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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
|
| pubmed:dateCreated |
1998-3-30
|
| pubmed:abstractText |
Many diabetics are cold-intolerant and experience dramatic changes in normal systemic function during hypothermia. Little is known of the cardiovascular adjustments in diabetics exposed to an acute cold stress. In an effort to identify the alterations in mean arterial blood pressure (MAP) and heart rate (HR) in the diabetic during environmental cooling (10 +/- 2 degrees C), we compared the in vivo MAP and HR responses of urethane-anaesthetized (1.5 g kg-1), streptozotocin-diabetic (STZ, 65 mg kg-1, n = 12) and control (CON, n = 10) rats during acute hypothermia. MAP was measured directly via an indwelling carotid artery cannula and HR was calculated from the peak systolic pressure waves. Overall, the STZ rats were more cold-intolerant than CON as evidenced by the greater rate of decline in colonic temperature (Tc) from 36 to 28 degrees C (STZ, 0.16 degree C min-1 vs. CON, 0.06 degree C min-1; P < 0.05). Prior to cooling, HR was significantly lower (P < 0.05) in STZ (282 +/- 9 beats min-1) than in CON rats (399 +/- 24 beats min-1); however, during the acute hypothermic period, HR displayed a similar rate of decline in both groups. With respect to MAP, both groups demonstrated similar pre-experimental pressor responses (CON, 81.7 +/- 5.4 vs. STZ, 83.2 +/- 5.1 mmHg, P > 0.05). During progressive hypothermia, MAP gradually increased (P < 0.05) in the CON group from baseline (Tc = 36 degrees C) and reached peak values (118.4 +/- 2.5 mmHg) at Tc = 30 degrees C, while the STZ group failed to exhibit any cold pressor response. At the conclusion of the experiment (Tc = 28 degrees C), the STZ group pressor response to hypothermia was not different from baseline (Tc = 36 degrees C, 83.2 +/- 5.1 vs. Tc = 28 degrees C, 77.4 +/- 3.4 mmHg; P > 0.05). The absence of any pressor response in the diabetic group during progressive hypothermia reflects the poor overall vasoconstrictive capacity to cooling and could partially explain the rapid decline of core temperature in this group.
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| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Jan
|
| pubmed:issn |
0001-6772
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
162
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
27-32
|
| pubmed:dateRevised |
2008-11-21
|
| pubmed:meshHeading |
pubmed-meshheading:9492899-Acute Disease,
pubmed-meshheading:9492899-Animals,
pubmed-meshheading:9492899-Blood Glucose,
pubmed-meshheading:9492899-Blood Pressure,
pubmed-meshheading:9492899-Body Temperature,
pubmed-meshheading:9492899-Body Weight,
pubmed-meshheading:9492899-Cold Temperature,
pubmed-meshheading:9492899-Diabetes Mellitus, Experimental,
pubmed-meshheading:9492899-Heart Rate,
pubmed-meshheading:9492899-Hypothermia,
pubmed-meshheading:9492899-Male,
pubmed-meshheading:9492899-Rats,
pubmed-meshheading:9492899-Rats, Wistar
|
| pubmed:year |
1998
|
| pubmed:articleTitle |
Diabetes affects blood pressure and heart rate responses during acute hypothermia.
|
| pubmed:affiliation |
Department of Exercise Science, Concordia University, Montreal, Quebec, Canada.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|