Identification and control of noncoronary collateral blood flow

S. F. Bolling, K. R. Kanter, J. T. Flaherty, Vincent L Gott, T. J. Gardner

Research output: Contribution to journalArticle

Abstract

To identify the source of noncoronary collateral myocardial blood flow and to establish methods to control it during induced ischemia, 29 dogs were placed on cardiopulmonary bypass. The right and left ventricles were vented, vent flows were measured volumetrically, and intracavitary left ventricular (LV) pressures were monitored. After induction of ischemia by aortic cross-clamping and infusion of cardioplegic solution, six different microspheres 7 to 10 μm in diameter were injected into the aorta at six different times to measure myocardial blood flow during the following interventions: vent drainage of the right or left ventricle or both, proximal ligation of both coronary arteries, severance of the proximal pulmonary artery or the ascending aorta or both, and ligation of the bronchial arteries. Without effective LV venting, LV intracavitary pressure rose to 7.0 ± 0.1 mm Hg (mean ± standard error of the mean) and myocardial blood flow in the anterior left ventricle was 2.3 ± 1.3 ml/100 gm/min. When the LV vent was opened, vent flow was 35.9 ± 3.5 ml/min and myocardial blood flow fell to 0.3 ± 0.2 ml/100 gm/min. Right ventricular (RV) vent flow was absent except when the LV vent was occluded, and this RV vent flow was abolished by ligating the coronary arteries. With bronchial artery ligation, LV vent flow ceased and myocardial blood flow was virtually absent. These studies demonstrate that myocardial blood flow does occur during induced ischemia, but that the source of this blood flow is primarily through systemic-pulmonary channels. True noncoronary collateral myocardial blood flow was virtually nonexistent.

Original languageEnglish (US)
Pages (from-to)232-236
Number of pages5
JournalAnnals of Thoracic Surgery
Volume38
Issue number3
DOIs
StatePublished - 1984

Fingerprint

Heart Ventricles
Bronchial Arteries
Ligation
Ischemia
Ventricular Pressure
Aorta
Coronary Vessels
Cardioplegic Solutions
Cardiopulmonary Bypass
Microspheres
Constriction
Pulmonary Artery
Drainage
Dogs
Lung

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Surgery

Cite this

Identification and control of noncoronary collateral blood flow. / Bolling, S. F.; Kanter, K. R.; Flaherty, J. T.; Gott, Vincent L; Gardner, T. J.

In: Annals of Thoracic Surgery, Vol. 38, No. 3, 1984, p. 232-236.

Research output: Contribution to journalArticle

Bolling, S. F. ; Kanter, K. R. ; Flaherty, J. T. ; Gott, Vincent L ; Gardner, T. J. / Identification and control of noncoronary collateral blood flow. In: Annals of Thoracic Surgery. 1984 ; Vol. 38, No. 3. pp. 232-236.
@article{732c72b7adc040d38a2f579c25c9378e,
title = "Identification and control of noncoronary collateral blood flow",
abstract = "To identify the source of noncoronary collateral myocardial blood flow and to establish methods to control it during induced ischemia, 29 dogs were placed on cardiopulmonary bypass. The right and left ventricles were vented, vent flows were measured volumetrically, and intracavitary left ventricular (LV) pressures were monitored. After induction of ischemia by aortic cross-clamping and infusion of cardioplegic solution, six different microspheres 7 to 10 μm in diameter were injected into the aorta at six different times to measure myocardial blood flow during the following interventions: vent drainage of the right or left ventricle or both, proximal ligation of both coronary arteries, severance of the proximal pulmonary artery or the ascending aorta or both, and ligation of the bronchial arteries. Without effective LV venting, LV intracavitary pressure rose to 7.0 ± 0.1 mm Hg (mean ± standard error of the mean) and myocardial blood flow in the anterior left ventricle was 2.3 ± 1.3 ml/100 gm/min. When the LV vent was opened, vent flow was 35.9 ± 3.5 ml/min and myocardial blood flow fell to 0.3 ± 0.2 ml/100 gm/min. Right ventricular (RV) vent flow was absent except when the LV vent was occluded, and this RV vent flow was abolished by ligating the coronary arteries. With bronchial artery ligation, LV vent flow ceased and myocardial blood flow was virtually absent. These studies demonstrate that myocardial blood flow does occur during induced ischemia, but that the source of this blood flow is primarily through systemic-pulmonary channels. True noncoronary collateral myocardial blood flow was virtually nonexistent.",
author = "Bolling, {S. F.} and Kanter, {K. R.} and Flaherty, {J. T.} and Gott, {Vincent L} and Gardner, {T. J.}",
year = "1984",
doi = "10.1016/S0003-4975(10)62244-8",
language = "English (US)",
volume = "38",
pages = "232--236",
journal = "Annals of Thoracic Surgery",
issn = "0003-4975",
publisher = "Elsevier USA",
number = "3",

}

TY - JOUR

T1 - Identification and control of noncoronary collateral blood flow

AU - Bolling, S. F.

AU - Kanter, K. R.

AU - Flaherty, J. T.

AU - Gott, Vincent L

AU - Gardner, T. J.

PY - 1984

Y1 - 1984

N2 - To identify the source of noncoronary collateral myocardial blood flow and to establish methods to control it during induced ischemia, 29 dogs were placed on cardiopulmonary bypass. The right and left ventricles were vented, vent flows were measured volumetrically, and intracavitary left ventricular (LV) pressures were monitored. After induction of ischemia by aortic cross-clamping and infusion of cardioplegic solution, six different microspheres 7 to 10 μm in diameter were injected into the aorta at six different times to measure myocardial blood flow during the following interventions: vent drainage of the right or left ventricle or both, proximal ligation of both coronary arteries, severance of the proximal pulmonary artery or the ascending aorta or both, and ligation of the bronchial arteries. Without effective LV venting, LV intracavitary pressure rose to 7.0 ± 0.1 mm Hg (mean ± standard error of the mean) and myocardial blood flow in the anterior left ventricle was 2.3 ± 1.3 ml/100 gm/min. When the LV vent was opened, vent flow was 35.9 ± 3.5 ml/min and myocardial blood flow fell to 0.3 ± 0.2 ml/100 gm/min. Right ventricular (RV) vent flow was absent except when the LV vent was occluded, and this RV vent flow was abolished by ligating the coronary arteries. With bronchial artery ligation, LV vent flow ceased and myocardial blood flow was virtually absent. These studies demonstrate that myocardial blood flow does occur during induced ischemia, but that the source of this blood flow is primarily through systemic-pulmonary channels. True noncoronary collateral myocardial blood flow was virtually nonexistent.

AB - To identify the source of noncoronary collateral myocardial blood flow and to establish methods to control it during induced ischemia, 29 dogs were placed on cardiopulmonary bypass. The right and left ventricles were vented, vent flows were measured volumetrically, and intracavitary left ventricular (LV) pressures were monitored. After induction of ischemia by aortic cross-clamping and infusion of cardioplegic solution, six different microspheres 7 to 10 μm in diameter were injected into the aorta at six different times to measure myocardial blood flow during the following interventions: vent drainage of the right or left ventricle or both, proximal ligation of both coronary arteries, severance of the proximal pulmonary artery or the ascending aorta or both, and ligation of the bronchial arteries. Without effective LV venting, LV intracavitary pressure rose to 7.0 ± 0.1 mm Hg (mean ± standard error of the mean) and myocardial blood flow in the anterior left ventricle was 2.3 ± 1.3 ml/100 gm/min. When the LV vent was opened, vent flow was 35.9 ± 3.5 ml/min and myocardial blood flow fell to 0.3 ± 0.2 ml/100 gm/min. Right ventricular (RV) vent flow was absent except when the LV vent was occluded, and this RV vent flow was abolished by ligating the coronary arteries. With bronchial artery ligation, LV vent flow ceased and myocardial blood flow was virtually absent. These studies demonstrate that myocardial blood flow does occur during induced ischemia, but that the source of this blood flow is primarily through systemic-pulmonary channels. True noncoronary collateral myocardial blood flow was virtually nonexistent.

UR - http://www.scopus.com/inward/record.url?scp=0021155064&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0021155064&partnerID=8YFLogxK

U2 - 10.1016/S0003-4975(10)62244-8

DO - 10.1016/S0003-4975(10)62244-8

M3 - Article

C2 - 6383241

AN - SCOPUS:0021155064

VL - 38

SP - 232

EP - 236

JO - Annals of Thoracic Surgery

JF - Annals of Thoracic Surgery

SN - 0003-4975

IS - 3

ER -