Effects of Pulsatile CPB on Interleukin‐8 and Endothelin‐1 Levels

Abstract

Studies on pulsatile and nonpulsatile perfusion have long been performed. However, investigators have not reached a conclusion on which is more effective. In the present study, pulsatile cardiopulmonary bypass (CPB) was investigated in terms of the effects on cytokines, endothelin, catecholamine, and pulmonary and renal functions. Twenty-four patients who underwent coronary artery bypass grafting were divided into a pulsatile CPB group and a nonpulsatile CPB group. Parameters examined were hemodynamics, interleukin-8 (IL-8), endothelin-1 (ET-1), epinephrine, norepinephrine, lactate, arterial ketone body ratio, urine volume, blood urea nitrogen, creatinine, renin activity, angiotensin-II, lactate dehydrogenase, plasma-free hemoglobin, tracheal intubation time, and respiratory index. The IL-8 at 0.5, 3, and 6 h after CPB, and ET-1 at 3, 6, 9, and 18 h after CPB were significantly lower in the pulsatile group. Both epinephrine and norepinephrine were significantly lower in the pulsatile group. The respiratory index was significantly higher in the pulsatile group. In the present study, inhibitory effects on cytokine activity, edema in pulmonary alveoli, and endothelial damage were shown in addition to the favorable effects on catecholamine level, renal function, and peripheral circulation that have already been documented.

Off-pump coronary artery bypass surgery versus standard linear or pulsatile cardiopulmonary bypass: endothelial activation and inflammatory response

“…Endothelial activation is critical to the development and maintenance of systemic inflammation and thus plays a pivotal role in post-CPB morbidity and mortality [1,4,10,11]. Accordingly, the clinical use of biochemical assays to detect and quantify circulating cytokines and chemokines -the main effectors of inflammatory response -may help increase our knowledge regarding SIRS [1,4].…”

“…Accordingly, the clinical use of biochemical assays to detect and quantify circulating cytokines and chemokines -the main effectors of inflammatory response -may help increase our knowledge regarding SIRS [1,4]. Despite the extensive literature, however, the mechanisms underlying post-CPB SIRS are not definitely understood, primarily because of extreme differences in inter-group settings in both animal and clinical studies [1][2][3][4][5][6][9][10][11][12]. The literature also lacks studies of endothelial response and cytokine leakage associated with PCPB versus OPCABG.…”

Pulse pressure-dependent cerebrovascular eNOS regulation in mice

“…[13][14][15] Similarly, non-pulsatile clinical cardiopulmonary by-pass increases sympathetic activity and plasma levels of renin, angiotensin II, norepinephrine, endothelin-1, TNFa and ROS, and inadequate synthesis of NO, inflammation and oxidative stress were also reported in the peripheral circulation ex vivo. 12,[16][17][18][19][20][21][22] While PP may modulate systemic neurohumoral control of hemodynamics, a direct regulatory effect on the endothelium is, however, poorly understood. A seminal study by Vanhoutte's group in 1986 showed that pulsatile flow increased endothelium-dependent relaxation of the canine femoral artery.…”

Pulsatile Cardiopulmonary Bypass With Intra-Aortic Balloon Pump Improves Organ Function and Reduces Endothelial Activation

“…12 Accordingly Orime et al found less endothelial damage and beneficial effects on the microcirculation with the pulsatile Jostra system, 14 as did Sezai et al, who demonstrated reduced endothelin-1 leakage and better peripheral circulation when pulsatile perfusion was used. 13 …”