***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: BACKGROUND Activation of the kinase cascade ( protein kinase C ( PKC ) , tyrosine kinase ( TK ) , and mitogen-activated protein kinase ( MAPK ) is a key feature of the transduction pathway , elicited by preconditioning signals and mediating their cardioprotective effects . We assessed whether such an activation occurred during cardiac operations and could thus represent a target for cardioprotective strategies . METHODS A total of 20 patients undergoing coronary artery bypass grafting surgery were studied . During the first 10 minutes of cardiopulmonary bypass ( CPB ) , 10 were treated with sevoflurane ( 2.5 minimum alveolar concentration ) , an inhalational anesthetic that mimics preconditioning through a similar activation of the kinase cascade . Ten case-matched patients undergoing 10 minutes of sevoflurane-free CPB served as controls . Right atrial biopsies were taken before and 10 minutes after CPB and were then processed for the measurement of PKC , TK , and p38 MAPK activities by enzyme assay techniques . Troponin I was also monitored over the first 2 postoperative days . RESULTS Compared with pre-CPB values , PKC and p38 MAPK activities ( in nanomoles per milligram of protein per minute and arbitrary units , respectively ) increased significantly and to the same extent in both groups : PKC , from 20.7+/-0.7 to 29.9+/-3.9 in controls ( p = 0.037 ) and from 18.4+/-1.1 to 23.9+/-1.8 in sevoflurane ( p = 0.016 ) ; p38 MAPK , from 88.6+/-8.5 to 312.9+/-66.2 in controls ( p = 0.005 ) and from 114.6+/-14.7 to 213.4+/-51.8 in sevoflurane ( p = 0.045 ) . Conversely , sevoflurane triggered a significant increase in TK activity ( from 68.5+/-1.4 to 83.7+/-2.9 picomoles per milligram of protein per minute p = 0.0015 ) which did not occur in controls ( from 67.5+/-1.9 to 76.8+/-4.2 picomoles per milligram of protein per minute , p = 0.09 ) . Likewise , the peak postoperative value of troponin I was not different between controls and sevoflurane-treated patients ( 3.4+/-0.6 vs 2.4+/-0.4 , p = 0.21 ) . CONCLUSIONS Cardiopulmonary bypass triggers an activation of the kinase cascade that is mechanistically linked to opening of potassium channels . The direct opening of these channels by the anesthetic sevoflurane does not increase kinase activation further , nor does it improve markers of cell necrosis , thus suggesting that pharmacologically targeting potassium channels may overlap the preconditioning-like effects of CPB alone Background : Experimental studies have related the cardioprotective effects of sevoflurane both to preconditioning properties and to beneficial effects during reperfusion . In clinical studies , the cardioprotective effects of volatile agents seem more important when administered throughout the procedure than when used only in the preconditioning period . The authors hypothesized that the cardioprotective effects of sevoflurane observed in patients undergoing coronary surgery with cardiopulmonary bypass are related to timing and duration of its administration . Methods : Elective coronary surgery patients were r and omly assigned to four different anesthetic protocol s ( n = 50 each ) . In a first group , patients received a propofol based intravenous regimen ( propofol group ) . In a second group , propofol was replaced by sevoflurane from sternotomy until the start of cardiopulmonary bypass ( SEVO pre group ) . In a third group , propofol was replaced by sevoflurane after completion of the coronary anastomoses ( SEVO post group ) . In a fourth group , propofol was administered until sternotomy and then replaced by sevoflurane for the remaining of the operation ( SEVO all group ) . Postoperative concentrations of cardiac troponin I were followed during 48 h. Cardiac function was assessed perioperatively and during 24 h postoperatively . Results : Postoperative troponin I concentrations in the SEVO all group were lower than in the propofol group . Stroke volume decreased transiently after cardiopulmonary bypass in the propofol group but remained unchanged throughout in the SEVO all group . In the SEVO pre and SEVO post groups , stroke volume also decreased after cardiopulmonary bypass but returned earlier to baseline values than in the propofol group . Duration of stay in the intensive care unit was lower in the SEVO all group than in the propofol group . Conclusion : In patients undergoing coronary artery surgery with cardiopulmonary bypass , the cardioprotective effects of sevoflurane were clinical ly most apparent when it was administered throughout the operation Background —Ventricular fibrillation ( VF ) and tachycardia ( VT ) are the common and potential life-threatening complications after CABG . Ischemic preconditioning ( IP ) has been proved effective in reducing ischemia reperfusion arrhythmia in animals and humans . Whether IP is effective in suppressing postoperative VF/VT in patients with CABG has not been studied . Methods and Results —Eighty-six patients with CABG with stable and unstable 3-vessel disease were equally r and omly assigned into an IP and a control group . The patients who received IP received 2 periods of 2-minute ischemia followed by 3-minute reperfusion . Twenty-four-hour electrocardiographic data were collected . IP result ed in fewer cases of VF after declamping ( 48.8 % versus 79.1 % in IP and control , P = 0.004 ) and a shorter VF period ( 2.28±0.44 versus 4.41±0.51 minutes , P = 0.002 ) . The episodes of VT were significantly reduced in patients in the IP group during early reperfusion and 24 hours after reperfusion ( 0.65±0.16 versus 3.71±0.46 , P = 0.000 and 0.07±0.04 versus 2.12±1.41 , P = 0.002 , respectively ) . De novo sustained VT occurred in 3 control patients as against none in the IP group after surgery . As a result , IP significantly curtailed the mechanical ventilation period and reduced the need for inotropes . Conclusions —IP significantly reduced postoperative VF/VT  in patients with CABG with 3-vessel disease . Suppression of VT during early reperfusion and 24 hours after reperfusion suggests early and delayed IP phenomena in patients undergoing CABG surgery Background : Sevoflurane induces preconditioning ( SevoPC ) . The effect of aprotinin and the involvement of endothelial nitric-oxide synthase ( NOS ) on SevoPC are unknown . We investigated ( 1 ) whether SevoPC is strengthened by multiple preconditioning cycles , ( 2 ) whether SevoPC is blocked by aprotinin , and ( 3 ) whether endothelial NOS plays a crucial role in SevoPC . Methods : Anesthetized male Wistar rats were r and omized to 15 groups ( each n = 6 ) and underwent 25-min regional myocardial ischemia and 2-h reperfusion . Controls were not treated further . Preconditioning groups inhaled 1 minimum alveolar concentration of sevoflurane for 5 min ( SEVO-I ) , twice for 5 min each ( SEVO-II ) , three times for 5 min each ( SEVO-III ) , or six times for 5 min each ( SEVO-VI ) . Aprotinin was administered with and without sevoflurane . Involvement of endothelial NOS was determined with the nonspecific NOS blocker N-nitro-l-arginine-methyl-ester , the specific neuronal NOS blocker 7-nitroindazole , and the specific inducible NOS blocker aminoguanidine . Results : SevoPC reduced infa rct size in all protocol s ( SEVO-I , 42 ± 6 % ; SEVO-II , 33 ± 4 % ; SEVO-III , 11 ± 5 % ; SEVO-VI , 16 ± 4 % ; all P < 0.001 vs. control , 67 ± 3 % ) and was least after three and six cycles of sevoflurane ( P < 0.001 vs. SEVO-II and -I , respectively ) . Aprotinin alone had no effect on infa rct size but blocked SevoPC . N-nitro-l-arginine-methyl-ester abolished SevoPC ( 67 ± 4 % ; P < 0.05 vs. SEVO-III ) . Aminoguanidine and 7-nitroindazole blocked SevoPC only partially ( 25 ± 6 and 31 ± 6 % , respectively ; P < 0.05 vs. SEVO-III and control ) . SevoPC induced endothelial NOS phosphorylation , which was abrogated by aprotinin . Conclusion : SevoPC is strengthened by multiple preconditioning cycles , and phosphorylation of endothelial NOS is a crucial step in mediating SevoPC . These effects are abolished by aprotinin UNLABELLED Ischaemic preconditioning , with brief periods of ischaemia separated by reperfusion , increases myocardial resistance to infa rct ion . In addition , preconditioning leads to preservation of myocardial adenosine triphosphate ( ATP ) during ischaemia . We propose that ischaemic preconditioning may share fundamental similarities with intermittent aortic cross-clamping utilised during aorto-coronary bypass surgery . The aim of this study was to test the hypothesis that controlled aortic cross-clamping is a form of preconditioning using conservation of ATP as the end point . Patients r and omised to the preconditioned group ( preconditioned , n = 10 patients ) , received a preconditioning stimulus of two 3-min periods of cross-clamping separated by 2 min of reperfusion prior to an ischaemic insult of 10 min ischaemia and ventricular fibrillation . In the control group ( control , n = 10 patients ) hearts received 10 min cross-clamping with fibrillation without prior preconditioning .  Myocardial ATP , creatine phosphate ( CP ) , and lactate were determined from biopsy specimens taken at the onset of cardiopulmonary bypass ( A ) , at the end of preconditioning ( B ) , and at the end of 10 min of ischaemic insult ( C ) . RESULTS expressed as mean + /- SE ( mumol/g dry weight ) . Preconditioning result ed in a significant depletion of the myocardial ATP content ( preconditioned , B : 11.7 + /- 0.9 vs A : 19.8 + /- 1.4 ; P < 0.01 ) . Furthermore 10 min of ischaemia result ed in a significant depletion of ATP in the control patients ( control , C : 7.2 + /- 0.3 vs B : 19.5 + /- 1.2 ; P < 0.005 ) . ( ABSTRACT TRUNCATED AT 250 WORDS Background —Postprocedural myocardial infa rct ion ( type 4a ) has been shown to be an adverse prognostic indicator after  elective percutaneous coronary intervention ( PCI ) . The Cardiac Remote Ischemic Preconditioning in Coronary Stenting ( CRISP Stent ) study demonstrated that remote ischemic preconditioning reduced procedural symptoms , ECG ST-segment deviation , and cardiac troponin I release after elective PCI and reduced the major adverse cardiac and cerebral event ( MACCE ) rate at 6 months . We were interested to confirm if this early benefit in MACCE rate in the remote ischemic preconditioning group was sustained long-term . Methods and Results — Patients were telephoned by research ers blinded to the r and omization details . MACCE , defined as all-cause mortality , nonfatal myocardial infa rct ion , transient ischemic attack or stroke , and heart failure requiring hospital admission , were adjudicated by case note and national data base review . One hundred ninety-two ( 89.3 % ) of the 225 patients with elective PCI r and omized in the original study were available for long-term follow-up ( mean time to event or last follow-up : 1579.7±603.6 days ) . There were a total of 59 ( 30.7 % ) MACCEs . Patients with an MACCE had a higher mean cardiac troponin I after PCI ( ±SD ) : 2.07±6.99 versus 0.91±2.07 ng/mL ( P=0.05 ) . The MACCE rate at 6 years remained lower in the remote ischemic preconditioning group ( hazard ratio , 0.58 ; 95 % confidence interval , 0.35–0.97 ; P=0.039 ; absolute risk reduction=0.13 and number needed to treat=8 to prevent the MACCE at 6 years ) . Conclusions —Remote ischemic preconditioning reduces the incidence of postprocedural cardiac troponin I after elective PCI and confers an MACCE-free survival benefit at both short- and long-term follow-up . Clinical Trial Registration —URL : http://www.uk 
    Output:
    
Conclusion Available evidence from the present systematic review and meta- analysis suggests that sevoflurane preconditioning may reduce troponin levels in on-pump CABG .