EFFECT OF HYPERTONIC SALINE DEXTRAN ON POSTSTENOTIC MYOCARDIAL PERFUSION, METABOLISM, AND FUNCTION DURING RESUSCITATION FROM HEMORRHAGIC-SHOCK IN ANESTHETIZED PIGS/

Resuscitation using small volumes of hypertonic saline solutions norma lizes cardiac output without fully restoring arterial pressure. This s tudy compared the efficacy of either 7.2% saline/10% dextran 60 (HSDex ) or the identical sodium load of normal saline (NS) to improve region al myocardial blood flow (MBF), contractile function, and oxygen metab olism in the presence of a critical coronary stenosis. Fourteen anesth etized, open-chest pigs (25+/-3.6 kg) were instrumented to assess left anterior descending coronary artery (LAD) flow, post-stenotic oxygen, and lactate metabolism, regional myocardial segment shortening (SS, s onomicrometry), and MBF(radioactive microspheres). After implementatio n of a critical LAD-stenosis, shock was induced by hemorrhage (mean ar terial pressure (MAP) 45-50 mmHg for 75 min). Resuscitation was starte d by infusion (2 min) of either HSDex (n=7, 80% of blood loss) or NS ( n=7, 80% of blood loss); 30 min later 6% dextran 60 (10% of blood loss ) was administered in both groups. The LAD-stenosis did not affect myo cardial metabolism, SS, or MBF at rest. After hemorrhage, MBF remained unchanged from baseline in non-stenotic but decreased by 53% in post- stenotic myocardium (p <.05). The endo-epicardial flow ratio fell belo w 1.0 in both areas. SS decreased by 10-15% only in post-stenotic myoc ardium (p <.05). Resuscitation with both HSDex and NS restored cardiac index (CI) but not MAP. MBF increased above baseline values with eith er solution in non-stenotic while it remained at shock levels in post- stenotic myocardium, where ischemia persisted as evidenced by lactate production and depressed SS. Neither in non-stenotic nor in post-steno tic myocardium was the epi-endocardial flow ratio normalized upon resu scitation with HSDex or NS. We conclude that in the presence of a flow -limiting coronary stenosis, initial fluid resuscitation with both HSD ex and the identical sodium load of NS failed to restore perfusion pre ssure, redistributed MBF in favor of normally perfused myocardium, and did not reverse ischemia in post-stenotic myocardium.