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Ulinastatin as a neuroprotective and anti‐inflammatory agent in infant piglets model undergoing surgery on hypothermic low‐flow cardiopulmonary bypass
Author(s) -
Wang Xiaocou,
Xue Qinghua,
Yan Fuxia,
Li Lihuan,
Liu Jinping,
Li Shoujun,
Hu Shengshou
Publication year - 2013
Publication title -
pediatric anesthesia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.704
H-Index - 82
eISSN - 1460-9592
pISSN - 1155-5645
DOI - 10.1111/pan.12073
Subject(s) - medicine , ulinastatin , cardiopulmonary bypass , anesthesia , neuroprotection , saline , enolase , immunohistochemistry
Summary Objective Infants are potentially more susceptible to brain injury mediated via cell death attributed to cardiopulmonary bypass (CPB) especially with prolonged hypothermic low flow ( HLF ). We hypothesized that a human urinary protease inhibitor (ulinastatin), by its anti‐inflammatory effect, would reduce central nervous system ( CNS ) injury during HLF . Methods Fifteen general‐type infant piglets were randomized to ulinastatin group ( G roup U , n  = 5), control group ( G roup C , n  = 5), and sham operation group ( G roup S , n  = 5). Routine CPB was established after median thoracotomy in G roup U and C under anesthesia. When the temperature of infant piglets dropped down to 25°C, low‐flow CPB (50 ml·kg −1 ·min −1 ) was instituted. After 120 min of aortic cross‐clamping and 20‐ to 30‐min rewarming, the aortic cross‐clamp was removed and finally the piglet was weaned from CPB . Five thousand units per killogram of ulinastatin and equivalently normal saline were, respectively, given at the beginning of and at aortic declamping in G roup U and G roup C . Group S just received sham median thoracotomy. Venous blood samples were taken immediately after anesthesia induction in all three groups, 5‐ and 120‐min post CPB in both Group U and C , respectively; plasma markers of inflammation and CNS injury were compared. Pathology results of hippocampus were observed by light microscopy. Results Statistically significant differences between Group C and U were noted in the expression of inflammatory markers such as IL ‐10, TNF ‐α and neuron‐specific enolase at 120‐min post CPB . Brain injuries were observed in both groups (index cases and controls) and were milder in G roup U . Conclusions In our study, HLF CPB on infant piglets resulted in brain injury, and ulinastatin might reduce the extent of such injury.

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