scholarly journals COMPARATIVE CHARACTERISTICS OF THE DYNAMICS OF CARDIOVASCULAR AND RESPIRATORY EFFECTS OF PNEUMOPERITONEUM BASED ON CARBON DIOXIDE AND ARGON IN LAPAROSCOPIC CHOLECYSTECTOMY

2021 ◽  
pp. 90-95
Author(s):  
O. L. Tkachuk ◽  
R. L. Parakhoniak ◽  
S. V. Melnyk ◽  
O. O. Tkachuk-Hryhorchuk
Keyword(s):  
Carbon Dioxide ◽  
Heart Rate ◽  
Cardiac Output ◽  
Laparoscopic Cholecystectomy ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Negative Impact ◽  
Abdominal Pressure ◽  
The Mean ◽  
Respiratory Systems

Pneumoperitoneum is one of the most critical components of laparoscopic surgery, which has a negative effect on gas exchange and stress to circulatory buffering system. One of the top priorities of laparoscopic technologies is to minimize the impact on the respiratory and cardiovascular systems, metabolic dynamics and compensatory abilities of homeostasis. The main goal of this research work is to compare the effects of carboxyperitoneum and argonoperitoneum on the intraoperative dynamics of CO2 concentration as well as cardiovascular and respiratory characteristics in patients undergoing laparoscopic cholecystectomy for various forms of cholelithiasis. Materials and methods. Four experimental groups involved patients based on their nosological form of cholelithiasis and the gas used to induce pneumoperitoneum. All patients underwent laparoscopic cholecystectomy by means of standard procedure. Either medical carbon dioxide or medical argon was used to induce pneumoperitoneum. Intraoperative monitoring of blood carbon dioxide levels PaCO2 was performed by taking venous blood every 15 minutes. Capnometry was performed by means of mainstream analysis using “BIOMED” BM1000C modular patient monitor by recording the discrete values of PetCO2 every 15 minutes, as well as by analyzing photocopies of capnography curves every 15 minutes. Intraoperative echocardiography was performed to identify the mean arterial pressure (MAP), heart rate (HR) and cardiac output (CO) in order to assess the effects of different types of pneumoperitoneum on the cardiovascular system. Results. The obtained data confirm the expected difference in the indices of cardiorespiratory functions between patients with acute cholecystitis and cholelithiasis without signs of inflammation. The investigation revealed that under the influence of pneumoperitoneum, heart rate and mean arterial pressure increase, while the cardiac output decreases. The respiratory pressure marker depends more on the intra-abdominal pressure and presumably the patient’s body type than on the presence of inflammatory syndrome. Argon insufflation has a slight negative impact on the cardiovascular system. Particularly, the mean arterial pressure and heart rate increase, while the cardiac output marker is less decreased as compared to the use of carbon dioxide. Abdominal pressure has a significant effect on the cardiovascular and respiratory systems regardless of the used type of gas. The combination of high intra-abdominal pressure with the elevated head end of the operating table, which is a common practise during cholecystectomy, has especially great influence on cardiovascular and respiratory functions. Operation which is carried out at decreased pressure allows reducing the deviations of practically all indices. Conclusions. Thus, the cardiovascular and respiratory systems adapt under the influence of pneumoperitoneum, providing compensation for the negative effects of mechanical and resorptive-metabolic character. Compensatory-adaptive abilities of the cardiovascular and respiratory systems increase with the decrease of intra-abdominal pressure. The use of argon as a working gas for insufflation into the abdominal cavity during laparoscopy reduces the negative impact of pneumoperitoneum on the cardiovascular and respiratory systems, providing a greater reserve of homeostatic and buffer systems of the body.

Hemodynamic response of normal men to graded treadmill exercise

1964 ◽  
Vol 19 (3) ◽  
pp. 457-464 ◽  
Author(s):  
Burton S. Tabakin ◽  
John S. Hanson ◽  
Thornton W. Merriam ◽  
Edgar J. Caldwell
Keyword(s):  
Carbon Dioxide ◽  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Treadmill Exercise ◽  
Minute Volume ◽  
Peripheral Vascular ◽  
Carbon Dioxide Elimination ◽  
Oxygen Utilization

The physiologic variables defining the circulatory and respiratory state in normal man have been measured in recumbency, standing at rest and during progressively severe grades of exercise approaching near-maximal levels. Indicator-dilution technique was used for determination of cardiac output with simultaneous radio-electrocardiographic recordings of heart rate. Direct intra-arterial pressure measurements were utilized for calculation of peripheral vascular resistance. Minute volume of ventilation, oxygen utilization, and carbon dioxide elimination were obtained from analysis of expired air collected at the time of each cardiac output determination. A peak mean workload of 1,501 kg-m/min was realized during the treadmill exercise. Increases in cardiac output over the range of exercise employed correlated well with indices of workload such as heart rate, oxygen utilization, and minute volume of ventilation. There was no correlation of stroke volume with these indices. It is concluded from examination of individual stroke-volume responses that a progressive increase in stroke volume is not a necessary or constant phenomenon in adapting to increasing workload. cardiac output in treadmill exercise; dye-dilution cardiac output determinations; arterial pressure during upright exercise; stroke-volume response to graded treadmill exercise; exercise response of cardiac output and stroke volume; peripheral vascular resistance response to position and exercise; treadmill exercise—effects on cardiac output, stroke volume, and oxygen uptake; minute ventilation, cardiac output, and stroke volume during exercise; carbon dioxide elimination during treadmill exercise; heart rate and cardiac output during treadmill exercise; exercise; physiology Submitted on July 12, 1963

Vascular Abnormalities and Pulmonary Hypertension in the Berkeley Sickle Mouse.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 3185-3185
Author(s):  
David R. Archer ◽  
Shawn Elms ◽  
Joshua Boutwell ◽  
Jennifer Perry ◽  
Roy Sutliff
Keyword(s):  
Pulmonary Hypertension ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Endothelial Dysfunction ◽  
Mouse Model ◽  
Arterial Pressure ◽  
Right Ventricular ◽  
The Mean

Abstract Clinically, pulmonary hypertension is a major risk factor for mortality in adults with sickle cell disease. Contributing factors probably include red cell hemolysis and vaso-occlusive injury with their associated oxidative and inflammatory stimuli. Previously, we have described RBC hemolysis and endothelial oxidative stress in the Berkeley sickle mouse model and extend those studies in this work to investigate cardiovascular and endothelial dysfunction. Eight to ten month old homozygous and hemizygous Berkeley sickle mice and C57BL/6 control mice were used for all aspects of these experiments. In vivo measurements of mean arterial pressure and right ventricular pressures were conducted in fully anesthetized mice using a pressure transducer inserted in the carotid and right ventricle respectively. Following in vivo readings hearts were excised for measurement of ventricular mass. The ascending aorta was removed and cut into 5 mm rings for in vitro studies of agonist- induced contractility and relaxation. The mean arterial pressure of the hemizygous sickle mice (70.6 ± 3.4) was significantly lower than the control mice (86.0 ± 3.1) and the mean arterial pressure of homozygous sickle mice (59.0 ± 2.2 mmHg) was significantly lower than the hemizygous and control mice (p≤0.05 and p≤0.001, respectively). The right ventricular pressure showed a trend that approached significance (p= 0.08) such that pressures in homozygous mice were ≥ than those in hemizygous which were ≥ than those in control mice. Increased basal cardiac output was suggested by significant left ventricular hypertrophy. In vitro examination of potassium chloride activation of voltage gated calcium channels showed no significant difference in sensitivity or maximal contraction. Similarly, there was no difference in sensitivity to the α1 agonist, phenylephrine. However, both hemi- and homozygous mice showed a significant reduction in maximal force of contraction (normalized to cross sectional area when compared to controls. Maximal acetylcholine induced relaxation of aortic rings was significantly reduced (p≤0.05) in homozygous sickle mice compared to controls. The same effect was not seen with sodium nitroprusside induced relaxation indicating that the acetylcholine effect was not due to effects on the smooth muscle but was endothelium-dependent. The Berkeley mouse model shows cardiac hypertrophy consistent with the increased cardiac output associated with chronic anemia and a reduced basal mean arterial blood pressure similar to that seen in humans. 8–10 month old mice have increased right ventricular pressure and RV mass indicative of pulmonary hypertension. Further endothelial dysfunction is characterized by a reduction in the maximal relaxation elicited by acetylcholine. Therefore, the Berkeley mouse is a good model for investigating sickle related endothelial dysfunction.

Responses of the Systemic Circulation and of the Renin—Angiotensin—Aldosterone System to Ketanserin at Rest and Exercise in Normal Man

1984 ◽  
Vol 66 (1) ◽  
pp. 17-25 ◽  
Author(s):  
Robert Fagard ◽  
Anne Cattaert ◽  
Paul Lijnen ◽  
Jan Staessen ◽  
Luc Vanhees ◽  
...  
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Catecholamines ◽  
Plasma Renin ◽  
Systemic Circulation ◽  
Work Rate ◽  
Plasma Aldosterone ◽  
Sitting Position ◽  
The Mean

1. The systemic circulation at rest and during exercise was studied in ten normal male volunteers, after placebo on one occasion and after acute intravenous administration of the serotonergic antagonist ketanserin on another occasion. The effects of ketanserin on the components of the renin—angiotensin—aldosterone system, on plasma catecholamines and on exercise capacity for graded uninterrupted exercise were also investigated. 2. At rest in recumbency rapid intravenous injection of 10 mg of ketanserin, followed by a continuous infusion of 2 mg/h, produced an acute but transient fall in mean intra-arterial pressure of 6 mmHg compared with placebo. After 15 min the mean arterial pressure with ketanserin was within 2 mmHg of the mean pressure with placebo. In the sitting position both at rest and up to 30% of maximal work rate, the mean arterial pressure during ketanserin did not differ from the pressure on placebo. However, at higher levels of physical activity the rise in mean arterial pressure was lower with ketanserin; the pressure achieved with placebo was 7.5 mmHg higher at maximal work rate. Heart rate and cardiac output were significantly higher during ketanserin. 3. When the subjects were lying down and resting, plasma noradrenaline and adrenaline levels, plasma renin activity and angiotensin II concentration were not affected by ketanserin; however, these values were higher in the sitting position both at rest and during exercise. Plasma aldosterone was reduced by ketanserin during exercise and also when the subject was resting in the recumbent position. 4. Exercise capacity as measured by peak oxygen uptake was similar during ketanserin (3.09 ± se 0.12 litres/min) and during placebo (3.11 ± 0.13). 5. The data suggest that 5-hydroxytryptamine can have only a small role, if any, in pressure homoeostasis in sodium replete man at rest in recumbency. At moderate and heavy levels of exercise, the results are compatible with a role for 5-hydroxytryptamine in pressure regulation. Activation of the sympathetic nervous system by ketanserin is suggested by increases of plasma catecholamines, heart rate, cardiac output and plasma renin. The suppression of plasma aldosterone suggests that 5-hydroxytryptamine may have a role in the regulation of aldosterone secretion which is independent of angiotensin II.

The Effects of Increasing Plasma Concentrations of Dexmedetomidine in Humans

2000 ◽  
Vol 93 (2) ◽  
pp. 382-394 ◽  
Author(s):  
Thomas J. Ebert ◽  
Judith E. Hall ◽  
Jill A. Barney ◽  
Toni D. Uhrich ◽  
Maelynn D. Colinco
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Pulmonary Artery ◽  
Arterial Pressure ◽  
Plasma Concentrations ◽  
Cold Pressor Test ◽  
Cold Pressor ◽  
Central Venous ◽  
Pressor Test

Background This study determined the responses to increasing plasma concentrations of dexmedetomidine in humans. Methods Ten healthy men (20-27 yr) provided informed consent and were monitored (underwent electrocardiography, measured arterial, central venous [CVP] and pulmonary artery [PAP] pressures, cardiac output, oxygen saturation, end-tidal carbon dioxide [ETCO2], respiration, blood gas, and catecholamines). Hemodynamic measurements, blood sampling, and psychometric, cold pressor, and baroreflex tests were performed at rest and during sequential 40-min intravenous target infusions of dexmedetomidine (0.5, 0.8, 1.2, 2.0, 3.2, 5.0, and 8.0 ng/ml; baroreflex testing only at 0.5 and 0.8 ng/ml). Results The initial dose of dexmedetomidine decreased catecholamines 45-76% and eliminated the norepinephrine increase that was seen during the cold pressor test. Catecholamine suppression persisted in subsequent infusions. The first two doses of dexmedetomidine increased sedation 38 and 65%, and lowered mean arterial pressure by 13%, but did not change central venous pressure or pulmonary artery pressure. Subsequent higher doses increased sedation, all pressures, and calculated vascular resistance, and resulted in significant decreases in heart rate, cardiac output, and stroke volume. Recall and recognition decreased at a dose of more than 0.7 ng/ml. The pain rating and mean arterial pressure increase to cold pressor test progressively diminished as the dexmedetomidine dose increased. The baroreflex heart rate slowing as a result of phenylephrine challenge was potentiated at both doses of dexmedetomidine. Respiratory variables were minimally changed during infusions, whereas acid-base was unchanged. Conclusions Increasing concentrations of dexmedetomidine in humans resulted in progressive increases in sedation and analgesia, decreases in heart rate, cardiac output, and memory. A biphasic (low, then high) dose-response relation for mean arterial pressure, pulmonary arterial pressure, and vascular resistances, and an attenuation of the cold pressor response also were observed.

scholarly journals Hemodynamic Changes Associated with Spinal Anesthesia for Cesarean Delivery in Severe Preeclampsia

2008 ◽  
Vol 108 (5) ◽  
pp. 802-811 ◽  
Author(s):  
Robert A. Dyer ◽  
Jenna L. Piercy ◽  
Anthony R. Reed ◽  
Carl J. Lombard ◽  
Leann K. Schoeman ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Spinal Anesthesia ◽  
Cesarean Delivery ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Severe Preeclampsia

Background Hemodynamic responses to spinal anesthesia (SA) for cesarean delivery in patients with severe preeclampsia are poorly understood. This study used a beat-by-beat monitor of cardiac output (CO) to characterize the response to SA. The hypothesis was that CO would decrease from baseline values by less than 20%. Methods Fifteen patients with severe preeclampsia consented to an observational study. The monitor employed used pulse wave form analysis to estimate nominal stroke volume. Calibration was by lithium dilution. CO and systemic vascular resistance were derived from the measured stroke volume, heart rate, and mean arterial pressure. In addition, the hemodynamic effects of phenylephrine, the response to delivery and oxytocin, and hemodynamics during recovery from SA were recorded. Hemodynamic values were averaged for defined time intervals before, during, and after SA. Results Cardiac output remained stable from induction of SA until the time of request for analgesia. Mean arterial pressure and systemic vascular resistance decreased significantly from the time of adoption of the supine position until the end of surgery. After oxytocin administration, systemic vascular resistance decreased and heart rate and CO increased. Phenylephrine, 50 mug, increased mean arterial pressure to above target values and did not significantly change CO. At the time of recovery from SA, there were no clinically relevant changes from baseline hemodynamic values. Conclusions Spinal anesthesia in severe preeclampsia was associated with clinically insignificant changes in CO. Phenylephrine restored mean arterial pressure but did not increase maternal CO. Oxytocin caused transient marked hypotension, tachycardia, and increases in CO.

Hemodynamic effects of neurohypophyseal peptides with antidiuretic activity in dogs

1985 ◽  
Vol 249 (5) ◽  
pp. H1001-H1008 ◽  
Author(s):  
J. Schwartz ◽  
J. F. Liard ◽  
C. Ott ◽  
A. W. Cowley
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Plasma Renin ◽  
Hemodynamic Effects ◽  
Antidiuretic Activity

Arginine vasopressin (AVP) is known to produce increases in total peripheral resistance (TPR) and mean arterial pressure (MAP) and decreases in heart rate (HR), cardiac output (CO), and plasma renin activity (PRA). Some recent observations with AVP and synthetic analogues have suggested that under certain conditions, AVP can induce cardiovascular and reninsecretory responses in the opposite directions. To characterize the receptors mediating these responses, the effects of AVP, oxytocin, and synthetic neurohypophyseal analogues with specific antidiuretic, vasoconstrictor, or oxytocic activities were studied in conscious dogs. AVP and 2-phenylalanine-8-ornithine-oxytocin (Phe2Orn8OT, a selective vasoconstrictor agonist) produced similar responses when infused at 10 ng X kg-1 X min-1. That is, TPR and MAP increased, and CO, HR, and PRA decreased. Pretreatment with a selective vasoconstrictor antagonist, [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid) 2-(O-methyl)tyrosine]AVP, abbreviated d(CH2)5Tyr(Me)-AVP (10 micrograms/kg), blocked the actions of Phe2Orn8OT. However, in the presence of d(CH2)5Tyr(Me)AVP, AVP actually decreased TPR and increased CO, HR, and PRA. An analogue with selective antidiuretic activity, 4-valine-8-D-AVP (VDAVP, 10 ng X kg-1 X min-1), produced the same effects as the combination of vasopressin plus d(CH2)5Tyr(Me)AVP. Neither the effects of VDAVP nor of AVP plus antagonist were blocked by propranolol (1 mg/kg). These data indicate that vasopressin, by its antidiuretic activity, produces cardiovascular effects that are opposite to many of those produced by its vasoconstrictor action and that these effects are not dependent on mediation by beta-adrenoceptors.

Dynamic exercise training in foxhounds. I. Oxygen consumption and hemodynamic responses

1985 ◽  
Vol 59 (1) ◽  
pp. 183-189 ◽  
Author(s):  
T. I. Musch ◽  
G. C. Haidet ◽  
G. A. Ordway ◽  
J. C. Longhurst ◽  
J. H. Mitchell
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Exercise Training ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Maximal Exercise ◽  
Submaximal Exercise ◽  
Maximal Heart Rate ◽  
O2 Consumption

Ten foxhounds were studied during maximal and submaximal exercise on a motor-driven treadmill before and after 8–12 wk of training. Training consisted of working at 80% of maximal heart rate 1 h/day, 5 days/wk. Maximal O2 consumption (VO2max) increased 28% from 113.7 +/- 5.5 to 146.1 +/- 5.4 ml O2 X min-1 X kg-1, pre- to posttraining. This increase in VO2max was due primarily to a 27% increase in maximal cardiac output, since maximal arteriovenous O2 difference increased only 4% above pretraining values. Mean arterial pressure during maximal exercise did not change from pre- to posttraining, with the result that calculated systemic vascular resistance (SVR) decreased 20%. There were no training-induced changes in O2 consumption, cardiac output, arteriovenous O2 difference, mean arterial pressure, or SVR at any level of submaximal exercise. However, if post- and pretraining values are compared, heart rate was lower and stroke volume was greater at any level of submaximal exercise. Venous lactate concentrations during a given level of submaximal exercise were significantly lower during posttraining compared with pretraining, but venous lactate concentrations during maximal exercise did not change as a result of exercise training. These results indicate that a program of endurance training will produce a significant increase in VO2max in the foxhound. This increase in VO2max is similar to that reported previously for humans and rats but is derived primarily from central (stroke volume) changes rather than a combination of central and peripheral (O2 extraction) changes.

scholarly journals Abnormal cardiovascular response to nitroglycerin in migraine

Cephalalgia ◽  
2019 ◽  
Vol 40 (3) ◽  
pp. 266-277
Author(s):  
Willebrordus PJ van Oosterhout ◽  
Guus G Schoonman ◽  
Dirk P Saal ◽  
Roland D Thijs ◽  
Michel D Ferrari ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Cardiovascular Response ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Initial Increase

Introduction Migraine and vasovagal syncope are comorbid conditions that may share part of their pathophysiology through autonomic control of the systemic circulation. Nitroglycerin can trigger both syncope and migraine attacks, suggesting enhanced systemic sensitivity in migraine. We aimed to determine the cardiovascular responses to nitroglycerin in migraine. Methods In 16 women with migraine without aura and 10 age- and gender-matched controls without headache, intravenous nitroglycerin (0.5 µg·kg−1·min−1) was administered. Finger photoplethysmography continuously assessed cardiovascular parameters (mean arterial pressure, heart rate, cardiac output, stroke volume and total peripheral resistance) before, during and after nitroglycerin infusion. Results Nitroglycerin provoked a migraine-like attack in 13/16 (81.2%) migraineurs but not in controls ( p = .0001). No syncope was provoked. Migraineurs who later developed a migraine-like attack showed different responses in all parameters vs. controls (all p < .001): The decreases in cardiac output and stroke volume were more rapid and longer lasting, heart rate increased, mean arterial pressure and total peripheral resistance were higher and decreased steeply after an initial increase. Discussion Migraineurs who developed a migraine-like attack in response to nitroglycerin showed stronger systemic cardiovascular responses compared to non-headache controls. The stronger systemic cardiovascular responses in migraine suggest increased systemic sensitivity to vasodilators, possibly due to insufficient autonomic compensatory mechanisms.

Dexmedetomidine as a Single Bolus Dose in Laparoscopic Cholecystectomy under General Anesthesia – A Comparison of Different Doses

2020 ◽  
Vol 5 (2) ◽  
pp. 1045-1049
Author(s):  
Kumud Pyakurel ◽  
Lalit Kumar Rajbanshi ◽  
Chitra Thapa ◽  
Gunjan Regmi
Keyword(s):  
Heart Rate ◽  
Laparoscopic Cholecystectomy ◽  
Mean Arterial Pressure ◽  
Adverse Events ◽  
Arterial Pressure ◽  
General Anesthesia ◽  
Induction Dose ◽  
Pharmacodynamic Profile ◽  
Duration Of Surgery ◽  
Sedation Scores

Introduction: Dexmedetomidine has an ideal pharmacodynamic profile for attenuation of stress response during general anesthesia for laparoscopic cholecystectomy. Since, the value of dexmedetomidine as a single premedication dose remains largely unexplored, this study compared dexmedetomidine in 0.5μg/kg and 1μg/kg dose for laparoscopic cholecystectomy under general anesthesia.  Objectives: The primary objective of this study was to compare dexmedetomidine in a single premedication dose of 0.5μg/kg and 1μg/kg in terms of hemodynamic (heart rate and mean arterial pressure) changes to critical incidences such as laryngoscopy, endotracheal intubation, pneumoperitoneum and extubation. The secondary objectives were to compare induction dose of propofol required, sedation scores in the immediate post anesthesia period and adverse events such as bradycardia and hypotension.  Methodology: This was a prospective double blind study. Ninety-two patients aged 18-55 years of either gender of American Society of Anesthesiologists physical status I-II were randomly allocated into two groups to receive either Dexmedetomidine 1μg/kg or 0.5μg/kg slowly IV over 10 minutes as a premedication before induction. Heart rate, Mean arterial pressure, induction dose of propofol, sedation scores, and adverse events were compared.  Results: The patient characteristics, Fentanyl consumption, duration of surgery and anesthesia in both groups were comparable. There was comparable attenuation of hemodynamics in both groups during laryngoscopy and intubation. Dexmedetomidine in 1μg/kg compared to 0.5μg/kg had significantly better attenuation of hemodynamics from 1 minute to 40 minutes of pneumoperitoneum. After 40 minutes, there was no attenuation in either group. The post anesthesia sedation scores were comparable. The induction dose of propofol was significantly less and the incidence of bradycardia was significantly higher with dexmedetomidine 1μg/kg.  Conclusion This study demonstrates that a premedication dose of Dexmedetomidine in 1μg/kg compared to 0.5μg/kg has significantly betier attenuation of hemodynamics from 1 minute to 40 minutes of pneumoperitoneum.

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