Mechanism of defective oxygen extraction following global ischemia

Kirk R. Kanter, Donald D. Glower, Hartzell V Schaff, Timothy J. Gardner

Research output: Contribution to journalArticle

22 Citations (Scopus)

Abstract

Prolonged global ischemia has been shown to result in a defect in oxygen extraction (O2E) which is not related to postischemic changes in coronary blood flow or ventricular contractility. Possible explanations for this defect include either (1) decreased O2 delivery due to diffusion barriers, arterial-venous (A-V) shunting, or myocardial flow maldistribution, or (2) an impaired cellular ability to utilize delivered O2. Studies were carried out in 24 isolated perfused feline hearts divided into three equal groups. Groups I and II were subjected to 60 min of 37°C ischemia; Group III was protected with hypothermia (27°C) and potassium cardioplegia during the 60 min of ischemia. Group II underwent hyperosmolar (340 mOsm) reperfusion with mannitol to improve subendocardial perfusion; Groups I and III had isosmolar postischemic reperfusion. In addition to O2E determinations, myocardial O2 (PmO2) was monitored continuously by mass spectrometry. Radioactive microspheres were used to measure both A-V shunting and endo/epi flow ratios. Postischemic O2E was depressed in Group I (70 ± 5% of control) and Group II (70 ± 4% of control) but was unaltered in Group III (105 ± 8% of control). This impairment of O2E was not associated with increased A-V shunting. PmO2 was not different among the three groups excluding diffusion barriers as a likely explanation. Improving transmural myocardial perfusion in Group II did not result in improvement in postischemic O2E making flow maldistribution an unlikely cause of this defect. The mechanism of defective postischemic O2E, therefore, must be an impaired capacity for utilization of delivered O2 at the cellular level.

Original languageEnglish (US)
Pages (from-to)482-488
Number of pages7
JournalJournal of Surgical Research
Volume30
Issue number5
DOIs
StatePublished - 1981
Externally publishedYes

Fingerprint

Ischemia
Oxygen
Reperfusion
Perfusion
Induced Heart Arrest
Felidae
Mannitol
Hypothermia
Microspheres
Mass Spectrometry
Potassium
Control Groups

ASJC Scopus subject areas

  • Surgery

Cite this

Mechanism of defective oxygen extraction following global ischemia. / Kanter, Kirk R.; Glower, Donald D.; Schaff, Hartzell V; Gardner, Timothy J.

In: Journal of Surgical Research, Vol. 30, No. 5, 1981, p. 482-488.

Research output: Contribution to journalArticle

Kanter, Kirk R. ; Glower, Donald D. ; Schaff, Hartzell V ; Gardner, Timothy J. / Mechanism of defective oxygen extraction following global ischemia. In: Journal of Surgical Research. 1981 ; Vol. 30, No. 5. pp. 482-488.
@article{f32d376d2718491da345a5609da2e2a7,
title = "Mechanism of defective oxygen extraction following global ischemia",
abstract = "Prolonged global ischemia has been shown to result in a defect in oxygen extraction (O2E) which is not related to postischemic changes in coronary blood flow or ventricular contractility. Possible explanations for this defect include either (1) decreased O2 delivery due to diffusion barriers, arterial-venous (A-V) shunting, or myocardial flow maldistribution, or (2) an impaired cellular ability to utilize delivered O2. Studies were carried out in 24 isolated perfused feline hearts divided into three equal groups. Groups I and II were subjected to 60 min of 37°C ischemia; Group III was protected with hypothermia (27°C) and potassium cardioplegia during the 60 min of ischemia. Group II underwent hyperosmolar (340 mOsm) reperfusion with mannitol to improve subendocardial perfusion; Groups I and III had isosmolar postischemic reperfusion. In addition to O2E determinations, myocardial O2 (PmO2) was monitored continuously by mass spectrometry. Radioactive microspheres were used to measure both A-V shunting and endo/epi flow ratios. Postischemic O2E was depressed in Group I (70 ± 5{\%} of control) and Group II (70 ± 4{\%} of control) but was unaltered in Group III (105 ± 8{\%} of control). This impairment of O2E was not associated with increased A-V shunting. PmO2 was not different among the three groups excluding diffusion barriers as a likely explanation. Improving transmural myocardial perfusion in Group II did not result in improvement in postischemic O2E making flow maldistribution an unlikely cause of this defect. The mechanism of defective postischemic O2E, therefore, must be an impaired capacity for utilization of delivered O2 at the cellular level.",
author = "Kanter, {Kirk R.} and Glower, {Donald D.} and Schaff, {Hartzell V} and Gardner, {Timothy J.}",
year = "1981",
doi = "10.1016/0022-4804(81)90094-9",
language = "English (US)",
volume = "30",
pages = "482--488",
journal = "Journal of Surgical Research",
issn = "0022-4804",
publisher = "Academic Press Inc.",
number = "5",

}

TY - JOUR

T1 - Mechanism of defective oxygen extraction following global ischemia

AU - Kanter, Kirk R.

AU - Glower, Donald D.

AU - Schaff, Hartzell V

AU - Gardner, Timothy J.

PY - 1981

Y1 - 1981

N2 - Prolonged global ischemia has been shown to result in a defect in oxygen extraction (O2E) which is not related to postischemic changes in coronary blood flow or ventricular contractility. Possible explanations for this defect include either (1) decreased O2 delivery due to diffusion barriers, arterial-venous (A-V) shunting, or myocardial flow maldistribution, or (2) an impaired cellular ability to utilize delivered O2. Studies were carried out in 24 isolated perfused feline hearts divided into three equal groups. Groups I and II were subjected to 60 min of 37°C ischemia; Group III was protected with hypothermia (27°C) and potassium cardioplegia during the 60 min of ischemia. Group II underwent hyperosmolar (340 mOsm) reperfusion with mannitol to improve subendocardial perfusion; Groups I and III had isosmolar postischemic reperfusion. In addition to O2E determinations, myocardial O2 (PmO2) was monitored continuously by mass spectrometry. Radioactive microspheres were used to measure both A-V shunting and endo/epi flow ratios. Postischemic O2E was depressed in Group I (70 ± 5% of control) and Group II (70 ± 4% of control) but was unaltered in Group III (105 ± 8% of control). This impairment of O2E was not associated with increased A-V shunting. PmO2 was not different among the three groups excluding diffusion barriers as a likely explanation. Improving transmural myocardial perfusion in Group II did not result in improvement in postischemic O2E making flow maldistribution an unlikely cause of this defect. The mechanism of defective postischemic O2E, therefore, must be an impaired capacity for utilization of delivered O2 at the cellular level.

AB - Prolonged global ischemia has been shown to result in a defect in oxygen extraction (O2E) which is not related to postischemic changes in coronary blood flow or ventricular contractility. Possible explanations for this defect include either (1) decreased O2 delivery due to diffusion barriers, arterial-venous (A-V) shunting, or myocardial flow maldistribution, or (2) an impaired cellular ability to utilize delivered O2. Studies were carried out in 24 isolated perfused feline hearts divided into three equal groups. Groups I and II were subjected to 60 min of 37°C ischemia; Group III was protected with hypothermia (27°C) and potassium cardioplegia during the 60 min of ischemia. Group II underwent hyperosmolar (340 mOsm) reperfusion with mannitol to improve subendocardial perfusion; Groups I and III had isosmolar postischemic reperfusion. In addition to O2E determinations, myocardial O2 (PmO2) was monitored continuously by mass spectrometry. Radioactive microspheres were used to measure both A-V shunting and endo/epi flow ratios. Postischemic O2E was depressed in Group I (70 ± 5% of control) and Group II (70 ± 4% of control) but was unaltered in Group III (105 ± 8% of control). This impairment of O2E was not associated with increased A-V shunting. PmO2 was not different among the three groups excluding diffusion barriers as a likely explanation. Improving transmural myocardial perfusion in Group II did not result in improvement in postischemic O2E making flow maldistribution an unlikely cause of this defect. The mechanism of defective postischemic O2E, therefore, must be an impaired capacity for utilization of delivered O2 at the cellular level.

UR - http://www.scopus.com/inward/record.url?scp=0019458740&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0019458740&partnerID=8YFLogxK

U2 - 10.1016/0022-4804(81)90094-9

DO - 10.1016/0022-4804(81)90094-9

M3 - Article

C2 - 7242065

AN - SCOPUS:0019458740

VL - 30

SP - 482

EP - 488

JO - Journal of Surgical Research

JF - Journal of Surgical Research

SN - 0022-4804

IS - 5

ER -