title: Reperfusion conditions: critical importance of total ventricular decompression during regional reperfusion.
abstract: This study tests the hypothesis that failure to minimize left ventricular oxygen demands by venting during reperfusion diminishes recovery after controlled blood cardioplegic reperfusion. Of 25 dogs undergoing 2 hours of left anterior descending coronary occlusion, nine were reperfused with normal blood without bypass and five were reperfused with normal blood during total vented bypass. Eleven other dogs were reperfused with aspartate-glutamate-enriched, diltiazem-supplemented blood cardioplegic solution for 20 minutes during cardiopulmonary bypass; the left ventricle was decompressed by venting in only five of them. Regional systolic shortening was measured by ultrasonic crystals and myocardial damage estimated from triphenyltetrazolium chloride staining. All segments developed systolic bulging during ischemia (-23% systolic shortening, p less than 0.05), with no segmental recovery after reperfusion with normal blood without bypass (-27% systolic shortening, p less than 0.05) and negligible recovery following reperfusion with normal blood during total vented bypass (6 +/- 2%, p less than 0.05). In contrast, there was immediate recovery of regional contractility (+ 53% systolic shortening, p less than 0.05) in bypassed hearts reperfused with aspartate-glutamate-enriched, diltiazem-supplemented blood cardioplegic solution when venting was used and triphenyltetrazolium chloride nonstaining fell from 43% to 12% (p less than 0.05). Conversely, there was no postischemic recovery (-8% systolic shortening, p less than 0.05) when the same blood cardioplegic reperfusate was given over a comparable time without venting; triphenyltetrazolium chloride damage increased to 25% (p less than 0.05). Minimizing O2 demands by left ventricular decompression with venting during blood cardioplegic reperfusion is essential to ensure immediate functional recovery and limit histochemical damage.
mesh_terms: D000818:Animals; D001224:Aspartic Acid / Q000627:therapeutic use; D002118:Calcium / Q000627:therapeutic use; D006328:Cardiac Catheterization; D003326:Coronary Circulation; D003327:Coronary Disease / Q000503:physiopathology / Q000628:therapy*; D004110:Diltiazem / Q000627:therapeutic use; D004285:Dogs; D005971:Glutamates / Q000627:therapeutic use; D018698:Glutamic Acid; D006324:Heart Arrest, Induced; D006352:Heart Ventricles; D009200:Myocardial Contraction / Q000187:drug effects; D011189:Potassium Chloride / Q000627:therapeutic use; D014325:Tromethamine / Q000627:therapeutic use
chemical_list: D005971:Glutamates; D014325:Tromethamine; D001224:Aspartic Acid; D018698:Glutamic Acid; D011189:Potassium Chloride; D004110:Diltiazem; D002118:Calcium