TY - JOUR
T1 - Regional vascular adjustments during recovery from myocardial infarction in rats
AU - Drexler, Helmut
AU - Toggart, Edward J.
AU - Glick, Mark R.
AU - Heald, Jim
AU - Flaim, Stephen F.
AU - Zelis, Robert
N1 - Funding Information:
From the Departments of Medicine and ysiologPhy, The Milton Hershey Medical Center, The Pennsylvania State University College of Medicine, Hershey, Pennsylvanai. This study swa supported in part by Public Health Service Grant HL 25186 from the National Heart, Lung, and Blood stitute,In Bethesda, Maryland, the Sam Ostrow Cardiology Research Fund, Hershey, the American Heart Association York-Adams Chapter, York, Pennsylvania and a gift from the Grand Pennsylvania Chapter Order of the Eastern Star, Harrisburg, Pennsylvania. Dr. Drexler was the recipient of a fellowship antgr from the scheDeut schungForsge meinschaft (DFGl, Federal Republic of Germany. Dr. Toggart was sup ported by the National Heart, Lung, and Blood stInitute, Bethesda, aryM land, Public Health Service Training Grant HL06239-02. Manuscript received January 13, 1986, accedpet January 29, 1986. Address orf reprints: Stephen F. Flaim, PhD, Department of oloigicalB Research, Section for Cardiovaculars Research, cNeMil Pharmaceutical, Spring House, Pennsylvania 19477.
PY - 1986
Y1 - 1986
N2 - Left ventricular function and systemic regional blood flow (radioactive microspheres, 15 ± 5 μ) were studied 1, 3, 10 or 42 days after left coronary occlusion in conscious rats. One day after coronary occlusion, vascular resistance in the skeletal muscle and cutaneous beds increased while stroke work and left ventricular systolic pressure were depressed. Regional blood flow and hemodynamic data were similar for sham and infarction groups at 3 and 10 days after surgery, except for left ventricular end-diastolic pressure, which was significantly increased in rats with infarction (sham versus infarct: 11.5 ± 1.0 versus 18.4 ± 3.2 at day 3 and 12.2 ± 1.4 versus 19.9 ± 3.2 at day 10) (p < 0.05). At 42 days after myocardial infarction, manifest heart failure occurred as documented by decreased cardiac output and left ventricular systolic pressure and elevated left ventricular end-diastolic pressure and vascular resistance in the cutaneous, skeletal muscle and renal beds. In a separate group of animals with moderate (33.2 ±2% of left ventricle) and large infarctions (45 ±1.3% of left ventricle), regional blood flow was compared with the sham group. Rats with a large infarct demonstrated significant (p < 0.05) reduction in flow to kidney, gut and liver. In rats with a medium sized infarct, only renal blood flow was significantly reduced. It is concluded that in this model of myocardial infarction, early cardiocirculatory depression is followed by a partially compensated state with increased left ventricular end-diastolic pressure and subsequent systemic and regional vasoconstriction which, in turn, may contribute to late deterioration of heart failure.
AB - Left ventricular function and systemic regional blood flow (radioactive microspheres, 15 ± 5 μ) were studied 1, 3, 10 or 42 days after left coronary occlusion in conscious rats. One day after coronary occlusion, vascular resistance in the skeletal muscle and cutaneous beds increased while stroke work and left ventricular systolic pressure were depressed. Regional blood flow and hemodynamic data were similar for sham and infarction groups at 3 and 10 days after surgery, except for left ventricular end-diastolic pressure, which was significantly increased in rats with infarction (sham versus infarct: 11.5 ± 1.0 versus 18.4 ± 3.2 at day 3 and 12.2 ± 1.4 versus 19.9 ± 3.2 at day 10) (p < 0.05). At 42 days after myocardial infarction, manifest heart failure occurred as documented by decreased cardiac output and left ventricular systolic pressure and elevated left ventricular end-diastolic pressure and vascular resistance in the cutaneous, skeletal muscle and renal beds. In a separate group of animals with moderate (33.2 ±2% of left ventricle) and large infarctions (45 ±1.3% of left ventricle), regional blood flow was compared with the sham group. Rats with a large infarct demonstrated significant (p < 0.05) reduction in flow to kidney, gut and liver. In rats with a medium sized infarct, only renal blood flow was significantly reduced. It is concluded that in this model of myocardial infarction, early cardiocirculatory depression is followed by a partially compensated state with increased left ventricular end-diastolic pressure and subsequent systemic and regional vasoconstriction which, in turn, may contribute to late deterioration of heart failure.
UR - http://www.scopus.com/inward/record.url?scp=0022636985&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0022636985&partnerID=8YFLogxK
U2 - 10.1016/S0735-1097(86)80104-8
DO - 10.1016/S0735-1097(86)80104-8
M3 - Article
C2 - 3711508
AN - SCOPUS:0022636985
SN - 0735-1097
VL - 8
SP - 134
EP - 142
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
IS - 1
ER -