Coronary vascular injury after transient coronary artery occlusion.
BACKGROUND
Microvascular function was examined in dog hearts subjected to transient coronary artery occlusion.


METHODS
Temporary coronary artery occlusion (15 or 30 minutes) followed by prolonged reperfusion (24 to 72 hours) was performed in dogs. Myocardial blood flow (radioactive microspheres), vascular permeability (human serum albumin uptake), and apparent vascular volume (radioactively labeled erythrocytes) were used as measures of vascular function. Myeloperoxidase was used as a measure of leukocyte uptake. Free radical formation was measured by electron spin resonance using a spin trapping agent (phenyl N-tert-butylnitrone).


RESULTS
A 30-minute occlusion followed by reperfusion produced prolonged hyperemia, increased vascular permeability, increased apparent vascular volume, and increased leukocyte uptake. Extravasation of red blood cells and carbon black was present within the coronary artery distribution. The altered vascular function was temporally correlated with prolonged leukocyte uptake and free radical production, returning to control values only at 72 hours. A 15-minute occlusion increased vascular permeability at 24 hours, without altering myocardial blood flow or apparent vascular volume. Transmural myocardial leukocyte accumulation after a 15-minute occlusion was minimal in the absence of myocardial infarction or other histologic alterations. Active free radical formation was minimal at 24 hours, with a return of vascular permeability to control values at 48 hours.


CONCLUSIONS
The data demonstrate prolonged dysfunction of the coronary microvasculature after a transient 30-minute occlusion of the left anterior descending coronary artery. The prolonged injury is associated temporally with leukocyte uptake and free radical formation in the presence of minimal infarction. A transient 15-minute occlusion produces a different pattern of vascular dysfunction with an abbreviated duration (24 hours), not associated with myocardial necrosis, extensive leukocyte uptake, nor prolonged free radical formation.
Patterson
E
E
Department of Pharmacology, University of Oklahoma Health Sciences Center, Oklahoma City.
Burow
R D
RD
Hung
C Y
CY
Scherlag
B J
BJ
D000818:Animals; D002199:Capillary Permeability; D003326:Coronary Circulation; D003331:Coronary Vessels / Q000000981:diagnostic imaging / Q000473:pathology* / Q000502:physiology*; D003497:Cyclic N-Oxides; D004285:Dogs; D004578:Electron Spin Resonance Spectroscopy; D005609:Free Radicals / Q000378:metabolism; D006801:Humans; D007962:Leukocytes / Q000502:physiology; D008833:Microcirculation / Q000000981:diagnostic imaging / Q000473:pathology*; D009589:Nitrogen Oxides; D010210:Papillary Muscles / Q000166:cytology / Q000473:pathology; D009195:Peroxidase / Q000378:metabolism; D011877:Radionuclide Imaging; D015424:Reperfusion; D012709:Serum Albumin / Q000378:metabolism; D013113:Spin Labels; D013668:Technetium Tc 99m Aggregated Albumin; D013997:Time Factors
D003497:Cyclic N-Oxides; D005609:Free Radicals; D009589:Nitrogen Oxides; D012709:Serum Albumin; D013113:Spin Labels; D013668:Technetium Tc 99m Aggregated Albumin; C029217:phenyl-N-tert-butylnitrone; D009195:Peroxidase