabetics (43.5±13.7μmol/L, p<0.01) were significantly lower compared to controls (66.5±3.4μmol/L). Only in the nondiabetic, CAD patient group was an increase in NOx levels observed with exercise. No increase in NOx with exercise was observed for the diabetic. CAD patient group or for the control group. In normal controls exercise induced no significant change in NOx levels. Exercise induced increase in systemic NOx levels in patients with atherosclerotic disease may indicate a compensatory mechanism which is not present or diminished in the diabetic subgroup .","PeriodicalId":14521,"journal":{"name":"IUFS Journal of Biology","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Nitric Oxide Response to Acute Exercise in Patients with Coronary Artery Disease\",\"authors\":\"A. Kaya, Alev Arat-Özkan, Özge Köner, H. Balcı, O. Abacı, T. Gürmen, S. Kucukoğlu, Z. Yiğit\",\"doi\":\"10.18478/IUFSJB.73777\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Nitric oxide (NO) has been identified as a vasodilatory substance released from the endothelium which decreases in the presence of atherosclerosis. This study aimed to evaluate the systemic NO response to acute exercise in untrained diabetic and nondiabetic patients with atherosclerotic coronary artery disease (CAD). This is a prospective, clinical study consisting of three groups. Group A (n=50) consisted of nondiabetic CAD patients,group B (n=20) consisting of diabetic, CAD patients and group C (n=20) of healthy controls. All patients underwent a standard symptom limited treadmill exercise test according to the modified Bruce protocol after 24 hours low nitrite/ nitrate diet. End products of nitric oxide metabolism (NOx) were determined as the half life of NO is very short. Basal serum NOx levels of both diabetics (24±8.4μmol/L,p<0.0001)and nondiabetics (43.5±13.7μmol/L, p<0.01) were significantly lower compared to controls (66.5±3.4μmol/L). Only in the nondiabetic, CAD patient group was an increase in NOx levels observed with exercise. No increase in NOx with exercise was observed for the diabetic. CAD patient group or for the control group. In normal controls exercise induced no significant change in NOx levels. Exercise induced increase in systemic NOx levels in patients with atherosclerotic disease may indicate a compensatory mechanism which is not present or diminished in the diabetic subgroup .\",\"PeriodicalId\":14521,\"journal\":{\"name\":\"IUFS Journal of Biology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2009-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"IUFS Journal of Biology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.18478/IUFSJB.73777\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"IUFS Journal of Biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.18478/IUFSJB.73777","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Nitric Oxide Response to Acute Exercise in Patients with Coronary Artery Disease
Nitric oxide (NO) has been identified as a vasodilatory substance released from the endothelium which decreases in the presence of atherosclerosis. This study aimed to evaluate the systemic NO response to acute exercise in untrained diabetic and nondiabetic patients with atherosclerotic coronary artery disease (CAD). This is a prospective, clinical study consisting of three groups. Group A (n=50) consisted of nondiabetic CAD patients,group B (n=20) consisting of diabetic, CAD patients and group C (n=20) of healthy controls. All patients underwent a standard symptom limited treadmill exercise test according to the modified Bruce protocol after 24 hours low nitrite/ nitrate diet. End products of nitric oxide metabolism (NOx) were determined as the half life of NO is very short. Basal serum NOx levels of both diabetics (24±8.4μmol/L,p<0.0001)and nondiabetics (43.5±13.7μmol/L, p<0.01) were significantly lower compared to controls (66.5±3.4μmol/L). Only in the nondiabetic, CAD patient group was an increase in NOx levels observed with exercise. No increase in NOx with exercise was observed for the diabetic. CAD patient group or for the control group. In normal controls exercise induced no significant change in NOx levels. Exercise induced increase in systemic NOx levels in patients with atherosclerotic disease may indicate a compensatory mechanism which is not present or diminished in the diabetic subgroup .