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Introduction: Laryngoscopy and endotracheal intubation lead to a strong sympathetic response, this study was done to compare clonidine, esmolol, and lignocaine as an adjuvant to fentanyl to attenuate the pressor response to laryngoscopy during endotracheal intubation. To compare clonidine, esmolol, and lignocaine as an a Objectives: djuvant to fentanyl to attenuate the pressor response to laryngoscopy during endotracheal intubation. A Randomized prospective study includi Material and Methods: ng 150 normotensive patients undergoing elective surgical procedures were included. Three groups were divided according to drug they received. After 3 minutes of drug , laryngoscopy and endotracheal intubation were done. Vitals (HR,SBP,DBP and MAP) were noted before laryngoscopy and endotracheal intubation and 1,2,4,6 and 8 minute after Laryngoscopy and endotracheal intubation and anaesthesia was continued with O2+N2O+Sevoflurane. Results: Rise in heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) at one minute following intubation in all three groups of drugs (p<0.001). SBP both esmolol and clonidine reached equal to baseline in 4 mins with their respective p-value as 0.293 and 0.097 and group lignocaine reached equal to baseline in 6 mins. DBP of group esmolol reached baseline at 4 mins (p-value- 0.090), group clonidine reached baseline in 6 mins. And group lignocaine does not reach baseline even after 8 mins. MAP in esmolol group reached to baseline in 4 mins, group clonidine reached to baseline in 6 mins and group lignocaine does not reach to baseline even after 8 mins. Conclusion: Considering all parameters, it was concluded that esmolol with fentanyl showed better response on all parameters.
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Objectives To compare the attenuation of pressor responses by intravenous clonidine and preservative-free lignocaine to laryngoscopy and endotracheal intubation. Materials and Methods A randomized, prospective, comparative, double-blinded study was conducted in 80 adult patients who were randomized into two groups of 40 each, group clonidine (Group C) and group lignocaine (Group L). Group C patients were given 2 µg/kg clonidine in 20 ml of normal saline as a slow infusion over 10 min prior to intubation. Group L patients were given 1.5 mg/kg of preservative-free 2% lignocaine in 20 ml of normal saline as a single-dose infusion over 3 min prior to intubation. Baseline vital and hemodynamic parameters were monitored during the perioperative period at 1-, 5-, and 10-min post-intubation. Results The attenuation of heart rate (HR) after intubation was much better with clonidine than lignocaine as there is statistically significant difference in the mean HR between the two groups at 1, 5, and 10 min after intubation with the HR significantly lesser in the Group C than the Group L at all times after intubation. Both clonidine and lignocaine were effective in attenuating systolic blood pressure response after intubation, but clonidine was more effective than lignocaine as systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) in the Group C remained much lower than the Group L and the difference between the two groups was statistically significant at all times after intubation. Conclusion Premedicating with a single slow infusion of 2 µg/kg i.v. clonidine has been proven to be effective in maintaining perioperative hemodynamic stability at 1, 5, and 10 min post-intubation than lignocaine.
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Endotracheal intubation is one of the most invasive stimuli in anaesthesia1 producing noxious haemodynamic response in the form of tachycardia, hypertension and increased stress hormones i.e., catecholamine levels.1 This airway stimulus may increase morbidity and mortality in patients with recent myocardial infarction, hypertension, preeclampsia and cerebrovascular pathology such as tumours, aneurysms etc. Many pharmacological and non-pharmacological methods have evolved over time to obtund these haemodynamic stress responses to laryngoscopy and intubation. One such method is the use of Intubating Laryngeal Mask Airway (ILMA). In the present study, we compared changes in haemodynamic responses during intubation with endotracheal tube versus intubating with laryngeal mask airway. METHODSFifty patients of either sex between 15-45 years were randomized in to two groups. Group I for ILMA (n=25) and group II for Laryngoscopy and endotracheal intubation (n=25). Hemodynamic responses such as heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP) were measured in either groups and compared at just before induction which was used as baseline, after intubation through ILMA/Laryngoscopy and at the end of 1, 2, 3, 5 and 10 minute intervals.RESULTSBoth intubation through ILMA and laryngoscopy insertion were associated with increase in HR, SBP and DBP but in Group II Laryngoscopy group, the increase was 46.09%, 24.28% and 26.00% from baseline. The rise in HR, SBP and DBP were statistically significant (p<0.05) just after intubation through ILMA/laryngoscopy, it remained significant in the post intubation period till 5 minutes. After 5 and 10 minutes the changes in HR, SBP and DBP were not significant (p>0.05) between the groups.CONCLUSIONSIn Group I ILMA insertion was carried out easily and laryngoscopy was not needed. ILMA insertion was associated with an attenuated pressor response in comparison with laryngoscopy and intubation. In Group II there was higher increase in pressor response to intubation than Group I because laryngoscopy was done. Haemodynamic responses such as HR, SBP, DBP were significantly less following ILMA insertion as compared to direct laryngoscopy. So ILMA appears to be more suitable in patients where pressor response is to be avoided as in high risk patients i.e. h/o recent myocardial infarction, hypertension, CAD, preeclampsia and cerebrovascular pathology such as tumours, aneurysms etc.
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The current Study was done to compare the efficacy of intravenous lignocaine 2% versus oropharyngeal topical 10% xylocaine spray before induction of anaesthesia in attenuating the pressor response to direct laryngoscopy and endotracheal intubation. A total of 60 patients were divided randomly into two groups of 30 patients each. Group I received intravenous lignocaine 2% @ 1.5 mg/kg. Group II received topical 10% xylocaine spray @ 1.5 mg/kg body weight just before induction of anaesthesia. All hemodynamic parameters were measured immediately after laryngoscopy and intubation and at 1, 3, 5 minutes after laryngoscopy and intubation in both the groups. Mean values of haemodynamic parameters in Group I increased after intubation and then started declining but did not reach the baseline even at 5 minutes. In Group II all mean values of haemodynamic parameters increased after intubation and then started declining to almost baseline at 5 minutes. The differences in mean values of haemodynamic between the two groups immediately after intubation and at 1, 3 and 5 minutes thereafter were statistically highly significant (p<0.001). Oropharyngeal topical xylocaine 10% when applied before induction of general anaesthesia is more effective method for attenuating the pressor response to direct laryngoscopy and endotracheal intubation when compared to intravenous lignocaine 2%
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Background: Laryngoscopy and endotracheal intubation, which are a basic and integral part of general anesthesia (GA), are associated with reflex sympathetic stimulation, manifested by tachycardia and hypertension. Aim: The aim was to compare the effect of dexmedetomidine and clonidine on the pressor response among patients undergoing tracheal intubation in elective surgeries under general anesthesia. Materials and methods: A prospective and randomized control study conducted in 80 adult patients of age 18-55 years in ASA I and II were included in this study. Patients were divided into Group D and Group C of 40 patients each. Results: Mean SBP, DBP and MAP in the dexmedetomidine group remained close to the baseline throughout the study period showing a significant difference from clonidine groups following the induction interval. In present study after intubation heart rate, SBP, and DBP was increased in all patients but the increase was more in patients of clonidine group when compared to dexmedetomidine group. There was statistically significant difference in heart rate between the two groups at 1, 3 and 4 min interval after intubation (p value<0.05). No significant changes in peripheral oxygen saturation K. Selvarju, Kondreddi Narayana Prasad, Ajay Kumar Reddy Bobba. Study between clonidine and dexmedetomidine in attenuation of pressor response during endotracheal intubation. IAIM, 2018; 5(8): 100-106. Page 101 (SpO2) and cardiac rhythm (ECG) were observed in any patients of both groups. Bradycardia (HR<50/min) was observed in one patient of dexmedetomidine group and two patients in clonidine group, five minutes after intubation. Intraoperative hypotension was observed in one patient of dexmedetomidine group and in two patients of clonidine group. Conclusion: Premedication with dexmedetomidine can safely be recommended for attenuation of provided more stable hemodynamics response to endotracheal intubation
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Background: Laryngoscopy and tracheal intubation is invariably associated with a reflex Sympathetic pressor response resulting in elevated heart rate and blood pressures. This may prove detrimental in high-risk patients. Objective of this study is to compare the effects of lignocaine and esmolol in attenuation of this response. Methods: 150 ASA I - II status normotensive patients scheduled for elective surgical procedures were selected randomly and divided into three groups of 50 each. All patients received premedication with pentazocine 0.5mg/kg i.m and midazolam 0.05 mg/kg i.m. Induction of anesthesia was standardized for all patients who received, thiopentone 5-mg/kg i.v. and Glycopyrrolate 0.01. mg/kg and were relaxed with succinylcholine 2mg/kg i.v. First group did not receive any attenuation. The second group received 2mg/kg lignocaine i.v. bolus and the third group received 1mg/kg Esmolol iv. bolus, 3 minutes before laryngoscopy and intubation. HR, systolic, diastolic blood pressure was recorded noninvasively before induction, post induction-1,3,5, 7 and 10 minutes from the onset of laryngoscopy. ‘z’ test was used for statistical analysis. Results: After intubation incidence of tachycardia (HR>100/min) was significantly greater in control and lignocaine group than in esmolol group (z>1.96, p<0.05- 0.001). Rise in SBP and DBP were also statistically significant in control and lignocaine group than in esmolol group (z>1.96, p<0.05). Conclusion: Attenuation of pressor response is seen both with lignocaine and with esmolol. Of the two drugs Esmolol 1mg/kg i.v. bolus provides a consistent, reliable and effective attenuation as compared to lignocaine 2mg/kg iv. bolus.
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Background: Laryngoscopy and endotracheal intubation are almost always associated with an increased sympathetic activity. To attenuate the presser response, various drugs have been tried. This study aims at finding out if the low dose of clonidine (1.5μg/kg) is best suited for this purpose. Methods: This was a prospective study which involved two groups of patients. Each group had 30 patients who presented for elective, non-cardiovascular surgeries. The patients in group-C received Clonidine (1.5 μg/kg) and the patients in group-N received Normal saline. Heart rate (HR), Systolic blood pressure (SBP), Diastolic blood pressure (DBP) and Mean blood pressure (MBP) were recorded before and after intubation and at 1, 5, and 10 mins. The obtained clinical data were analyzed statistically with analysis of variance. Results: In our study, HR, SBP, and DBP and MBP all increased during intubation and thereafter in the control groups. Pretreatment with clonidine (1.5 μg/kg) significantly attenuated the cardiovascular and catecholamine responses to tracheal intubation Conclusion: Preoperative administration of a single dose of clonidine blunted the hemodynamic responses more then the placebo during Laryngoscopy and Intubation with reduced anesthetic requirements.
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Background: The objectives of the present study were to compare the effect of lignocaine (1.5 mg/kg IV given 3 mins before laryngoscopy and intubation), esmolol (300 μg/kg as a bolus 2 mins before intubation), and dexmedetomidine (0.5 μg/kg IV over 10 mins) on the pressor response in non-hypertensive American Society of Anesthesiologists (ASA) Grade I and II patients posted for elective surgery and the pharmacoeconomic and pharmacoepidemiological inferences drawn on comparison of these drugs. Methods: After approval by the Institutional Ethics Committee, 90 consenting adult patients aged 18-65 years of age of either sex of non-hypertensive ASA Grade I or II undergoing elective surgery under general anesthesia with endotracheal intubation were included in this randomized, prospective study protocol. (1) Group L: Patients were given IV lignocaine 1.5 mg/kg. (2) Group E: Patients were given IV esmolol 300 μg/kg. (3) Group D: Patients were given IV dexmedetomidine 0.5 μg/kg. Adequate monitoring, oxygenation, and hydration were established on the entry in the operating room (OR). All hemodynamic data were measured on arrival in OR, before induction, before intubation, and at 1, 3, 5 mins after intubation by an independent observer. Anesthesia was induced with thiopental sodium and fentanyl 2 μg/kg; intubation was performed with cuffed oral endotracheal tube of appropriate size for airway management. Surgery was allowed to start only after 5 mins of intubation. Results: Esmolol effectively blunted the blood pressure response to intubation, but incompletely attenuated the increase in heart rate (HR). Dexmedetomidine was more effective than lignocaine in minimizing the increase in HR, systolic blood pressure (SBP), and diastolic blood pressure (DBP) subsequent to endotracheal intubation. Conclusion: Dexmedetomidine 0.5 μg/kg has manifested to maintain hemodynamic stability associated with intubation and hence may prove benefi cial for cardiac patients where the stress response to laryngoscopy and intubation is highly undesirable.
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Background: Laryngoscopy and endotracheal intubation are associated with an increase in blood pressure (BP) and heart rate (HR). The present study was conducted to evaluate the role of gabapentin in attenuation of these hemodynamic changes. Methods: Forty patients undergoing elective laparoscopic cholecystectomy under general anesthesia with standardized premedication and anesthetics were randomized to receive gabapentin or a matching placebo. The patients of Group I received gabapentin 600 mg orally 2 hrs before surgery and patients in Group II received a matching placebo. Patient’s HR, systolic BP (SBP), diastolic BP (DBP), mean BP (MBP), were monitored before and after 1, 2, 5, and 10 mins of endotracheal intubation. Results: Comparison of SBP, DBP, and MBP at 1, 2, 5 and 10 mins after endotracheal intubation showed statistically significant attenuation in the gabapentin group when compared to placebo. Changes in the HR were not significant. Conclusion: Gabapentin 600 mg, given 2 hrs before induction is effective in attenuating the pressor response to laryngoscopy and tracheal intubation.
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Objective The present study was to analyze the role of ACh-lateral septum(SL)pressor system in the Central amygdaloid nucleus(AC)-emotional pressor circuit.Method Interurban microinjection of different drugs,then blood pressure and heart vate were vecorded.Results(1)CRF(corticotropin releasing factor)or SP(substance P)microinjection into the SL can induced pressor responses.The AC pressor responses to glutamate(Glu)could be attenuated by preinjection of CRF antagonist or SP antagonist into bilateral SL.(2)the AC pressor responses to Glu were also reduced by preinjection of atropine into either bilateral HBL,LC or RVL respectively,(3)Since lateral HB(HBL)projects to the posterior hypothalamus(HP)containing ACh-ergic neurons,and excitation of the latter produces pressor response via the RVL and LC-RVL;atropine preinjection into the HP could also decrease the HBL-and AC-pressor response.Conclusion The present results indicate that the AC produce pressor responses involved with the SL via their CRF and SP,mechanism underlying pressor response of SL is involved in pressor response of AC.
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In the present study, we examined cardiovascular response to static and dynamic hand-grip exercise at equivalent work load (peak tension) and tension-time index (TTI, integrated tension for time) in healthy young (n=8) and elderly (n=8) males. Static and dynamic exercises were conducted for 75 s and 150 s at 30% of maximal voluntary contraction (MVC) and for 45 s and 90 s at 50%MVC, respectively. Arterial pressure was continuously measured on a beat basis. Blood pressure at the end of exercise and the magnitude of pressor response induced by exercise did not differ significantly between static and dynamic exercises at the two work loads. The magnitude of pressor response tended to depend on work load. These findings were the same in both age groups. Consequently, it was indicated that blood pressure responses to static and dynamic hand-grip exercise at equivalent work load and TTI did not differ both in young and elderly people. Furthermore, it was suggested that central command and muscle metabolite induced stimulation of the exercise pressor reflex during static and dynamic exercise were similar based on the results of relative perceived exertion and blood pressure response during post-exercise arterial occlusion.
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@#ObjectiveTo investigate the effect and mechanisms of rostral ventrolateral medulla (RVL) on the pressor response of lateral hypothalamus-perifornical region (LH/PF) in rats.Methods30 healthy Wistar rats were randomly divided into four groups: the phentolamine group; propranolol group; atropine group and glutamate diethyl ester group, saline was as the control in every group. After microinjection of Glu into LH/PF, the blood pressure and heart rate were observed. Then phentolamine, propranolol, atropine and glutamate diethyl ester were microinjected into RVL and the blood pressure and heart rate changes induced by microinjection of Glu were observed again.ResultsMicroinjection of Glu into LH/PF can cause the blood pressure elevating and heart rate accelerating. The pressor response of Glu to excited LH/PF could be attenuated after response of phentolamine, propranolol, atropine and glutamate diethyl ester microinjected into RVL. The blood pressures of phentolamine group; propranolol group; atropine group and glutamate diethyl ester group reduced significantly different from those in the saline control group (P<0.01).ConclusionThe α-,β-,M- and Glu-receptors in the RVL induce the pressor response of LH/PF region.
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Changes of blood pressure, heart rate, ECG, respiration rate and pupil size by intracerebroventricular(ICV) infusion of hypertonic NaCl with 0.04 ml/min for 5 min(total 0.2ml) were observed in urethane-anesthetized rabbits. ICV infusion of 0.75M NaCl produced slight pressor effect (11mmHg) and did not affect other parameters. ICV infusion of 1.5M NaCl began to increase blood pressure from 2~3 min after the infusion and produced maximal increase(24mmHg) at 5~10 min. Then the pressor effect was recovered to the original level at 30~60 min. Change of heart rate by the infusion was not clear, but ST-segment of ECG was markedly depressed. Respiration rate increased about 1.5 times than the control in accordance with the pressor effect and the state was continued even after the recover of the pressor effect. Both pupils dilated markedly and light-reflex was lost. Changes of parameters by ICV infusion of 3.0M NaCl were similar to those by 1.5M NaCl and some rabbits caused severe arrhythmias and died. The purpose of present study is to investigate the mechansim(s) of the pressor effect induced by the ICV infusion of 1.5M NaCl. The pressor effect of 1.5M NaCl was attenuated by the continuous infusion of vasopressin antagonist(20microm/kg/min) but not affected by intravenous treatment with 2mg/kg phentolamine, 2mg/kg propranolol and 1mg/kg chlorisondamine. The pressor effect was not altered with ICV 0.12mg/kg phenoxybenzamine, 0.4mg diltiazem, 0.1mg/kg mecamylamine and 0.2mg/kg atropine. After ICV infusion of 25microg/kg/min of diazepam, however, the pressor effect was completely abolished and restored 3~4 hours after stopping diazepam infusion. The pressor effect was rather potentiated than inhibited in bilateral adrenalectomized or nephrectomized rabbits. Infusion of 2microg/kg/min of saralasin for 10 min in the bliateral adrenalectomized rabbit did not affect the pressor effect at all. These results suggest that hypertensive effect induced by ICV infusion of hypertonic NaCl is mediated by the increase of vasopressin secretion.
Sujets)
Lapins , Troubles du rythme cardiaque , Atropine , Pression sanguine , Chlorisondamine , Diazépam , Diltiazem , Électrocardiographie , Rythme cardiaque , Perfusions intraventriculaires , Mécamylamine , Phénoxybenzamine , Phentolamine , Propranolol , Pupille , Fréquence respiratoire , Saralasine , VasopressinesRésumé
AIM: To study the central mechanism of intracerebral interleukin-1? in restraint stress-induced pressor response in rats. METHODS: Cardiovascular radio-telemetry system, stereotaxic microinjection system and neuroelectrophysiological methods were used to investigate the role of intracerebral interleukin-1? in pressor response induced by restraint stress, and the relation with the changes of discharge in the rostral ventrolateral medulla (RVL) neuron. RESULTS: The pressor response was induced by restraint stress and was reduced by intracerebral-ventricular injection of (icv) IL-1 receptor antagonist (IL-Ira) in conscious rats. The pressor response was directly induced by IL-1 (icv), which is related to increase of the extracellular discharge frequency in RVL neurons. CONCLUSION: Intracerebral IL-1? mediates pressor response induced by restraint stress, the mechanism may be closely related to RVL.
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Hypoxic pulmonary pressor response (HPPR) was observed witb a preparation of perfused lungs in situ in rats, and the effects of deoxy-2-glucose (2DG), verapamil, and dipyridamole on HPPR were studied.During bypoxia (inhalation of 3% oxygen for 10 minutes) , there was a 50% increase on average in pulmonary arterial pressure in the perfused lungs in situ in rats. 2DG inhibited the first and second but enhanced the seventh and eighth HPPR. Both verapamil and dipyridamole depressed HPPR.On the basis of the results, the author suggests that the mechanism of HPPR might originate from the lungs themselves. There might be a close relation between the glucose-energy metabolism and the occurrence of HPPR, the trans-membranous influx of calcium might play a certain role in the development of HPPR, and adenosine would probably participate in the regulation of HPPR.