TY - JOUR T1 - Renal effects of nitric oxide in endotoxemia. AU - Cohen,R I, AU - Hassell,A M, AU - Marzouk,K, AU - Marini,C, AU - Liu,S F, AU - Scharf,S M, PY - 2001/12/6/pubmed PY - 2002/1/19/medline PY - 2001/12/6/entrez SP - 1890 EP - 5 JF - American journal of respiratory and critical care medicine JO - Am J Respir Crit Care Med VL - 164 IS - 10 Pt 1 N2 - Nitric oxide (NO) is postulated to play a key role in the pathophysiology of renal failure in sepsis. Whether the renal effects of increased NO are beneficial or harmful remains unclear. In a porcine model of lipopolysaccharide (LPS)-induced shock, we evaluated the effect of LPS on glomerular filtration rate (GFR) and renal blood flow (RBF). We then administered the nonselective nitric oxide synthase (NOS) inhibitor N(G)-L-arginine methyl ester (L-NAME), and compared its effects on GFR and RBF with those of S-methylisothiourea (SMT), a selective NOS inhibitor, and those of saline. We postulated that SMT, by maintaining constitutive NO, would be more beneficial than either L-NAME or saline. LPS infusion decreased mean arterial pressure (MAP), and increased cardiac output, RBF, and medullary NO content. The increased RBF was diverted to the medulla. There was no evidence of renal dysfunction in the saline-resuscitated group. Both NOS inhibitors increased MAP but decreased RBF, but only L-NAME reduced GFR and increased sodium excretion and renal oxygen extraction. We conclude that NO in endotoxemia is beneficial because it maintains RBF and GFR. Additionally, selective NOS inhibition did not offer any advantages over saline resuscitation. SN - 1073-449X UR - https://www.unboundmedicine.com/medline/citation/11734442/Renal_effects_of_nitric_oxide_in_endotoxemia_ L2 - https://www.atsjournals.org/doi/10.1164/ajrccm.164.10.2103140?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -