Circulation, Vol 86, 255-262, Copyright © 1992 by American Heart Association
H Drexler, E Hablawetz, W Lu, U Riede and A Christes
BACKGROUND. Large myocardial infarction is associated with reactive
hypertrophy and dilation of the left ventricle, depressed coronary flow
reserve, and the development of heart failure including systemic
vasoconstriction. We hypothetized that changes in endothelial function,
e.g., in the synthesis or action of nitric oxide in the coronary and
peripheral vasculatures, might be involved in the depressed coronary flow
reserve and increased systemic vascular resistance observed in
postinfarction myocardial hypertrophy and failure. METHODS AND RESULTS. The
regional blood flow changes that occur as a result of inhibiting the basal
release of nitric oxide with NG-monomethyl-L-arginine (L- NMMA) and how
this regional pattern may be altered in large MI (infarct size, 30-51% of
left ventricle) were examined. Measurements were made 24 hours and 8 weeks
after myocardial infarction or sham operation in conscious rats. The left
ventricular end-diastolic pressure and effects of L-NMMA on left
ventricular end-diastolic pressure was similar 24 hours and 8 weeks after
myocardial infarction. The effects of L-NMMA (30 mg/kg i.v.) on heart rate
and blood pressure were similar in infarcted and sham animals. L-NMMA
exerted a marked vasoconstriction in the renal, splanchnic, cutaneous, and
cerebral circulations of similar magnitude in sham-operated rats and
animals with myocardial infarction. The coronary vasoconstrictor effect of
L-NMMA was attenuated significantly in the hypertrophied right and
noninfarcted left ventricle of 8-week-old infarcted rats (p less than 0.01
versus sham- operated animals) but not 24 hours after induction of
myocardial infarction when cardiac hypertrophy has not yet developed. The
increase in left ventricular coronary resistance in 8-week-old infarcted
animals was inversely related to infarct size (r = -0.787, p = 0.012, n =
9). Nitroglycerin exerted similar increases in coronary blood flow in rats
with chronic myocardial infarction and sham-operated animals, arguing
against a reduced vascular responsiveness to nitric oxide. Transmission
electron microscopy of coronary resistance vessels in 8-week-old infarcted
animals did not reveal endothelial abnormalities. CONCLUSIONS. These data
suggest that the basal release of nitric oxide in the renal, intestinal,
and cutaneous circulations is not affected adversely in this model of
myocardial infarction and failure. However, the blunted coronary
vasoconstrictor effect of L-NMMA late after large myocardial infarction
supports the view that the basal release of nitric oxide is impaired in
postinfarction reactive cardiac hypertrophy.
ARTICLES
Effects of inhibition of nitric oxide formation on regional blood flow in experimental myocardial infarction
Medizinische Klinik III, University of Freiburg, FRG.
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