Objective To observe the changes of serum potassium level and the factors that affected it when preoperative intravenous administration of gelofusine was given rapidly at high dose. Methods Thirty patients scheduled for upper abdominal operation were selected for the study and they were randomizely divided into test group (gelofusion group) and control group with 15 cases in each group. The first blood and urine sample was taken after epidural puncture and the potassium value was used as basic values. Then an intravenous administration of gelofusion at a dose of 10ml/kg was given in gelofusion group within 30min and then the second sample was obtained. Another intravenous administration of gelofusion at a dose of 10 ml/kg was given within 1 hour and the third sample was taken, while the fourth and fifth samples were taken 30 and 90 minutes after the third samples taken respectively. All the blood samples were tested for serum level of electrolytes (Na+,K+,Cl-,Ca2+,Mg2+), pH, Osm, Hct. The value of electrolytes (Na+,K+,Cl-,Ca2+,Mg2+) of urine samples were determined too. The intracellular levels of K+ and Mg2+ of erythrocyte were tested. The gelofusion were replaced by saline solution in control group and the other procedures were the same.Results The serum level of potassium was decreased progressively after rapid intravenous administration of gelofusine at high dose. Conclusion The serum level of potassium will decrease significantly after rapid intravenous administration of gelofusion at high dose during operation.
In order to observe electrolyte changes before and after scheduled abdominal surgery and effect of prompt potassium supplement on the recovery of gastrointestinal function, electrolytes in 69 patients were tested before and after surgery, and the recovery of the gastrointestinal function was observed.The results showed that after surgery the levels of K＋, Na＋ and Cl＋ were decreased dramatically (Ｐ＜0.05) but still within the normal range, with no distinctive change in Ca２＋ and Mg２＋. No correlation between the amount of blood transfusion and potassium was detected. Prompt potassium supplement contributed to the quick recovery of gastrointestinal function.This suggests that with normal renal function, blood transfusion during the operation will not cause hyperkalemia, potassium supplement might begin on the first day when the patient begins to urinale.
The effects on rat’s liver preservation using HX solation with high potassium and low sodium or HXm solution with high sodium and low potassium were studied with isolated perfusion of rat livers (IPRL). Sixty inbred Wistar rats were randomly divided into group HX (preserved with HX solution, n=30) and group HXm (preserved with HXm solution,n=30). The preservation effects of the storage solutions were assessed by measuring the sinunoidal lining cell mortality (SLCM), the Krebs-hense-leit perfusate ketone bidy ratio (PKBR), the hepatic sugar release (SL), and the hepatic tissue water content (HTWC). The results showed that there no significant differences between the two storage solutions after 6 hours preservation. If the preserved time was prolonged to 12 hours or more, the effect of rat’s liver preservation using HX solution were much superior to those using HXmsolutin.
Objective To explore the activity of Ca2 + -activated K+ ( KCa) inairwaysmoothmuscle cells( ASMCs) in a rat model of chronic obstructive pulmonary disease( COPD) , and to observe the effect of 11, 12-Epoxyeicosatrienoic acid( 11, 12-EETs) on the KCa channel of ASMCs. Methods Forty male Sprague-Dawley rats were randomly assigned to a COPD group and a normal control group. The rats in the COPD group were exposed to cigarette smoking in a relatively closed chamber to induce COPD. The ASMCs were isolated from small bronchi using an acute enzymatic digestion method. In the symmetrical high K+ solution,the KCa currents were separated with inside-out configuration using the patch clamp technique. The activity of KCa currents in ASMCs between the COPD group and the normal group were compared and the effect of 11, 12-EETs on KCa channel was recorded. The opening probability( Po) , opening time( To) and closing time ( Tc) of the KCa were measured. Results Compared with the normal group, Po of KCa in the COPD rats was much shorter ( 0. 084 ±0. 028 vs 0. 198 ±0. 029, P lt; 0. 01) , To was shorter [ ( 0. 732 ±0. 058) ms vs ( 1. 648 ±0. 152) ms, P lt; 0. 01] and Tc was longer[ ( 12. 259 ±2. 612) ms vs ( 6. 753 ±1. 237) ms, P lt;0. 01] . 11, 12-EETs can evoke the activity of KCa currents of ASMCs in the COPD rats while Po was increased( 0. 227 ±0. 059 vs 0. 084 ±0. 028, P lt; 0. 01) , To was much longer[ ( 2. 068 ±0. 064) ms vs ( 0. 732 ±0. 058) ms, P lt; 0. 01] , and Tc was shorter [ ( 4. 273 ±0. 978) ms vs ( 12. 259 ±2. 612) ms, P lt;0. 01] .Conclusions The results suggest that the decreasing of KCa activity plays an important role in the development of COPD. 11,12-EETs can directly evoke the activity of KCa channel in COPD rats, thus relax the airway smooth muscles.
Objective To investigate the role of Kv1. 5 in the pathogenesis of pulmonary hypertension simulated by hypobaria and hypoxia, and the effects of dichloroacetate ( DCA) on the Kv1. 5 expression in pulmonary arterial smooth muscle cells ( PASMCs ) and mean pulmonary arterial pressure ( mPAP) . Methods Twenty-four SD rats were randomly divided into a normal group ( N group) , a high altitude group ( HA group) , and a DCA treated group ( DCA group) . The N group were fed in normalconditions, the HA group and DCA group were fed in a hypobaria and hypoxia chamber simulated to an altitude of 5000 meters. In addition, the DCA group rats were gastric gavaged with DCA ( 70 mg · kg - 1 · d - 1 ) .Twenty-one days later, percentage of wall thickness ( WT% ) and percentage of wall area ( WA% ) of the pulmonary arteriole, mPAP, and the ratio of right ventricle / left ventricle and septum ( RV/ LV + S) were evaluated. Real-time PCR, immunohistochemistry and Western blot were carried out to detect the Kv1. 5 expression in PASMCs. Results In the HA group, WT% , and WA% of pulmonary arteriole, mPAP and RV/ ( LV + S) all increased significantly compared with the N group ( P lt;0. 01) . These changes in the DCA group were significantly lower than those in the HA group( P lt; 0. 01) . Furthermore, the protein and mRNA expression of Kv1. 5 in the PASMCs deceased significantly in the HA group compared with the N group( P lt;0. 01) , but recovered in the DCA group ( P lt;0. 01) . Conclusions The expression of Kv1. 5 in PASMCs is tremendously inhibited in rats fed in high altitude, which might be a important role of pulmonaryhypertension. DCA can inhibit the remodeling of pulmonary arterials probably by recovering Kv1. 5 expression.
Objective To investigate whether sodium tanshinone ⅡA sulphonate ( STS) treatment attenuates pulmonary edema of seawater drowning ( PE-SWD) , and examine the effects of STS on Na-KATPase(NKA) in PE-SWD. Methods Thirty-six rats were randomly divided into there groups, ie. a normal group ( NG) , a seawater group ( SG) , and a STS treatment group ( TG) . The rat model of PE-SWD was established by seawater instillation. PaO2 , histological changes of lungs, lung wet /dry weight ratio ( W/D) ,pulmonary microvascular permeability ( PMVP) , and NKA activity were detected. Western blot were used to test the effects of STS on NKA-α1 expression. Results Seawater instillation decreased PaO2 and the expression of NKA, while increased W/D ratio and PMVP. At 2 h after seawater instillation, the PaO2 in the TG group were significantly higher than those in the SG group, and peaked at 4 h after seawater instillation.Histological examination showed that there were hemorrhage, edema, markedly thickened alveolar wall, and infiltration of inflammatory cells in alveolar spaces in the SG group, but lung injury was significantly alleviated in the TG group. W/D ratio and PMVP in the TG group were significantly lower than those in the SG group. Additionally, NKA activity and NKA-α1 expression were significantly higher in the TG group than those in the SG group. Conclusion STS treatment can attenuate pulmonary edema of seawater drowning which may be related with up-regulating Na-K-ATPase activity and expression.
Objective To investigate the role of mitochondrial adenosine triphosphatesensitive potassium channel(mitoKATP) in immature myocardial ischemic preconditioning, and to provide evidence for immature myocardial protection. Methods Langendorff isolated heart infused model was used in the experiment. Twentyfour rabbits (aged from 14 to 21 days) were randomly divided into 4 groups：ischemiareperfusion group（I/R group）, myocardial ischemic preconditioning group(E1 group), 5hydroxydecanoate(5-HD) group (E2 group) and Diazoxide (Diaz) group(E3 group). Hemodynamics recovery rate, myocardial water content(MWC), the leakage rates of serum creatine kinase and lactate dehydrogenase, adenosine triphosphate content, superoxide dismutase activity, malondialdehyde content, myocardial cell Ca2+ content and myocardial mitochondrial Ca2+ content, myocardial mitochondrial Ca2+-ATPase activity, the adenosine triphosphate(ATP) synthesizing ability of myocardial mitochondria were tested, and myocardial ultrastructure was observed via electron microscopy. Results The hemodynamics recovery rate, myocardial water content(P＜0.05), adenosine triphosphate content, superoxide dismutase activity, myocardial mitochondrial Ca2+-adenosine triphosphyatase(ATPase) activity and the ATP synthesizing ability of myocardial mitochondria of the rabbits in E1 and E3 group were significantly better than that in I/R group and E2 group(P＜0.05). Malondialdehyde content, the leakage rates of serum creatine kinase and lactate dehydrogenase, myocardial cell Ca2+ content and myocardial mitochondrial Ca2+ content of the rabbits in E1 group and E3 group were significantly lower than that in I/R group and E2 group (P＜0.05). The myocardial ultrastructure injury in E1 and E3 group were significantly reduced compared with that in I/R and E2 group. Conclusion Myocardial ischemic preconditioning has significant protective effects on immature myocardium. Its mechanism may be related to the activation of mitoKATP.
Objective To investigate the protective effects of ischemic postconditioning (IPo) on ischemiareperfusion (I/R) myocardium and the relationship with mitochondrial adenosine triphosphate (ATP) sensitive K+ channels (mitoKATP) and provide evidences to the development of druginduced postconditioning. Methods Langendorff models were established in 40 Wistar rats which were divided into 5 groups by random number table with 8 rats in each group. Normal control group(NC group): the rat hearts were continuously reperfused by KrebsHenseleit bicarbonate buffer (K-HB) for 100 min without any other treatment; I/R group: the rat hearts underwent a 40-min global ischemia followed by a 60-min reperfusion; IPo group: after a 40-min global ischemia, the process of 10-second reperfusion followed by a 10-second ischemia was repeated 6 times, then there was a continuous 58min reperfusion; 5-hydroxydecanoic acid(5-HD) group: after a 40min global ischemia, hearts with 5HD(100 μmol/L) K-HB were reperfused for 15min and then perfused without 5HD for 45min；IPo+5-HD group: after a 40-min global ischemia, the process that the isolated hearts with 5-HD(100 μmol/L) KHB were reperfused for 10second followed by a 10second ischemia was repeated 6 times, then the hearts with 5-HD(100 μmol/L) KHB were continuously [CM(159mm]perfused for 13-min followed by reperfusion without 5-HD(100 μmol/L) K-HB for 45-min. The cardiac function,coronary flow(CF), cardiac troponin I(cTnI) content in coronary effluent, the area of acute myocardial infarction (AMI) and myocardial ultrastructure were observed. Results Left ventricular developed pressure(74.3±3.3 mm Hg vs. 57.1±3.3 mm Hg,t=1300, P=0.000),+dp/dtmax(1 706.6±135.6 mm Hg/s vs. 1 313.3±96.2 mm Hg/s,t=6.28,P=0.000),－dp/dtmax(1 132.8±112.1 mm Hg/s vs. 575.7±67.7 mm Hg/s,t=13.48, P=0.000) and CF(6.49±0.30 ml/min vs. 3.70±0.24 ml/min,t=28.6,P=0.000) in IPo group were higher than those in I/R group. Left ventricular enddiastolic pressure(10.9±1.7mm Hg vs. 26.2±1.5 mm Hg,t=－19.21, P=0000)and cTnI content in coronary effluent (0.62±0.01 ng/ml vs. 0.71±0.01 ng/ml, t=-12.00,P=0.000) were lower than those in I/R group; the area of AMI decreased 20.8％ compared with that in I/R group (Plt;0.05). The myocardial protective effect in IPo+5HD group was similar with that in IPo group, but lower than that in IPo group. The electron microscope showed that IPo and IPo+5HD could reduce myocardial fiber damage and mitochondrial damage caused by I/R. Conclusion IPo can protect I/R myocardium, which is achieved mainly by activating mitoK-ATP channels.
Objective To investigate the effects of diazoxide （DIA）cardioplegic solution on the reduction of donor cardiomyocyte apoptosis, Methods In a Krebs-Henseleit （KH） solution perfused isolated rabbit heart Langendorff model, 32 rabbit hearts were divided into four groups with simple random sampling （8 rabbits in each group ）： DIA group （50μmol/L diazoxide mixed in KH solution）,STH group （ST, Thomas＇ solution）, 5-HD group （50μmol/L diazoxide and 100μmol/L 5-hydroxydecanoic acid mixed in KH solution）, KH group （KH solution）, The rabbit hearts of each group underwent 6 hours of hypothermic （4 C） storage in the corresponding cardioplegic solution. Left ventricular developed pressure （LVDP）, maximal values of positive rate of left ventricular pressure （＋dp/dtmax） were measured before and after storage, The post-storage values of LVDP and ＋dp/dtmax were expressed as the percentage of pre-storage control values. Apoptotic cardiomyocytes were detected by the TdT- mediated dUTP-biotin nick end labeling （TUNEL）. Malonaldehyde （MDA） contents and adenosine triphosphate （ATP） contents were also measured after storage. Results Recovery rates of LVDP, ＋dp/dtmax, and ATP contents in DIA group were higher than those of other 3 groups respectively（P〈0. 05）, Cardiomyocytes apoptosis percentage and MDA content were lower than other 3 groups respectively（P〈0. 05）, Conclusions Diazoxide cardioplegic solution can protect the isolated hearts and this may be relates to opening selective mitochondrial KATP channels. The selective mitochondrial KATP channel antagonist 5-hydroxydecanoic acid can block the cardioprotective effect of diazoxide.