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(Circulation. 1997;95:1623-1634.)
© 1997 American Heart Association, Inc.

Articles

Effects of L-Arginine and N-Nitro-L-Arginine Methyl Ester on Cardiac Perfusion and Function After 1-Day Cold Preservation of Isolated Hearts

David F. Stowe, MD, PhD; Mladen Boban, MD; David L. Roerig, PhD; David Chang, MD; Barbara W. Palmisano, MD; Zeljko J. Bosnjak, PhD

From the Anesthesiology Research Laboratory, Departments of Anesthesiology (D.F.S., M.B., D.L.R, D.C., B.W.P., Z.J.B.) and Physiology (D.F.S., Z.J.B.), Cardiovascular Research Center, Medical College of Wisconsin, and Veterans Affairs Medical Center, Milwaukee, Wisc.

Correspondence to David F. Stowe, MD, PhD, 462 Medical Education Bldg, Medical College of Wisconsin, Milwaukee Regional Medical Center, 8701 W Watertown Plank Rd, Milwaukee, WI 53226.

Background Coronary flow responses to endothelium-dependent (acetylcholine [ACh] or 5-hydroxytryptamine [5-HT]) and endothelium-independent (adenosine [ADE] or nitroprusside [NP]) vasodilators may be altered before and after 1-day hypothermia during the perfusion of arginine vasopressin (AVP), D-arginine (D-ARG), L-arginine (L-ARG), or nitro-L-arginine methyl ester (L-NAME).

Methods and Results Four groups of guinea pig hearts (37.5°C [warm]) were perfused for 6 hours with AVP, L-ARG, L-NAME, or nothing (control). Five heart groups (cold) were perfused with AVP, D-ARG, L-ARG, L-NAME, or nothing (control), but after 2 hours they were perfused at low flow for 22 hours at 3.7°C and again for 3 hours at 37.5°C. ADE, butanedione monoxime, and NP were given for cardioprotection before, during, and after hypothermia. In warm groups, L-ARG did not alter basal flow or ADE, ACh, 5-HT, or NP responses, whereas L-NAME and AVP reduced basal flow and the ADE response, abolished ACh and 5-HT responses, and increased the NP response. In cold groups after hypothermia, L-ARG did not alter basal flow, but L-NAME, AVP, D-ARG, and control reduced flow. In the postcold L-ARG group, ACh increased peak flow, but NP did not increase flow in other cold groups. Effluent L-ARG and L-CIT in the cold control group fell from 64±9 and 9±1 µg/L at 1 hour to 36±5 and 5±1 µg/L at 25 hours, respectively. Left ventricular pressure and cardiac efficiency improved more in the postcold L-ARG group than in the postcold D-ARG, AVP, and L-NAME groups.

Conclusions Endogenous effluent levels of L-ARG and L-CIT decrease after 24 hours in isolated hearts, whereas perfusion of L-ARG improves cardiac performance, basal coronary flow, and vasodilator responses. In contrast, L-NAME, L-ARG, and AVP limit flow and performance but maintain a partial vasodilatory response to NP. Sustained release of NO may account for improved performance after L-ARG after hypothermia.

Key Words: vascular endothelium • 2,3 butanedione monoxime • cardiac hypothermia

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