Effects of acute lung injury and anesthesia on left ventricular mechanics

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Abstract
Traditional left ventricular (LV) function curves are frequently depressed in patients with acute lung injury. Similar findings in pentobarbital sodium-anesthetized dogs with oleic acid lung injury (OALI) have been observed. To test the hypothesis that acute OALI produces a significant injury to the heart, the LV mechanics of pentobarbital-anesthetized dogs with (n = 6) and without (n = 6) OALI were evaluated. End-systolic force-length and force-velocity relations determined echocardiographically during afterload manipulation with sodium nitroprusside demonstrated a marked deterioration in LV shortening characteristics over 90 min in both groups of pentobarbital-anesthetized dogs. In contrast, LV mechanics studied using the same protocol in fentanyl-anesthetized dogs were unchanged in both the injured (n = 6) and noninjured (n = 6) lung groups. Comparisons with data acquired over a wide range of LV afterload from six conscious, instrumented dogs showed that LV contractile state was normal to slightly increased with fentanyl and markedly depressed with pentobarbital. Diastolic properties, as assessed by end-diastolic pressure-dimension relations, were essentially unchanged in all anesthetized animals. We conclude that OALI has no effect on LV systolic or diastolic mechanics; the LV dysfunction attributed to OALI in previous studies is due to an acute, severe cardiomyopathy induced by pentobarbital; and unlike pentobarbital, anesthesia with fentanyl has no discernible time-dependent effect on LV mechanics. These findings have important implications for future studies of canine cardiovascular physiology employing anesthetized animal preparations.

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