Myocyte contracture, vascular resistance, and vascular permeability after global ischemia in isolated hearts from alloxan-induced diabetic rabbits

Ronald Tilton, A. Daugherty, S. P. Sutera, K. B. Larson, M. P. Land, D. L. Rateri, C. Kilo, J. R. Williamson

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

Coronary vascular hemodynamics, albumin permeation, and myocyte contractility were assessed in isolated hearts from 6-mo alloxan-induced diabetic (ALX-D) rabbits during 3 h of reperfusion after 40 min of global no-flow ischemia. Residue-detection data, generated during the single passage of a bolus of 125I-labeled bovine serum albumin (125I-BSA) through the coronary vasculature, were used to estimate indices of vascular function, including the mean transit time of 125I-BSA, the fractional rate of intravascular clearance of 125I-BSA, and 125I-BSA permeation of coronary vessels. During reflow after ischemia in hearts from control rabbits, vascular resistance increased approximately three times that at baseline, left ventricular end-diastolic pressure (LVEDP) increased 8-10 times, and maximum +dP/dt recovered 0.4 times baseline, whereas the fractional rate of washout of intravascular 125I-BSA decreased to less than one-half of baseline values (was prolonged 2-fold), and albumin permeation and mean-transit time were increased 3 and 5 times baseline, respectively. In hearts from diabetic rabbits, vascular resistance was similar to the control group before ischemia but increased only one-third as much during reflow after ischemia. Increases in LVEDP during reflow were ~50% lower than controls, and +dP/dt recovered ~2.5 times more than in control hearts. 125I-BSA permeation in diabetics was similar to controls before ischemia, but during reflow increased 6 times (~2 times controls). Washout of intravascular 125I-BSA was prolonged ~20% versus baseline during 3 h of reflow in hearts from diabetic rabbits. Thus, ALX-D in the rabbit delayed ischemia-reperfusion injury to myocytes and vascular smooth muscle cells while increasing vascular albumin permeation.

Original languageEnglish (US)
Pages (from-to)1484-1491
Number of pages8
JournalDiabetes
Volume38
Issue number11
StatePublished - 1989
Externally publishedYes

Fingerprint

Alloxan
Capillary Permeability
Contracture
Bovine Serum Albumin
Vascular Resistance
Muscle Cells
Ischemia
Rabbits
Blood Vessels
Albumins
Blood Pressure
Reperfusion Injury
Vascular Smooth Muscle
Reperfusion
Smooth Muscle Myocytes
Coronary Vessels
Hemodynamics
Control Groups

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Internal Medicine

Cite this

Tilton, R., Daugherty, A., Sutera, S. P., Larson, K. B., Land, M. P., Rateri, D. L., ... Williamson, J. R. (1989). Myocyte contracture, vascular resistance, and vascular permeability after global ischemia in isolated hearts from alloxan-induced diabetic rabbits. Diabetes, 38(11), 1484-1491.

Myocyte contracture, vascular resistance, and vascular permeability after global ischemia in isolated hearts from alloxan-induced diabetic rabbits. / Tilton, Ronald; Daugherty, A.; Sutera, S. P.; Larson, K. B.; Land, M. P.; Rateri, D. L.; Kilo, C.; Williamson, J. R.

In: Diabetes, Vol. 38, No. 11, 1989, p. 1484-1491.

Research output: Contribution to journalArticle

Tilton, R, Daugherty, A, Sutera, SP, Larson, KB, Land, MP, Rateri, DL, Kilo, C & Williamson, JR 1989, 'Myocyte contracture, vascular resistance, and vascular permeability after global ischemia in isolated hearts from alloxan-induced diabetic rabbits', Diabetes, vol. 38, no. 11, pp. 1484-1491.
Tilton, Ronald ; Daugherty, A. ; Sutera, S. P. ; Larson, K. B. ; Land, M. P. ; Rateri, D. L. ; Kilo, C. ; Williamson, J. R. / Myocyte contracture, vascular resistance, and vascular permeability after global ischemia in isolated hearts from alloxan-induced diabetic rabbits. In: Diabetes. 1989 ; Vol. 38, No. 11. pp. 1484-1491.
@article{c07ffc9bd01e4b689fdec2d1d023f71f,
title = "Myocyte contracture, vascular resistance, and vascular permeability after global ischemia in isolated hearts from alloxan-induced diabetic rabbits",
abstract = "Coronary vascular hemodynamics, albumin permeation, and myocyte contractility were assessed in isolated hearts from 6-mo alloxan-induced diabetic (ALX-D) rabbits during 3 h of reperfusion after 40 min of global no-flow ischemia. Residue-detection data, generated during the single passage of a bolus of 125I-labeled bovine serum albumin (125I-BSA) through the coronary vasculature, were used to estimate indices of vascular function, including the mean transit time of 125I-BSA, the fractional rate of intravascular clearance of 125I-BSA, and 125I-BSA permeation of coronary vessels. During reflow after ischemia in hearts from control rabbits, vascular resistance increased approximately three times that at baseline, left ventricular end-diastolic pressure (LVEDP) increased 8-10 times, and maximum +dP/dt recovered 0.4 times baseline, whereas the fractional rate of washout of intravascular 125I-BSA decreased to less than one-half of baseline values (was prolonged 2-fold), and albumin permeation and mean-transit time were increased 3 and 5 times baseline, respectively. In hearts from diabetic rabbits, vascular resistance was similar to the control group before ischemia but increased only one-third as much during reflow after ischemia. Increases in LVEDP during reflow were ~50{\%} lower than controls, and +dP/dt recovered ~2.5 times more than in control hearts. 125I-BSA permeation in diabetics was similar to controls before ischemia, but during reflow increased 6 times (~2 times controls). Washout of intravascular 125I-BSA was prolonged ~20{\%} versus baseline during 3 h of reflow in hearts from diabetic rabbits. Thus, ALX-D in the rabbit delayed ischemia-reperfusion injury to myocytes and vascular smooth muscle cells while increasing vascular albumin permeation.",
author = "Ronald Tilton and A. Daugherty and Sutera, {S. P.} and Larson, {K. B.} and Land, {M. P.} and Rateri, {D. L.} and C. Kilo and Williamson, {J. R.}",
year = "1989",
language = "English (US)",
volume = "38",
pages = "1484--1491",
journal = "Diabetes",
issn = "0012-1797",
publisher = "American Diabetes Association Inc.",
number = "11",

}

TY - JOUR

T1 - Myocyte contracture, vascular resistance, and vascular permeability after global ischemia in isolated hearts from alloxan-induced diabetic rabbits

AU - Tilton, Ronald

AU - Daugherty, A.

AU - Sutera, S. P.

AU - Larson, K. B.

AU - Land, M. P.

AU - Rateri, D. L.

AU - Kilo, C.

AU - Williamson, J. R.

PY - 1989

Y1 - 1989

N2 - Coronary vascular hemodynamics, albumin permeation, and myocyte contractility were assessed in isolated hearts from 6-mo alloxan-induced diabetic (ALX-D) rabbits during 3 h of reperfusion after 40 min of global no-flow ischemia. Residue-detection data, generated during the single passage of a bolus of 125I-labeled bovine serum albumin (125I-BSA) through the coronary vasculature, were used to estimate indices of vascular function, including the mean transit time of 125I-BSA, the fractional rate of intravascular clearance of 125I-BSA, and 125I-BSA permeation of coronary vessels. During reflow after ischemia in hearts from control rabbits, vascular resistance increased approximately three times that at baseline, left ventricular end-diastolic pressure (LVEDP) increased 8-10 times, and maximum +dP/dt recovered 0.4 times baseline, whereas the fractional rate of washout of intravascular 125I-BSA decreased to less than one-half of baseline values (was prolonged 2-fold), and albumin permeation and mean-transit time were increased 3 and 5 times baseline, respectively. In hearts from diabetic rabbits, vascular resistance was similar to the control group before ischemia but increased only one-third as much during reflow after ischemia. Increases in LVEDP during reflow were ~50% lower than controls, and +dP/dt recovered ~2.5 times more than in control hearts. 125I-BSA permeation in diabetics was similar to controls before ischemia, but during reflow increased 6 times (~2 times controls). Washout of intravascular 125I-BSA was prolonged ~20% versus baseline during 3 h of reflow in hearts from diabetic rabbits. Thus, ALX-D in the rabbit delayed ischemia-reperfusion injury to myocytes and vascular smooth muscle cells while increasing vascular albumin permeation.

AB - Coronary vascular hemodynamics, albumin permeation, and myocyte contractility were assessed in isolated hearts from 6-mo alloxan-induced diabetic (ALX-D) rabbits during 3 h of reperfusion after 40 min of global no-flow ischemia. Residue-detection data, generated during the single passage of a bolus of 125I-labeled bovine serum albumin (125I-BSA) through the coronary vasculature, were used to estimate indices of vascular function, including the mean transit time of 125I-BSA, the fractional rate of intravascular clearance of 125I-BSA, and 125I-BSA permeation of coronary vessels. During reflow after ischemia in hearts from control rabbits, vascular resistance increased approximately three times that at baseline, left ventricular end-diastolic pressure (LVEDP) increased 8-10 times, and maximum +dP/dt recovered 0.4 times baseline, whereas the fractional rate of washout of intravascular 125I-BSA decreased to less than one-half of baseline values (was prolonged 2-fold), and albumin permeation and mean-transit time were increased 3 and 5 times baseline, respectively. In hearts from diabetic rabbits, vascular resistance was similar to the control group before ischemia but increased only one-third as much during reflow after ischemia. Increases in LVEDP during reflow were ~50% lower than controls, and +dP/dt recovered ~2.5 times more than in control hearts. 125I-BSA permeation in diabetics was similar to controls before ischemia, but during reflow increased 6 times (~2 times controls). Washout of intravascular 125I-BSA was prolonged ~20% versus baseline during 3 h of reflow in hearts from diabetic rabbits. Thus, ALX-D in the rabbit delayed ischemia-reperfusion injury to myocytes and vascular smooth muscle cells while increasing vascular albumin permeation.

UR - http://www.scopus.com/inward/record.url?scp=0024463232&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024463232&partnerID=8YFLogxK

M3 - Article

VL - 38

SP - 1484

EP - 1491

JO - Diabetes

JF - Diabetes

SN - 0012-1797

IS - 11

ER -