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The occurrence of PRS was associated with the use of NM (odds ratio [95% CI]= 0.190 [0.055�C0.660]; p = 0.009) and patient age (odds ratio [95% http://www.selleckchem.com/products/nutlin-3a.html CI]= 1.085 [1.017�C1.159]; p = 0.014). Perioperative lab data and recovery patterns were similar between the two groups (Figure 3). In both groups normal values were recovered by postoperative day 30. The ICU length of stay was shorter in the NM group compared to the control group (control group vs. NM group, 7 [4�C14] vs. 6 [4�C13] days, p = 0.019). Univariate logistic regression analyses determined pH and serum potassium concentration before graft reperfusion, dopamine use during the late postreperfusion period, occurrence of PRS, use of NM and diagnosis of the patient as potential http://www.selleck.cn/products/Romidepsin-FK228.html variables associated with the length of ICU stay. However, partial correlation analysis and nonparametric ANCOVA revealed that the diagnosis was the only significant factor when other factors were corrected (p http://www.selleckchem.com/products/AC-220.html 0.02 mg/kg of NM before reperfusion of the liver graft was associated with less frequent PRS and a faster recovery to a hemodynamically stable state requiring less vasopressors. Many surgical and anesthetic techniques have been tried to prevent and attenuate the PRS with varying degrees of success (3,12�C14). The association between PRS and clinical factors such as characteristics of recipient and donor graft, surgical techniques and anesthetic management is yet to be determined. In the early observation of PRS, Aggarwal and colleagues suspected that hypotension after reperfusion of the liver graft is caused by the release of ��yet to be defined vasodilating substances�� from the liver graft (15). Subsequent studies demonstrated that undefined substances released during ischemia reperfusion of the liver graft contribute toward cardiovascular instability through activation of the complement system and the kallikrein�Ckinin system, negative effect on cardiac performance, or inhibition of nitric oxide synthase (8,16�C18).