| BackgroundOperation treatments are the important measures to cardiovascular surgicaldisorders, and cardiopulmonary bypass (CPB) is the prerequisite condition ofopen heart operation. But so far, CPB is the greatest impact treatment measure tophysiological state, and the following organ injuries and complications are themain reasons for the poor prognosis of patients. CPB not only evokes strongstress and inflammation, but also leads to hyperglycemia and hyperinsulinemia,suggesting that CPB can induce acute insulin resistance (IR). How to reduce and avoid the injury occurring as far as possible in the CPB at the same time has beenan important research direction in the field of cardiac surgery. Glucose-insulin-potassium chloride polarized liquid (GIK) has more than40years of history incardiac operation perioperative application, but the method and the formula ofGIK differ in thousands of ways in heart centers, and the clinical effects are notthe same. This paper takes patients undergoing CPB mitral valve replacement(MVR) as the research objects to find out whether CPB can induce IR and theheart and other organs function and mechanism of modified GIK, thereforeproviding new clues for organ protections in the period of CPB.Purpose1. To observe whether CPB will induce acute IR, as well as the effects ofmodified GIK.2. To observe the changes of heart and other organs function in patientsundergoing MVR, and the effects modified GIK.3. To investigate the mechanism of modified GIK in the acute IR andmultiorgan function by CPB.MethodsThe experiment1(1) Select40patients of heart surgical diagnosis of mitralstenosis with or without regurgitation, and divide into2groups:21cases in GIKgroup,19cases in the control group, according to computer random number.(2)GIK group received GIK solution (20%glucose500mL, insulin33IU,10%potassium chloride30mL) via central venous catheter at60ml per hour beforeinduction of anesthesia and ended about six hours after aortic cross clamp (AXC)removal. The control group received equivalent0.9%Sodium chloride in the same fashion.(3)All patients were given routine examination and treatment,percutaneous thoracic incision approach, the ascending aorta and inferior venacava cannulation, on the establishment of CPB, and received conventional MVR.(4) Arterial blood samples were obtained respectively from patients of the twogroups before the operation, after anesthetic, CPB15min,5min following releaseof AXC, the end of CPB,30min，6h,12h,24h following the end of operation. Thelevels of blood glucose, insulin, lactic acid were measured, and the insulinresistance index (HOMA-IRI) was calculated using the HOMA Calculator V2.2.In the preoperative, CPB30min, postoperative1h,6h,12h,24h,48h, heart rate(HR), mean arterial pressure (MAP), mean pulmonary arterial pressure (MPAP),central venous pressure (CVP) were recorded.(5) Count data were analysedusing chi-square analysis, and measurement data were performed as mean plus SD(x+SD), using SPSS17statistical software. P <0.05was considered statisticallysignificant. Experiment2(1) Select40patients of heart surgical diagnosis ofmitral stenosis with or without regurgitation, and divide into2groups:21cases inGIK group,19cases in the control group, according to computer random number.(2) All of the patients were placed catheter placement of Swan-Ganz (7F, Arrow,USA) via right internal jugular vein before operation. GIK group received GIKsolution500ml (glucose20%, insulin33IU,10%potassium chloride30mL) viacentral venous catheter at60ml per hour before induction of anesthesia and endedabout six hours after aortic cross clamp (AXC) removal. The control groupreceived equivalent0.9%Sodium chloride in the same fashion.(3) All patientswere given routine examination and treatment, percutaneous thoracic incisionapproach, the ascending aorta and inferior vena cava cannulation, on theestablishment of CPB, and received conventional MVR.(4) Arterial bloodsamples were obtained respectively from patients of the two groups before the operation,12h,24h following the end of operation. The levels of AST, CK, LDH,CK-MB, ALT, TBA, BUN, CR were measured. Peri-operative hemodynamic dataand left ventricular ejection fraction (LVEF) were measured.(5) Count data wereanalysed using chi-square analysis, and measurement data were performed asmean plus SD (x+SD), using SPSS17statistical software. P <0.05wasconsidered statistically significant. Experiment3(1) Select40patients of heartsurgical diagnosis of mitral stenosis with or without regurgitation, and divide into2groups:21cases in GIK group,19cases in the control group, according tocomputer random number.(2) GIK group received GIK solution500ml (glucose20%, insulin33IU,10%potassium chloride30mL) via central venous catheter at60ml per hour before induction of anesthesia and ended about six hours after aorticcross clamp (AXC) removal. The control group received equivalent0.9%Sodiumchloride in the same fashion.(3) All patients were given routine examination andtreatment, percutaneous thoracic incision approach, the ascending aorta andinferior vena cava cannulation, on the establishment of CPB, and receivedconventional MVR.(4) Arterial blood samples were obtained respectively frompatients of the two groups before the operation, CPB15min, the end of CPB,24hfollowing the end of operation. The levels of epinephrine, glucocorticoids, CRP,IL-1, IL-10, and TNF-α were measured. Positive inotropic drug index (IS) wascalculated.(5) Count data were analysed using chi-square analysis, andmeasurement data were performed as mean plus SD (x+SD), using SPSS17statistical software. P <0.05was considered statistically significant.ResultsExperiment1: Perioperative blood glucose, insulin, and lactic in both groups ofpatients rised of different levels.However, blood glucose of GIK group was higher than that of the control group in the period of CPB, then lower than that ofcontrol group in postoperative. Blood insulin of GIK group was higher than thatof the control group in the period of CPB and postoperative6hrs. The peak ofblood glucose in the period of CPB was less than200mg per deciliter, and lessthan that of control group significantly in the postoperative6h,12h. The level oflactate was lower than that of the control group during the whole study period.patients of both groups showed marked insulin resistance phenomenon in theperioperative period, but the insulin resistance index (HOMA-IRI) of patients inGIK group was significantly lower than that of control group (P <0.05) in thepostoperative12h,24h. Experiment2: The cardiac index（CI）at postoperative24and48hours of GIK group increased significantly compared with control group;the LVEF of GIK group was higher than that of control group. The systemicvascular resistance (SVR) and pulmonary circulation resistance (PVR) atpostoperative24and48hours in GIK group decreased significantly comparedwith control group. AST, CK, LDH, CK-MB, ALT, TBA, BUN, CR of thepatients in GIK group at post-operative12,24h were lower than those of controlgroup. Experiment3: The level of blood glucocorticoid of GIK group was lowerand the level of blood epinephrine of GIK group was higher than that of controlgroup at the end of CPB. The level of CRP, IL-1, and TNF-αof GIK group werelower than that of control group at the period of CPB and postoperation, and thelevel of IL-10of GIK group was higher than that of control group at the sametime. GIK treatment was associated with a significant reduction in inotrope use24hrs postoperatively.ConclusionMVR patients showed significant acute IR, and GIK therapy improved this pathological condition. MVR patients showed significant multiple organs injuries,and GIK therapy during the CPB period can significantly improve the multipleorgans function. GIK therapy in the CPB period showed an benefit on multipleorgan protection effect and decreasing acute IR, and its mechanism may beassociated with lowered stress levels, improved metabolism and maintainence ofa stable inner environment. |
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