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Objective:To evaluate the effect of controlled low central venous pressure with milrinone on laparoscopic hepatectomy in the patients.Methods:Fifty American Society of Anesthesiologists physical statusⅠ-Ⅲ patients of both sexes, aged 18-64 yr, with body mass index of 18-30 kg/m 2, of Child-Pugh grade A or B, undergoing elective laparoscopic hepatectomy, were divided into 2 groups ( n=25 each) using a random number table method: milrinone group (group M) and nitroglycerin group (group NG). After the start of surgery, milrinone 0.5 μg·kg -1·min -1 was continuously infused in group M, and nitroglycerin was continuously infused with the initial dose of 0.5 μg·kg -1·min -1 to maintain central venous pressure (CVP)≤5 mmHg in group NG.Mean arterial pressure and heart rate were recorded on admission to the operation room (T 0), at skin incision (T 1), at the beginning of liver resection (T 2), at completion of liver resection (T 3), at the end of operation (T 4), and CVP, cardiac index and stroke volume variation were recorded at T 1-4.Internal jugular vein blood samples were collected to determine the concentrations of hemogloblin, blood lactate at T 1 and T 4, and serum alanine aminotransferase, aspartate aminotransferase and creatinine concentrations at 1, 3 and 7 days after surgery.The score of blood oozing in hepatic surgical field, amount of norepinephrine used, blood loss, postoperative recovery and occurrence of complications within 7 days after operation were recorded. Results:Compared with group NG, cardiac index was significantly increased at T 2, 3, the CVP was decreased at T 2, the blood oozing score, blood loss, consumption of norepinephrine, and concentrations of blood lactate were decreased, and the postoperative drainage indwelling time was shortened in group M ( P<0.05). There was no significant difference in the serum alanine aminotransferase, aspartate aminotransferase and creatinine concentrations and incidence of postoperative complications at 1, 3 and 7 days after operation between the two groups ( P>0.05). Conclusions:Milrinone is better than nitroglycerin in decreasing central venous pressure, reducing blood loss, maintaining stable circulatory function and tissue perfusion in laparoscopic hepatectomy.
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Objective To evaluate the effect of ulinastatin on the activity of Janus kinase 2/signaling transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway during focal cerebral ischemia-reperfusion (I/R) in rats.Methods Forty-eight clean-grade healthy adult male Sprague-Dawley rats,aged 6-8 weeks,weighing 230-280 g,were divided into 3 groups (n=16 each) using a random number table:sham operation group (S group),cerebral I/R group (I/R group) and ulinastatin group (U group).Focal cerebral I/R was induced by occlusion of the middle cerebral artery for 2 h followed by reperfusion.Ulinastatin 100 000 U/kg was injected via the femoral vein immediately after beginning of cerebral ischemia in group U.Neurologic deficit was evaluated and scored (NDS) at 24 h of reperfusion.The rats were then sacrificed and brains were removed for measurement of the cerebral infarct size (by TTC staining) and for determination of the expression of total JAK2,total STAT3 and phosphorylated JAK2 (p-JAK2) and phosphorylated STAT3 (p-STAT3) in the cerebral cortex.Results Compared with S group,NDS and cerebral infarct size were significantly increased,and the expression of p-STAT3 and p-JAK2 in the cerebral cortex was up-regulated in I/R group and U group (P＜0.05).Compared with I/R group,NDS and cerebral infarct size were significantly decreased,and the expression of p-STAT3 and p-JAK2 in the cerebral cortex was down-regulated in U group (P＜0.05).There was no significant difference in the expression of total JAK2 and total STAT3 in the cerebral cortex between three groups (P＞0.05).Conclusion Ulinastatin can inhibit the activity of JAK2/STAT3 signaling pathway during cerebral I/R,which may be involved in the brain protective mechanism of ulinastatin in rats.
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Objective To evaluate the effect of intrathecal dexmedetomidine on the expression of G-protein-coupled inwardly rectifying K+ channel 1 (GIRK1) in dorsal root ganglia of rats with diabetic neuropathic pain (DNP).Methods A total of 144 healthy adult male SPF Sprague-Dawley rats,aged 8-10 weeks,weighing 200-220 g,were randomly divided into 4 groups (n =36 each) using a random number table:control group (group C),dexmedetomidine group (group D),group DNP,and DNP + dexmedetomidine group (group DD).DNP model was established by single intraperitoneal injection of streptozotocin (STZ) 60 mg/kg.In D and DD groups,dexmedetomidine 1.5 μg/kg was injected intrathecally at 14 days after citrate buffer or STZ injection,while the equal volume of normal saline was given in group C.The mechanical pain threshold was measured before STZ injection (T0),at 14 days after STZ injection (T1),and at 2,4 and 6 h after intrathecal injection (T:2-4).After measurement of the mechanical pain threshold at T2-4,the rats were sacrificed,and the dorsal root ganglia of the lumbar segment (L4-6) were removed for determination of the number of GIRK1 positive cells and expression of GIRK1 protein by immunofluorescence and Western blot,respectively.Results Compared with group DNP,the mechanical pain threshold was significantly increased,the number of GIRK1 positive cells in dorsal root ganglia was significantly increased,and the expression of GIRK1 was significantly up-regulated at T2-4 in group DD (P＜0.05).Compared with group D,the number of GIRK1 positive cells in dorsal root ganglia was significantly increased,and the expression of GIRK1 was significantly up-regulated at T2-4 in group DD (P＜0.05).Compared with group C,the mechanical pain threshold was significantly decreased at T1-4 in group DNP (P＜0.05).Conclusion Intrathecal dexmedetomidine attenuates DNP through up-regulating the expression of GIRK1 in dorsal root ganglia of rats.
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Objective To investigate the protective effects of ulinastatin on express of GRP 78、CHOP and caspase-12, the molecules related to endoplasmic reticulum stress (ERS),after ischemia reperfusion injury in rats.Methods Ninety rats were equally randomized into 3 groups(n=30): Sham group (S group,n=30), Ischemia -reperfusion group (I/R group, n=30), Ulinastatin group (U group, n=30).Focal transient cerebral ischemia model was established with intralu-minal occlusion fo left meddle cerebral artery .Made through 2 hours of temporary middle cerebral artery occlusion , followed with 24 hours of reperfusion .The pathological results were investigated by HE staining and the cerebral injury situation was e -valuated by neurological deficit scores .Infract volume was measured by TTC staining , apoptosis was detected by TdT -medi-ated dUTP and nick end labeling (TUNEL), and expression of GRP78, CHOP and caspase -12 were meastured by western blot.Results Compared with the S group , the number of apoptotic cells were significantly increase in I /R group and U group (P<0.05);infarct volume and expression of GRP -78, CHOP and caspase-12 were significantly increased in I/R group and U group (P<0.05).The infarct volume and the number of apoptotic cells were significantly less in U group than in I/R group ( P<0.05 ) .GRP78 expression was higher in U group than in I/R group ( P<0.05 ) , however CHOP and caspase-12 expression was less in U group than in I/R group (P<0.05).Conclusion Ulinastatin has a protective effect on cerebral ischemia reperfusion injury , which may related to increased GRP 78, decreased CHOP and caspase -12 expres-sion and to inhibition of the ERS -induced apoptosis pathway .