Cerebral blood flow responsivity to CO2 in anesthetized chronically diabetic dogs

Frederick Sieber, P. R. Brown, Y. Wu, Raymond C Koehler, R. J. Traystman

Research output: Contribution to journalArticle

Abstract

The effect of diabetes mellitus on the cerebrovascular response to CO2 is unclear. We examined the effects of diabetes on cerebral blood flow (CBF) and cerebral oxygen uptake (CMR(O2)) during CO2 alterations. Four groups of dogs were studied: nondiabetic, normoglycemic controls; nondiabetic, acute hyperglycemia; diabetic (pancreatectomy) with high-dose insulin treatment to maintain blood glucose between 4.0 and 6.0 mM; and diabetic with low-dose insulin treatment to maintain blood glucose at 13.2 ± 0.4 mM. Six weeks after either sham surgery or pancreatectomy, dogs were anesthetized with fentanyl (50 μg/kg) plus pentobarbital (10 mg/kg), and microsphere determinations of CBF were made during normo-, hypo-, and hypercapnia. On the day of the study, arterial glucose levels in the control, acute hyperglycemia, and high- and low-dose insulin diabetic groups were 4.0 ± 0.3, 14.9 ± 2.5, 3.3 ± 0.8, and 13.3 ± 0.7 mM, respectively, at control. The corresponding baseline CMR(O2) levels were 2.8 ± 0.2, 3.0 ± 0.2, 4.1 ± 0.4, and 4.0 ± 0.3 ml O2 · 100 g-1 · min-1, and the values in both diabetic groups were higher than control. Normocapnic CBF in the acute hyperglycemia, high-dose insulin, and low-dose insulin groups was elevated from control (54 ± 3, 50 ± 3, 51 ± 3 vs. 36 ± 1 ml · 100 g-1 · min- 1) and cerebrovascular resistance was lower (2.24 ± 0.15, 2.51 ± 0.14, 2.38 ± 0.21 vs. 3.35 ± 0.18 mmHg · ml-1 · 100 g · min). CBF responses to both hypercapnia and hypocapnia were similar among groups. Thus both acute hyperglycemia and diabetes decrease cerebrovascular resistance and increase CBF. In the diabetic groups elevated CBF was attributable to elevated CMR(O2) in the anesthetized state. However, we found no evidence of impaired cerebrovascular CO2 responsivity after a 6-wk duration of diabetes.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume264
Issue number4 33-4
StatePublished - 1993

Fingerprint

Cerebrovascular Circulation
Dogs
Hyperglycemia
Insulin
Hypocapnia
Pancreatectomy
Hypercapnia
Blood Glucose
Fentanyl
Pentobarbital
Microspheres
Diabetes Mellitus
Oxygen
Glucose

Keywords

  • brain
  • diabetes
  • glucose

ASJC Scopus subject areas

  • Physiology

Cite this

Cerebral blood flow responsivity to CO2 in anesthetized chronically diabetic dogs. / Sieber, Frederick; Brown, P. R.; Wu, Y.; Koehler, Raymond C; Traystman, R. J.

In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 264, No. 4 33-4, 1993.

Research output: Contribution to journalArticle

@article{7f006dae39994a14adf4975857e70b04,
title = "Cerebral blood flow responsivity to CO2 in anesthetized chronically diabetic dogs",
abstract = "The effect of diabetes mellitus on the cerebrovascular response to CO2 is unclear. We examined the effects of diabetes on cerebral blood flow (CBF) and cerebral oxygen uptake (CMR(O2)) during CO2 alterations. Four groups of dogs were studied: nondiabetic, normoglycemic controls; nondiabetic, acute hyperglycemia; diabetic (pancreatectomy) with high-dose insulin treatment to maintain blood glucose between 4.0 and 6.0 mM; and diabetic with low-dose insulin treatment to maintain blood glucose at 13.2 ± 0.4 mM. Six weeks after either sham surgery or pancreatectomy, dogs were anesthetized with fentanyl (50 μg/kg) plus pentobarbital (10 mg/kg), and microsphere determinations of CBF were made during normo-, hypo-, and hypercapnia. On the day of the study, arterial glucose levels in the control, acute hyperglycemia, and high- and low-dose insulin diabetic groups were 4.0 ± 0.3, 14.9 ± 2.5, 3.3 ± 0.8, and 13.3 ± 0.7 mM, respectively, at control. The corresponding baseline CMR(O2) levels were 2.8 ± 0.2, 3.0 ± 0.2, 4.1 ± 0.4, and 4.0 ± 0.3 ml O2 · 100 g-1 · min-1, and the values in both diabetic groups were higher than control. Normocapnic CBF in the acute hyperglycemia, high-dose insulin, and low-dose insulin groups was elevated from control (54 ± 3, 50 ± 3, 51 ± 3 vs. 36 ± 1 ml · 100 g-1 · min- 1) and cerebrovascular resistance was lower (2.24 ± 0.15, 2.51 ± 0.14, 2.38 ± 0.21 vs. 3.35 ± 0.18 mmHg · ml-1 · 100 g · min). CBF responses to both hypercapnia and hypocapnia were similar among groups. Thus both acute hyperglycemia and diabetes decrease cerebrovascular resistance and increase CBF. In the diabetic groups elevated CBF was attributable to elevated CMR(O2) in the anesthetized state. However, we found no evidence of impaired cerebrovascular CO2 responsivity after a 6-wk duration of diabetes.",
keywords = "brain, diabetes, glucose",
author = "Frederick Sieber and Brown, {P. R.} and Y. Wu and Koehler, {Raymond C} and Traystman, {R. J.}",
year = "1993",
language = "English (US)",
volume = "264",
journal = "American Journal of Physiology",
issn = "0363-6135",
publisher = "American Physiological Society",
number = "4 33-4",

}

TY - JOUR

T1 - Cerebral blood flow responsivity to CO2 in anesthetized chronically diabetic dogs

AU - Sieber, Frederick

AU - Brown, P. R.

AU - Wu, Y.

AU - Koehler, Raymond C

AU - Traystman, R. J.

PY - 1993

Y1 - 1993

N2 - The effect of diabetes mellitus on the cerebrovascular response to CO2 is unclear. We examined the effects of diabetes on cerebral blood flow (CBF) and cerebral oxygen uptake (CMR(O2)) during CO2 alterations. Four groups of dogs were studied: nondiabetic, normoglycemic controls; nondiabetic, acute hyperglycemia; diabetic (pancreatectomy) with high-dose insulin treatment to maintain blood glucose between 4.0 and 6.0 mM; and diabetic with low-dose insulin treatment to maintain blood glucose at 13.2 ± 0.4 mM. Six weeks after either sham surgery or pancreatectomy, dogs were anesthetized with fentanyl (50 μg/kg) plus pentobarbital (10 mg/kg), and microsphere determinations of CBF were made during normo-, hypo-, and hypercapnia. On the day of the study, arterial glucose levels in the control, acute hyperglycemia, and high- and low-dose insulin diabetic groups were 4.0 ± 0.3, 14.9 ± 2.5, 3.3 ± 0.8, and 13.3 ± 0.7 mM, respectively, at control. The corresponding baseline CMR(O2) levels were 2.8 ± 0.2, 3.0 ± 0.2, 4.1 ± 0.4, and 4.0 ± 0.3 ml O2 · 100 g-1 · min-1, and the values in both diabetic groups were higher than control. Normocapnic CBF in the acute hyperglycemia, high-dose insulin, and low-dose insulin groups was elevated from control (54 ± 3, 50 ± 3, 51 ± 3 vs. 36 ± 1 ml · 100 g-1 · min- 1) and cerebrovascular resistance was lower (2.24 ± 0.15, 2.51 ± 0.14, 2.38 ± 0.21 vs. 3.35 ± 0.18 mmHg · ml-1 · 100 g · min). CBF responses to both hypercapnia and hypocapnia were similar among groups. Thus both acute hyperglycemia and diabetes decrease cerebrovascular resistance and increase CBF. In the diabetic groups elevated CBF was attributable to elevated CMR(O2) in the anesthetized state. However, we found no evidence of impaired cerebrovascular CO2 responsivity after a 6-wk duration of diabetes.

AB - The effect of diabetes mellitus on the cerebrovascular response to CO2 is unclear. We examined the effects of diabetes on cerebral blood flow (CBF) and cerebral oxygen uptake (CMR(O2)) during CO2 alterations. Four groups of dogs were studied: nondiabetic, normoglycemic controls; nondiabetic, acute hyperglycemia; diabetic (pancreatectomy) with high-dose insulin treatment to maintain blood glucose between 4.0 and 6.0 mM; and diabetic with low-dose insulin treatment to maintain blood glucose at 13.2 ± 0.4 mM. Six weeks after either sham surgery or pancreatectomy, dogs were anesthetized with fentanyl (50 μg/kg) plus pentobarbital (10 mg/kg), and microsphere determinations of CBF were made during normo-, hypo-, and hypercapnia. On the day of the study, arterial glucose levels in the control, acute hyperglycemia, and high- and low-dose insulin diabetic groups were 4.0 ± 0.3, 14.9 ± 2.5, 3.3 ± 0.8, and 13.3 ± 0.7 mM, respectively, at control. The corresponding baseline CMR(O2) levels were 2.8 ± 0.2, 3.0 ± 0.2, 4.1 ± 0.4, and 4.0 ± 0.3 ml O2 · 100 g-1 · min-1, and the values in both diabetic groups were higher than control. Normocapnic CBF in the acute hyperglycemia, high-dose insulin, and low-dose insulin groups was elevated from control (54 ± 3, 50 ± 3, 51 ± 3 vs. 36 ± 1 ml · 100 g-1 · min- 1) and cerebrovascular resistance was lower (2.24 ± 0.15, 2.51 ± 0.14, 2.38 ± 0.21 vs. 3.35 ± 0.18 mmHg · ml-1 · 100 g · min). CBF responses to both hypercapnia and hypocapnia were similar among groups. Thus both acute hyperglycemia and diabetes decrease cerebrovascular resistance and increase CBF. In the diabetic groups elevated CBF was attributable to elevated CMR(O2) in the anesthetized state. However, we found no evidence of impaired cerebrovascular CO2 responsivity after a 6-wk duration of diabetes.

KW - brain

KW - diabetes

KW - glucose

UR - http://www.scopus.com/inward/record.url?scp=0027511823&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027511823&partnerID=8YFLogxK

M3 - Article

C2 - 8476084

AN - SCOPUS:0027511823

VL - 264

JO - American Journal of Physiology

JF - American Journal of Physiology

SN - 0363-6135

IS - 4 33-4

ER -