scholarly journals COMPARATIVE ASSESSMENT OF DIFFERENT TYPES OF LARYNGOSCOPES BLADES - MACINTOSH, MILLER AND MCCOY FOR LARYNGEAL VIEW AND PRESSOR RESPONSE

Author(s):  
Dr Sanjay Kumar ◽  
Dr Urmila Sinha ◽  
Dr Sanjeev Sinha ◽  
Dr Ranju Sinha

The laryngoscopy is known to have profound cardiovascular effects. This includes pressor response and tachycardia along with an increase in catecholamine concentration, mainly norepinephrine. The major cause of the sympathoadrenal response is believed to arise from stimulation of supraglottic region by laryngoscopic blade with tracheal tube placement and cuff inflation contributing little additional stimulation. Complications of pressor respo laryngoscopy include myocardial ischemia, cardiac failure, intracranial haemorrhage and increase in intracranial pressure. Hence the present study planned to evaluate the laryngeal view and pressor response by using three different blades – Macintosh, McCoy and Miller laryngoscopes. The study was planned in the Department of Anaesthesia in Andaman and Nicobar Islands Institute of Medical Science (ANIIMS), Port Blair India, From Jun 2016 to Jun 2017 . The 30 patient undergoing the Laryngoscopy were enrolled in the present study. For the 10 patients using the Macintosh Blade were divided in Group I. The next 10 patients using the Miller blade were considered in the Group II. The remaining 10 patients were studied by use of McCoy blade. The results in our study show that the MacCoy laryngoscope blade improves the visualization of the larynx and significantly attenuates haemodynamic parameters during laryngoscopy and intubation as compared to that with Macintosh laryngoscope blade. Keywords: Laryngoscopy, Intubation, pressor  response, Macintosh,  miller  and  Mccoy  laryngoscopes, etc

1980 ◽  
Vol 59 (s6) ◽  
pp. 235s-237s ◽  
Author(s):  
R. W. Rockhold ◽  
J. T. Crofton ◽  
L. Share

1. The cardiovascular effects of an enkephalin analogue were examined in spontaneously hypertensive and normotensive Wistar-Kyoto rats. (D-Ala2)-methionine enkephalin caused a biphasic increase in blood pressure and an increase in heart rate after intracerebroventricular injection. 2. The initial pressor response to (D-Ala2)-methionine enkephalin was greater in hypertensive than in normotensive rats. No difference was noted between groups during the secondary pressor response. Heart rate increases paralleled the secondary increase in blood pressure. 3. Naloxone pretreatment abolished the secondary increase in blood pressure and the tachycardia, but did not blunt the initial pressor response in female Wistar-Kyoto rats. 4. Plasma levels of arginine vasopressin were depressed during the plateau phase of the pressor response in hypertensive rats given intracerebroventricular (d-Ala2)-methionine enkephalin. 5. The results suggest that the cardiovascular effects of central enkephalin are not due to vasopressin, but may involve activation of the sympathetic nervous system.


1990 ◽  
Vol 258 (2) ◽  
pp. R325-R331 ◽  
Author(s):  
D. A. Morilak ◽  
G. Drolet ◽  
J. Chalmers

We have examined the influence of endogenous opioids on the basal and reflex control of arterial blood pressure in the pressor region of the rostral ventrolateral medulla (RVLM) of chloralose-anesthetized rabbits. We tested basal effects both in intact animals and after hypotensive hemorrhage. Bilateral administration of the opiod antagonist naloxone (20 nmol, 100 nl) directly into the RVLM induced a gradual and prolonged increase in mean arterial pressure (MAP) (+17 +/- 2 mmHg). This was preceded by a brief and mild depressor effect (-9 +/- 3 mmHg), which was attributable to a transient reduction in excitability immediately after naloxone injection. When naloxone was administered into the RVLM after hemorrhage (20 ml/kg), it improved recovery of MAP relative to saline controls, again producing a gradual, prolonged pressor response (+29 +/- 5 mmHg). The effect of naloxone on a baroreflex in intact animals was only transient, with a brief, nonsignificant attenuation of the reflex depressor response to aortic nerve stimulation. We conclude that endogenous opioids exert a tonic inhibitory influence on RVLM pressor neurons and that this input remains active after hemorrhage. The RVLM may thus be one site for the beneficial effects of naloxone in preventing circulatory decompensation after hemorrhage. In contrast, opioid neurons are not an essential component of baroreflex-mediated sympathoinhibition in the RVLM.


1956 ◽  
Vol 185 (3) ◽  
pp. 510-514 ◽  
Author(s):  
Faith K. Brown

Cardiovascular effects of acute elevations of intracranial pressure were studied, with special reference to three questions: a) whether vasoconstriction or cardiac stimulation is primarily responsible for the pressor response to this stimulus; b) whether the ultimate nature of the stimulus is neurogenic or humoral; and c) whether or not changes in venous tone occur in response to ICP elevation. It is concluded from the experimental findings that vasoconstriction was the dominant factor in the response, that the reflex is primarily neurogenic, and that the venomotor system shows an active constriction which accompanies the arterial pressure rise.


2008 ◽  
Vol 18 (11) ◽  
pp. 1035-1039 ◽  
Author(s):  
SEYED-MOHAMMAD MIRESKANDARI ◽  
NAHID ASKARIZADEH ◽  
MOHAMMAD-ESMAEEL DARABI ◽  
EIMAN RAHIMI ◽  
HOSSEIN-ALI ATAEE ◽  
...  

1994 ◽  
Vol 266 (4) ◽  
pp. R1148-R1153 ◽  
Author(s):  
A. Bataillard ◽  
J. Sassard

Cardiovascular effects of human recombinant interleukin-1 beta (hrIL-1 beta) were investigated in normotensive rats using a computerized analysis of arterial blood pressure in conscious, unrestrained animals. Intravenous injection of hrIL-1 beta induced a rapid and short-lasting rise in blood pressure associated with a first slight tachycardia followed by a second sustained and pronounced increase in heart rate. These effects occurred in a dose-related manner. Pretreatment with a converting-enzyme inhibitor (perindopril) did not modify the hrIL-1 beta-induced increase in blood pressure. Blockade of beta 1-adrenoceptors (atenolol) prevented the tachycardia, but did not significantly affect the pressor response to hrIL-1 beta. On the contrary, the hrIL-1 beta-induced increase in blood pressure was inhibited by an alpha 1-adrenoceptor antagonist (prazosin), whereas the tachycardia was untouched. Finally, pretreatment with a cyclooxygenase inhibitor (indomethacin) completely abolished the cardiovascular response to hrIL-1 beta. These results suggest that the hrIL-1 beta-induced pressor response and associated tachycardia require the synthesis of prostaglandins and involve a sympathetic nervous system activation but do not depend on the renin-angiotensin system.


1996 ◽  
Vol 270 (1) ◽  
pp. H167-H173 ◽  
Author(s):  
S. Lon ◽  
E. Szczepanska-Sadowska ◽  
M. Szczypaczewska

Five series of experiments were performed on conscious trained dogs to find out whether intracranially released arginine vasopressin (AVP) is involved in mediation of central cardiovascular effects of angiotensin II (ANG II). The dogs were implanted with guide tubes leading to the third cerebral ventricle (ICV) and implanted with the intra-arterial catheters. Blood pressure and heart rate were continuously monitored during intracerebroventricular administration of 1) ANG II alone (250 ng), 2) AVP alone (0.01 ng/min during 10 min), 3) ANG II together with AVP, 4) AVP together with AVP V1-receptor antagonist 1(1-mercapto-4-methylcyclohexaneacetic acid)-8-AVP [MeCAAVP, V1ANT,100 ng/min], and 5) ANG II together with V1ANT. The results revealed that 1) ANG II and AVP applied separately elicited significant, long-lasting increases of blood pressure; 2) the maximum pressor effect after ANG II and AVP applied together did not differ from that after separate application of either of these peptides, but the duration of the pressor response was significantly shorter; 3) pretreatment with V1ANT effectively prevented blood pressure increases elicited by central administration of AVP and ANG II; and 4) after blockade of V1 receptors administration of AVP resulted in a significantly delayed decrease of blood pressure below baseline. The results strongly suggest that 1) centrally released AVP mediates the pressor effect of intracerebroventricularly applied ANG II by means of V1 receptors; 2) intracerebroventricularly applied ANG II and AVP interact to activate the mechanism involved in extinction of their pressor effect; and 3) blockade of central V1 receptors uncovers the hypotensive action of centrally applied AVP.


Anaesthesia ◽  
2015 ◽  
Vol 70 (9) ◽  
pp. 1094-1095 ◽  
Author(s):  
B. M. A. Pieters ◽  
A. A. J. van Zundert

Author(s):  
S Sakila ◽  
N Begum ◽  
S Kawsar ◽  
ZA Begum ◽  
MS Zola

Aims: This study was aimed to find out anti-fertility effects of Andrographis paniculata (AP) plant. Study design & Methodology: A prospective case control animal study with 85 female and 30 male rats (Total 115 rats) was done in the Department of Pharmacology of Dhaka Medical College and Bangladesh Medical College, Dhaka, Bangladesh from July 2002 to December 2003. The total 85 female rats were grouped into case study or exposure group (N=60 female rats) exposed to water extract of AP & control or non exposure group (N=25 female rats, 30 male rats also considered as control group) Exposure group (water extract) of female were again subdivided in 3 groups according to duration of (A.P) exposure (N=20 in each group) e.g. 4 weeks, 6 weeks and 8 weeks. Mating schedules were done after the completion of scheduled duration of exposure with A.P (Dose was 1 gm/kg). Results: In group I percentage of infertility was 33.33% in 4 weeks exposure, 50% in 6 weeks exposure & 100% in 8 weeks exposure respectively. In control group (Group II) percentage of infertility was 0%. In case study group of female rats the value of FSH was 1.20 1U/L (4 weeks), 1.12 1U/L (6 weeks), 1.00 1U/L (8 weeks), LH 0.78 1U/L (4 weeks), 0.70 1U/L (6 weeks), 0.64 1U/L (8 weeks), Estrogen 45.30 pg/ml (4 weeks), 44.80 pg/ml (6 weeks), 44.20 pg/ml (8 weeks) and Progesterone 4.84 nmol/L (4 weeks), 4.72 nmol/L (6 weeks) and 3.80 nmol/L (8 weeks). In non exposure group the value of FSH was 1.23 1U/L, LH 0.80 1U/L, Estrogen 47.05 pg/L and Progesterone 5.50 nmol/L. In exposure group all the values were lesser than the normal hormonal value. Conclusion: This study suggests that due to lower level of hormone, female rats have promising percentage of infertility with AP. Further study is needed with rat as well as clinical trial with human being. Key Words: Andrographis paniculata, Antifertility effects doi: 10.3329/bjms.v8i1.3183 Bangladesh Journal of Medical Science Vol.8 No. 1-2; 2009 10-14


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