DIABETES AFFECTS BLOOD-PRESSURE AND HEART-RATE RESPONSES DURING ACUTEHYPOTHERMIA

Citation
Rd. Kilgour et Pa. Williams, DIABETES AFFECTS BLOOD-PRESSURE AND HEART-RATE RESPONSES DURING ACUTEHYPOTHERMIA, Acta Physiologica Scandinavica, 162(1), 1998, pp. 27-32
Citations number
23
Categorie Soggetti
Physiology
ISSN journal
00016772
Volume
162
Issue
1
Year of publication
1998
Pages
27 - 32
Database
ISI
SICI code
0001-6772(1998)162:1<27:DABAHR>2.0.ZU;2-W
Abstract
Many diabetics are cold-intolerant and experience dramatic changes in normal systemic function during hypothermia. Little is known of the ca rdiovascular adjustments in diabetics exposed to an acute cold stress. In an effort to identify the alterations in mean arterial blood press ure (MAP) and heart rate (HR) in the diabetic during environmental coo ling (10 +/- 2 degrees C). we compared the in vivo MAP and HR response s of urethane-anaesthetized (1.5 g kg(-1)), streptozotocin-diabetic (S TZ, 65 mg kg(-1), n = 12) and control (CON, n = 10) rats during acute hypothermia. MAP was measured directly via an indwelling carotid arter y 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 (T-c) from 36 t o 28 degrees C (STZ, 0.16 degrees C min(-1) vs. CON, 0.06 degrees C mi n(-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 beat s min(-1)); however, during the acute hypothermic period, HR displayed a similar rate of decline in both groups. With respect to MAP, both g roups demonstrated similar pre-experimental presser responses (CON, 81 .7 +/- 5.4 vs. STZ, 83.2 +/- 5.1 mmHg, P > 0.05). During progressive h ypothermia, MAP gradually increased (P < 0.05) in the CON group from b aseline (T-c = 36 degrees C) and reached peak values (118.4 +/- 2.5 mm Hg) at T-c = 30 degrees C, while the STZ group failed to exhibit any c old presser response. At the conclusion of the experiment( T-c = 28 de grees C), the STZ group pressor response to hypothermia was not differ ent from baseline (T-c = 36 degrees C, 83.2 +/- 5.1 vs. T-c = 28 degre es C, 77.4 +/- 3.4 mmHg; P > 0.05). The absence of any presser respons e in the diabetic group during progressive hypothermia reflects the po or overall vasoconstrictive capacity to cooling and could partially ex plain the rapid decline of core temperature in this group.