Tissue P(O2) in the intestinal muscle layer of rats during chronic diabetes

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Chronic diabetes mellitus induced in rats by streptozotocin or of genetic origin in Db/Db mice is associated with a loss of capillaries, arteriolar constriction, and a decrease in resting and maximum blood flow. As a result of these vascular changes, as well as glycosylation of hemoglobin, it is possible that tissue P(O2) is reduced at rest and cannot be substantially increased during dilatation. Tissue P(O2) in the intestinal muscle layer was measured at rest and during maximal dilation. In addition, the spacing between capillaries with active flow and the velocity of red blood cell flow in capillaries were measured at rest and at maximum dilation. These measurements were made in normal and diabetic rats (streptozotocin) at age 26-30 weeks; the diabetic animals had been hyperglycemic (>350 mg/100 ml) for 12-15 weeks. Tissue P(O2) at a distance of about 15 μm from the arterial, mid-point, and venous end of capillaries in normal rats was 24.8 ± 1.1 (SE), 23.1 ± 1.2, and 22.4 ± 0.9 mm Hg, respectively, compared with 25.8 ± 0.9, 24.1 ± 1.2, and 22.4 ± 1.1 mm Hg, respectively, in diabetic rats. The maximum mid-capillary tissue P(O2) during dilation was 27.7 ± 1.3 mm Hg in normal rats and 29.7 ± 1.5 mm Hg in diabetic rats. The average distance between capillaries was 37.6 ± 2.0 μm in normal rats and 46.8 ± 2.9 μm in diabetic animals; vasodilation did not change the capillary spacing in either group of animals. Capillary red cell velocity in normal rats increased from 0.98 ± 0.11 mm/sec at rest to 2.1 ± 0.4 mm/sec during dilatation. For comparable conditions in diabetic rats, the velocities were 0.41 ± 0.07 and 1.06 ± 0.19 mm/sec. The data presented indicate that the diabetic animals have tissue P(O2) equivalent to those in normal rats, both at rest and during maximum vasodilation. The loss of capillaries and decreased resting and maximum capillary red cell velocity in diabetic rats would decrease the delivery of oxygen, but apparently, a decrease in oxygen consumption occurred that allowed the intestinal tissue to have a normal P(O2).

Original languageEnglish
Pages (from-to)677-682
Number of pages6
JournalCirculation Research
Volume52
Issue number6
StatePublished - 1983

Fingerprint

Muscles
Dilatation
Streptozocin
Vasodilation
Glycosylation
Constriction
Oxygen Consumption
Blood Vessels
Diabetes Mellitus
Hemoglobins
Erythrocytes
Oxygen

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Tissue P(O2) in the intestinal muscle layer of rats during chronic diabetes. / Bohlen, H.

In: Circulation Research, Vol. 52, No. 6, 1983, p. 677-682.

Research output: Contribution to journalArticle

@article{b0dd21d4485d4330bc33d4308d536666,
title = "Tissue P(O2) in the intestinal muscle layer of rats during chronic diabetes",
abstract = "Chronic diabetes mellitus induced in rats by streptozotocin or of genetic origin in Db/Db mice is associated with a loss of capillaries, arteriolar constriction, and a decrease in resting and maximum blood flow. As a result of these vascular changes, as well as glycosylation of hemoglobin, it is possible that tissue P(O2) is reduced at rest and cannot be substantially increased during dilatation. Tissue P(O2) in the intestinal muscle layer was measured at rest and during maximal dilation. In addition, the spacing between capillaries with active flow and the velocity of red blood cell flow in capillaries were measured at rest and at maximum dilation. These measurements were made in normal and diabetic rats (streptozotocin) at age 26-30 weeks; the diabetic animals had been hyperglycemic (>350 mg/100 ml) for 12-15 weeks. Tissue P(O2) at a distance of about 15 μm from the arterial, mid-point, and venous end of capillaries in normal rats was 24.8 ± 1.1 (SE), 23.1 ± 1.2, and 22.4 ± 0.9 mm Hg, respectively, compared with 25.8 ± 0.9, 24.1 ± 1.2, and 22.4 ± 1.1 mm Hg, respectively, in diabetic rats. The maximum mid-capillary tissue P(O2) during dilation was 27.7 ± 1.3 mm Hg in normal rats and 29.7 ± 1.5 mm Hg in diabetic rats. The average distance between capillaries was 37.6 ± 2.0 μm in normal rats and 46.8 ± 2.9 μm in diabetic animals; vasodilation did not change the capillary spacing in either group of animals. Capillary red cell velocity in normal rats increased from 0.98 ± 0.11 mm/sec at rest to 2.1 ± 0.4 mm/sec during dilatation. For comparable conditions in diabetic rats, the velocities were 0.41 ± 0.07 and 1.06 ± 0.19 mm/sec. The data presented indicate that the diabetic animals have tissue P(O2) equivalent to those in normal rats, both at rest and during maximum vasodilation. The loss of capillaries and decreased resting and maximum capillary red cell velocity in diabetic rats would decrease the delivery of oxygen, but apparently, a decrease in oxygen consumption occurred that allowed the intestinal tissue to have a normal P(O2).",
author = "H. Bohlen",
year = "1983",
language = "English",
volume = "52",
pages = "677--682",
journal = "Circulation Research",
issn = "0009-7330",
publisher = "Lippincott Williams and Wilkins",
number = "6",

}

TY - JOUR

T1 - Tissue P(O2) in the intestinal muscle layer of rats during chronic diabetes

AU - Bohlen, H.

PY - 1983

Y1 - 1983

N2 - Chronic diabetes mellitus induced in rats by streptozotocin or of genetic origin in Db/Db mice is associated with a loss of capillaries, arteriolar constriction, and a decrease in resting and maximum blood flow. As a result of these vascular changes, as well as glycosylation of hemoglobin, it is possible that tissue P(O2) is reduced at rest and cannot be substantially increased during dilatation. Tissue P(O2) in the intestinal muscle layer was measured at rest and during maximal dilation. In addition, the spacing between capillaries with active flow and the velocity of red blood cell flow in capillaries were measured at rest and at maximum dilation. These measurements were made in normal and diabetic rats (streptozotocin) at age 26-30 weeks; the diabetic animals had been hyperglycemic (>350 mg/100 ml) for 12-15 weeks. Tissue P(O2) at a distance of about 15 μm from the arterial, mid-point, and venous end of capillaries in normal rats was 24.8 ± 1.1 (SE), 23.1 ± 1.2, and 22.4 ± 0.9 mm Hg, respectively, compared with 25.8 ± 0.9, 24.1 ± 1.2, and 22.4 ± 1.1 mm Hg, respectively, in diabetic rats. The maximum mid-capillary tissue P(O2) during dilation was 27.7 ± 1.3 mm Hg in normal rats and 29.7 ± 1.5 mm Hg in diabetic rats. The average distance between capillaries was 37.6 ± 2.0 μm in normal rats and 46.8 ± 2.9 μm in diabetic animals; vasodilation did not change the capillary spacing in either group of animals. Capillary red cell velocity in normal rats increased from 0.98 ± 0.11 mm/sec at rest to 2.1 ± 0.4 mm/sec during dilatation. For comparable conditions in diabetic rats, the velocities were 0.41 ± 0.07 and 1.06 ± 0.19 mm/sec. The data presented indicate that the diabetic animals have tissue P(O2) equivalent to those in normal rats, both at rest and during maximum vasodilation. The loss of capillaries and decreased resting and maximum capillary red cell velocity in diabetic rats would decrease the delivery of oxygen, but apparently, a decrease in oxygen consumption occurred that allowed the intestinal tissue to have a normal P(O2).

AB - Chronic diabetes mellitus induced in rats by streptozotocin or of genetic origin in Db/Db mice is associated with a loss of capillaries, arteriolar constriction, and a decrease in resting and maximum blood flow. As a result of these vascular changes, as well as glycosylation of hemoglobin, it is possible that tissue P(O2) is reduced at rest and cannot be substantially increased during dilatation. Tissue P(O2) in the intestinal muscle layer was measured at rest and during maximal dilation. In addition, the spacing between capillaries with active flow and the velocity of red blood cell flow in capillaries were measured at rest and at maximum dilation. These measurements were made in normal and diabetic rats (streptozotocin) at age 26-30 weeks; the diabetic animals had been hyperglycemic (>350 mg/100 ml) for 12-15 weeks. Tissue P(O2) at a distance of about 15 μm from the arterial, mid-point, and venous end of capillaries in normal rats was 24.8 ± 1.1 (SE), 23.1 ± 1.2, and 22.4 ± 0.9 mm Hg, respectively, compared with 25.8 ± 0.9, 24.1 ± 1.2, and 22.4 ± 1.1 mm Hg, respectively, in diabetic rats. The maximum mid-capillary tissue P(O2) during dilation was 27.7 ± 1.3 mm Hg in normal rats and 29.7 ± 1.5 mm Hg in diabetic rats. The average distance between capillaries was 37.6 ± 2.0 μm in normal rats and 46.8 ± 2.9 μm in diabetic animals; vasodilation did not change the capillary spacing in either group of animals. Capillary red cell velocity in normal rats increased from 0.98 ± 0.11 mm/sec at rest to 2.1 ± 0.4 mm/sec during dilatation. For comparable conditions in diabetic rats, the velocities were 0.41 ± 0.07 and 1.06 ± 0.19 mm/sec. The data presented indicate that the diabetic animals have tissue P(O2) equivalent to those in normal rats, both at rest and during maximum vasodilation. The loss of capillaries and decreased resting and maximum capillary red cell velocity in diabetic rats would decrease the delivery of oxygen, but apparently, a decrease in oxygen consumption occurred that allowed the intestinal tissue to have a normal P(O2).

UR - http://www.scopus.com/inward/record.url?scp=0020645713&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0020645713&partnerID=8YFLogxK

M3 - Article

C2 - 6861285

AN - SCOPUS:0020645713

VL - 52

SP - 677

EP - 682

JO - Circulation Research

JF - Circulation Research

SN - 0009-7330

IS - 6

ER -