title: Comparative effects of hypotension due to isoflurane, nitroglycerin, and adenosine on subendocardial microcirculation: observation of the in situ beating swine heart under critical stenosis.
abstract: BACKGROUND
  Although isoflurane may cause subendocardial hypoperfusion in the presence of coronary stenosis because of its coronary arteriolar dilatory effects, it is not known how the subendocardial microcirculation is affected. The authors examined the effects of isoflurane on poststenotic subendocardial microvessels with coronary stenosis.
  
  
  METHODS
  The authors observed subendocardial microvessels in in situ beating swine hearts with or without critical stenosis of the left anterior descending coronary artery (LAD) with a needle-type videomicroscope during isoflurane- (ISO-H), adenosine- (ADE-H), and nitroglycerin- (NTG-H) induced hypotension (mean arterial pressure, 55 mmHg). Regional myocardial function, oxygen balance, and lactate metabolism in the region perfused by the LAD also were determined.
  
  
  RESULTS
  In swine with stenosis, there were no differences in heart rate, cardiac output, and LAD blood flow among the three types of hypotension. Regional lactate production and anterior interventricular venous pO2 were similar during ISO-H and NTG-H but higher during ADE-H. With videomicroscopy, about half as many subendocardial microvessels could be visualized during ADE-H as with ISO-H and NTG-H. The average decrease in the systolic diameter of subendocardial microvessels of greater than 100 microm was 9 +/- 6% during ISO-H and 12 +/- 5% during NTG-H, but no consistent phasic diameter changes were observed during ADE-H. In swine without stenosis, a systolic diameter decrease was observed during all three types of hypotension.
  
  
  CONCLUSIONS
  These findings suggest that hypotension induced by isoflurane or nitroglycerin preserves phasic diameter changes in subendocardial microvessels in the presence of critical coronary stenosis, whereas that induced by adenosine does not.
authors.affiliation: Institute for Surgical Research, Klinikum Grosshadern, Ludwig-Maximilians University, Munich, Germany. fujitay@med.kawasaki-m.ac.jp
authors.forename: Y
authors.initials: Y
authors.lastname: Fujita
authors.forename: H
authors.initials: H
authors.lastname: Habazettl
authors.forename: C O
authors.initials: CO
authors.lastname: Corso
authors.forename: K
authors.initials: K
authors.lastname: Messmer
authors.forename: T
authors.initials: T
authors.lastname: Yada
mesh_terms: D000241:Adenosine / Q000494:pharmacology*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D003327:Coronary Disease / Q000503:physiopathology*; D004699:Endocardium; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D006863:Hydrogen-Ion Concentration; D007530:Isoflurane / Q000494:pharmacology*; D008297:Male; D008833:Microcirculation / Q000187:drug effects; D005996:Nitroglycerin / Q000494:pharmacology*; D013552:Swine
chemical_list: D007530:Isoflurane; D005996:Nitroglycerin; D000241:Adenosine