{"title":"Effects of meals on peripheral blood flow reduction by cold exposure in rabbit ears.","authors":"T. Wakabayashi","doi":"10.11480/BTMD.390102","DOIUrl":null,"url":null,"abstract":"Although insulin is known to have various actions on the cardiovascular system, its effects on the microvessels in vivo have not been fully elucidated. This study was aimed to examine the effects of the increased endogenous insulin release after meals on the reflex vasoconstriction induced by cold exposure in the rabbit ears using a laser Doppler flowmeter. A reflex blood flow reduction by cold exposure was tested 3-4 hours after meals in the rabbits with or without pretreatment with a somatostatin analogue (Sandostatin, 100 micrograms/body). The degrees of the blood flow reduction were decreased after the diet intake compared to the responses in the fasting state. The blood flow reduction after diet intake in the non-treated group was significantly attenuated compared to the treated group (88.4 +/- 13.0% in the non-treated group vs. 47.5 +/- 13.4% in the treated group at 1 minute of cold exposure; p less than 0.05, and 87.6 +/- 20.2% vs. 40.2 +/- 24.8%, respectively, at 5 minutes of cold exposure; p less than 0.05). The somatostatin-treated rabbits showed a significant suppression of the increase in the serum insulin levels after meals compared to the non-treated control rabbits (17.8 +/- 10.2 microU/ml in the treated group vs. 78.6 +/- 38.3 microU/ml in the non-treated group, p less than 0.05). In the somatostatin-treated rabbits, the exogenously applied insulin caused a decreased response of blood flow to cold exposure. These findings suggest that in the postprandial state the endogenous insulin release may regulate the reactivity of the microvessels to the sympathetic stimuli.","PeriodicalId":22311,"journal":{"name":"The Bulletin of Tokyo Medical and Dental University","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1992-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"The Bulletin of Tokyo Medical and Dental University","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.11480/BTMD.390102","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
Although insulin is known to have various actions on the cardiovascular system, its effects on the microvessels in vivo have not been fully elucidated. This study was aimed to examine the effects of the increased endogenous insulin release after meals on the reflex vasoconstriction induced by cold exposure in the rabbit ears using a laser Doppler flowmeter. A reflex blood flow reduction by cold exposure was tested 3-4 hours after meals in the rabbits with or without pretreatment with a somatostatin analogue (Sandostatin, 100 micrograms/body). The degrees of the blood flow reduction were decreased after the diet intake compared to the responses in the fasting state. The blood flow reduction after diet intake in the non-treated group was significantly attenuated compared to the treated group (88.4 +/- 13.0% in the non-treated group vs. 47.5 +/- 13.4% in the treated group at 1 minute of cold exposure; p less than 0.05, and 87.6 +/- 20.2% vs. 40.2 +/- 24.8%, respectively, at 5 minutes of cold exposure; p less than 0.05). The somatostatin-treated rabbits showed a significant suppression of the increase in the serum insulin levels after meals compared to the non-treated control rabbits (17.8 +/- 10.2 microU/ml in the treated group vs. 78.6 +/- 38.3 microU/ml in the non-treated group, p less than 0.05). In the somatostatin-treated rabbits, the exogenously applied insulin caused a decreased response of blood flow to cold exposure. These findings suggest that in the postprandial state the endogenous insulin release may regulate the reactivity of the microvessels to the sympathetic stimuli.