***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 and objective : The aim of this study was to evaluate the efficacy of dexmedetomidine , an & agr;2‐adrenoceptor agonist , on intraoperative bleeding , anaesthetic drug requirement and postoperative pain . Methods : Forty patients scheduled for elective tympanoplasty and septorhinoplasty operations under general anaesthesia were included in the study . The patients were r and omly assigned to receive either a dexmedetomidine 1 & mgr;g kg−1 bolus 10 min before induction of anaesthesia plus 0.5 & mgr;g kg−1 h−1 infusions during maintenance or placebo . Mean arterial pressure was maintained between 60 and 80 mmHg . Perioperative mean arterial pressure , heart rate , time to extubation and time to awakening were recorded . Bleeding during surgery was assessed by the surgeon , blinded to the study drugs , both intraoperatively and postoperatively as a final personal opinion about the whole surgical process . Results : The heart rate and mean arterial pressure were significantly lower during induction , operation and extubation in the dexmedetomidine group ( P < 0.05 ) . Blood losses were lower in the dexmedetomidine group ( P < 0.05 ) . Propofol dose required for induction , and fentanyl and isoflurane consumption were significantly reduced in the dexmedetomidine group ( P < 0.05 ) . The total amounts of nitroglycerin and meperidine used were higher in the control group ( P < 0.05 ) . Conclusions : Dexmedetomidine  decreased bleeding , postoperative analgesic requirements and intraoperative anaesthetic requirements and was associated with more stable haemodynamic responses to anaesthesia . We conclude that dexmedetomidine is a useful adjuvant to decrease bleeding when a bloodless surgical field is requested Background : Clonidine has been shown to reduce perioperative circulatory instability . This postoperative analgesic effect of clonidine was also known in previous studies . The aim of the study was to investigate the clinical efficiency of oral clonidine premedication in anesthesia and analgesia in patients undergoing laparoscopic cholecystectomy We have studied the effect of clonidine pretreatment on cardiovascular responses to various stimuli during craniotomy . Fifty-eight patients ( ASA Class I – II ) , scheduled for supratentorial surgery , were r and omly given either oral clonidine , mean dose 3.6 μg/kg ( n = 28 ) , or oral diazepam , 0.2 mg/kg ( n = 30 ) , ninety to one hundred minutes before surgery . Anaesthesia was induced with thiopentone and maintained with nitrous oxide : oxygen , pentazocine and halothane . Pancuronium was used as a neuromuscular blocker . Mean arterial pressure and heart rate were recorded before and after several stimuli . In the clonidine group hypertensive response was significantly less on laryngoscopy ( 6.5 % increases versus 11.2 % in the diazepam group ) , intubation ( 9.2 % versus 16.5 % ) , Mayfield clamp application ( 14.5 % versus 29.91 % ) and after skin infiltration with lignocaine-adrenaline solution ( 2.95 % versus 5.42 % ) . Heart rate response to laryngoscopy , intubation and skin infiltration was also significantly attenuated in the clonidine group . The sleep dose of thiopentone was smaller in patients pretreated with clonidine . Patients in the diazepam group required more medical intervention . No adverse effect occurred in any patient The effect of clonidine on intracranial pressure ( ICP ) , mean arterial pressure ( MAP ) , cerebral perfusion pressure ( CPP ) , heart rate ( HR ) , and drug requirements was studied in 24 patients scheduled for elective cerebral tumor resection ( ICP ≤20 mm Hg ) . The patients were r and omly assigned to one of two groups : Group P ( placebo ) , 12 patients ; Group C ( clonidine 3 μg/kg 10 min before induction ) , 12 patients . In all patients , anesthesia was induced with a propofol infusion ( 500 μg/kg/min ) combined with fentanyl 2 μg/kg , lidocaine 1.5 mg/kg , and vecuronium 0.1 mg/kg . Propofol was also used for maintenance . During the preinduction period , clonidine had no effect on ICP or HR , but in clonidine-treated patients , MAP and CPP decreased significantly in comparison to those of the placebo group . During induction , ICP and HR were stable and similar in both groups . MAP and CPP remained significantly lower in Group C. At intubation and Mayfield clamp application , ICP increased in both groups , with similar values at all times . MAP increased in both groups at intubation , Mayfield clamp application , and incision , staying lower , however , in Group C. CPP followed a pattern similar to that of MAP . Propofol requirements up to the 20th min were lower in Group C than in Group P ( 2.08 ± 0.83 vs. 3.3 ± 0.7 mg/kg , p < 0.05 ) . Finally , throughout the study , eight patients in Group C versus two in Group P had a CPP value < 60 mm Hg for ≥1 min ( p < 0.05 ) . In contrast , eight patients in Group P , but only one in Group C , had a CPP > 110 mm Hg . In conclusion , in normotensive neurosurgical patients with a baseline  ICP ≤20 mm Hg , clonidine had no effect on ICP or HR . It decreased MAP and CPP to lower values than those recorded in the placebo group throughout the study without altering the increase in these variables after intraoperative noxious stimulation . Therefore , it would seem that an appropriate use of clonidine would be in the patient in whom MAP control is otherwise difficult despite relatively high doses of anesthetic agents OBJECTIVES We investigated endocrine correlates of the hemodynamic changes induced by carbon dioxide pneumoperitoneum ( PNO ) . We then studied whether clonidine might modulate the hemodynamic changes induced by PNO by reducing release of catecholamines and vasopressin . BACKGROUND Both mechanical and neurohumoral factors contribute to the hemodynamic changes induced by carbon dioxide PNO . Several mediators have been proposed , but no study has correlated hemodynamic changes with changes in levels of these potential mediators . METHODS We conducted two studies , each including 20 healthy patients scheduled for elective laparoscopic cholecystectomy .  In the first study serial measurements of hemodynamics ( thermodilution technique ) were done during laparoscopy and after exsufflation . Plasma concentrations of cortisol , catecholamines , vasopressin , renin , endothelin and prostagl and ins were measured at the same time points . In the second study patients were r and omly allocated to receive 8 microg/kg clonidine infused over 1 h or placebo before PNO . Hemodynamics and plasma levels of cortisol , catecholamines and vasopressin were measured during PNO and after exsufflation . RESULTS Peritoneal insufflation result ed in a significant reduction of cardiac output ( 18+/-4 % ) and increases in mean arterial pressure ( 39+/-8 % ) and systemic ( 70+/-12 % ) and pulmonary ( 98+/-18 % ) vascular resistances . Laparoscopy result ed in progressive and significant increases in plasma concentrations of cortisol , epinephrine , norepinephrine and renin . Vasopressin plasma concentrations markedly increased immediately after the beginning of PNO ( before PNO 6+/-4 pg/ml ; during PNO 129+/-42 pg/ml ; p < 0.05 ) . The profile of vasopressin release paralleled the time course of changes in systemic vascular resistance . Prostagl and ins and endothelin did not change significantly . Clonidine significantly reduced mean arterial pressure , heart rate and the increase in systemic vascular resistance . Clonidine also significantly reduced catecholamine concentrations but did not alter vasopressin and cortisol plasma concentrations . CONCLUSIONS Vasopressin and catecholamines probably mediate the increase in systemic vascular resistance observed during PNO . Clonidine before PNO reduces catecholamine release and attenuates hemodynamic changes during laparoscopy This r and omised , placebo-controlled , double-blind study was design ed to assess the effect of intravenous clonidine and magnesium sulphate on intraoperative haemodynamics , anaesthetic consumption and postoperative recovery .  Seventy five patients undergoing elective upper limb orthopaedic surgery were r and omised into three groups . Group C received clonidine 3 μg/kg as a bolus before induction and 1μg/kg/hour by infusion intraopertively . Group M received magnesium sulphate 30 mg/kg as a bolus before induction and 10 mg/kg/hour by infusion . Group P received same volume of isotonic saline . Anaesthesia was induced and maintained with fentanyl citrate and propofol . Muscular relaxation was achieved by vecuronium bromide .  Induction time , recovery time and consumption of propofol as well as fentanyl citrate were recorded . Induction of anaesthesia was rapid with both clonidine and magnesium  sulphate . Time of bispectral index ( BIS ) to reach 60 was significantly lower in Group C and Group M ( P < 0.0001 ) . Requirements of propofol and fentanyl were significantly less in Group C and Group M ( P < 0.001 ) . Postoperative recovery was slower in Group M compared with other two groups ( P < 0.001 ) . Perioperative use of both clonidine and magnesium sulphate significantly reduced the consumption of propofol and fentanyl citrate . Magnesium sulphate  caused a delayed recovery Background and objective : Preoperative oral dextromethorphan and intravenous clonidine attenuate arterial pressure and heart rate increases during tourniquet inflation under general anaesthesia . The effect of preoperative oral clonidine on these variables has not been investigated . Methods : We design ed this study to compare the effect of preoperative oral dextromethorphan or clonidine on haemodynamic changes during tourniquet inflation in 75 patients undergoing lower limb surgery under general anaesthesia . Patients were r and omly assigned into three groups : dextromethorphan 30 mg ( n = 25 ) , clonidine 3 & mgr;g kg−1 ( n = 25 ) and placebo ( n = 25 ) . Anaesthesia was maintained with isoflurane 1.2 % and N2O 50 % in oxygen with endotracheal intubation . Dextromethorphan , clonidine or placebo was given orally in a double‐blinded fashion 90 min before induction of anaesthesia . Systolic , diastolic and mean arterial pressure and heart rate were measured at 0 , 30 , 45 , 60 min after the start of tourniquet inflation , before tourniquet release and 20 min after tourniquet deflation . Results : Systolic , diastolic and mean arterial pressure were significantly lower in the clonidine group compared with control after 45 , 60 min tourniquet inflation and before tourniquet release ( P < 0.05 ) . Twenty minutes after deflation , diastolic and mean arterial pressure in the control group were still increased and significantly higher compared with the clonidine group ( P < 0.05 ) . Development of more than a 30 % increase in systolic arterial pressure during tourniquet inflation was more frequent in the control group than in the other groups . Conclusions : Preoperative oral clonidine 3 & mgr;g kg−1 significantly prevented tourniquet‐induced systemic arterial pressure increase in patients under general anaesthesia better than oral dextromethorphan The alpha2-agonist dexmedetomidine ( Dex ) , a sedative and analgesic , reduces heart rate ( HR ) and blood pressure , and has been used in the practice of anesthesia . In this study , we aim ed to evaluate the effects of Dex on hemodynamic variables , anesthetic sparing effects , and recovery profiles in patients who underwent surgery in prone position . The prone position itself can cause a decrease in the systemic blood pressure .  Forty patients who undergo lumbar discectomy were r and omly assigned to receive either Dex ( a loading dose 1 microg/ kg in 10 minutes followed by an infusion rate of 0.2 microg/ kg/ hr ) or saline . In both groups , the anesthesia was induced with fentanyl , thiopental and rocuronium , and maintained with desflurane in 50 % N(2)O. Mean arterial blood pressure ( MAP ) , HR , cardiac output ( CO ) , and level of anesthesia were monitored . Recovery times and analgesic requirements were also recorded . As a response to endotracheal intubation , a significant increase in MAP and HR was observed in the control group compared to the Dex group , but no difference in CO . The recovery times were significantly shorter in the Dex group compared to the control group . Anesthetic and analgesic requirements of the Dex group were lower than controls . Thus , the use of Dex caused no detrimental effects on the hemodynamic variables in prone position . In addition , Dex decreased pressure response to intubation , and anesth 
    Output:
    
However , their effects appeared to vary with the surgical procedure .
Our study provides encouraging evidence that alpha-2 adrenergic agonists may reduce cardiac risk , especially during vascular surgery .