Effects of Ganglionic and Cholinergic Blocking Drugs on the Pressor Response to Central Vagal Stimulation

Pharmacology ◽  
1970 ◽  
Vol 4 (2) ◽  
pp. 120-128 ◽  
Author(s):  
W.M. Pedersoli
Keyword(s):  
Vagal Stimulation ◽  
Pressor Response

The ganglionic blocking properties of the cholinesterase reactivator, HS-6

1978 ◽  
Vol 56 (5) ◽  
pp. 857-862 ◽  
Author(s):  
Paul M. Lundy
Keyword(s):  
Animal Species ◽  
Vagal Stimulation ◽  
Pressor Response ◽  
Blood Levels ◽  
Pressor Effect ◽  
Nictitating Membrane ◽  
Beneficial Effects ◽  
Depressor Effect ◽  
Ganglionic Blocking ◽  
Cholinesterase Reactivator

Following intravenous administration of the cholinesterase reactivator HS-6 (30 mg/kg), blood pressure fell (up to 50 mmHg) and maximal blood levels of HS-6 reached 242 μg/ml. HS-6 attenuated the pressor response resulting from carotid occlusion and the depressor effect of vagal stimulation. Doses of HS-6 below those used to protect against soman in different animal species (10–30 μmol/kg) progressively blocked the ganglion-stimulating effects of nicotine and dimethylphenylpiperazinium but not the pressor effect following adrenaline, a pattern similar to that produced by hexamethonium but only [Formula: see text] as potent. HS-6, like hexamethonium and mecamylamine, progressively blocked the contraction of the nictitating membrane of the cat resulting from preganglionic stimulation.The results indicate that HS-6 possesses ganglion-blocking properties at doses likely to be used in the protection against soman poisoning. The ganglion-blocking properties of the drug may be a factor in the beneficial effects of HS-6.

Involvement of the ventrolateral medulla in the mediation of pressor responses of the rat to afferent vagal stimulation

1985 ◽  
Vol 63 (12) ◽  
pp. 1612-1614 ◽  
Author(s):  
T. Kubo
Keyword(s):  
Spinal Cord ◽  
Vagal Stimulation ◽  
Pressor Response ◽  
Ventrolateral Medulla ◽  
Vasopressin Antagonist ◽  
Caudal Ventrolateral Medulla ◽  
Pressor Responses ◽  
Electrolytic Lesions ◽  
Afferent Vagal ◽  
Stimulation Of

Electrical stimulation of afferent vagal fibres evoked a pressor response in rats after transection of the spinal cord. The pressor response was accounted for by an increased release of vasopressin because it was abolished by the intravenous injection of a vasopressin antagonist. Bilateral electrolytic lesions at the sites of the caudal ventrolateral medulla markedly reduced the pressor response to afferent vagal stimulation but not that to carotid occlusion. It is concluded that the area of the caudal ventrolateral medulla is involved in mediation of the vasopressin-induced pressor response to afferent vagal stimulation.

Pregabalin As A Premedicant To Attenuate Pressor Response In Patients Undergoing Laparoscopic Cholecystectomy: A Prospective, Randomized, Double-Blind, Placebo-Controlled Study

2020 ◽  
Vol 11 (3) ◽  
pp. 3418-3423
Author(s):  
Sweety Agrawal ◽  
Shubdha Bhagat ◽  
Pratibha Deshmukh ◽  
Amol Singham
Keyword(s):  
Laparoscopic Cholecystectomy ◽  
Pressor Response ◽  
Controlled Study ◽  
Double Blind ◽  
Co2 Insufflation ◽  
Ramsay Sedation Scale ◽  
Minute Interval ◽  
Group A ◽  
Group B ◽  
Induction Of Anaesthesia

The present study was done to evaluate the ability of oral pregabalin to attenuate the pressor response to airway instrumentation in patients undergoing laparoscopic cholecystectomy under general anesthesia. Sixty-four adult patients aged between 25-55 year of either gender belonging to ASA-1 or ASA2 physical status weighing 50-70 kg were enrolled in this study. Thirty-two patients each were randomized to group A, or group B. Patients in group A received tablet Pregabalin (150mg) and those in group B received placebo orally one hour before induction of anaesthesia. Heart rate, blood pressure, and sedation were assessed preoperatively before giving the tablets and after 30 minutes, and just before induction of anaesthesia. Intraoperative, pulse rate, mean arterial pressure, ECG in the lead II, SPO2 and ETCO2 were monitored. All the above parameters were noted during laryngoscopy and intubation, 3 minutes after CO2 insufflation, and then at every 10-minute interval till the end of surgery. These parameters were also recorded after extubating the patient. The Ramsay sedation scale was used to assess the sedation at the baseline, one hour after drug intake , one hour after extubation and 4 hour after surgery. Any adverse effects in the postoperative period were recorded. The result of our study shows that pre-emptive administration of oral pregabalin 150 mg significantly reduced the pressor response at the time of laryngoscopy and intubation, after CO2 insufflation and just after extubation. We conclude that oral pregabalin premedication is effective in successful attenuation of hemodynamic pressor response to laryngoscopy, intubation and pneumoperitoneum in patients undergoing laparoscopic cholecystectomy

scholarly journals Nifedipine prevents the pressor response to laryngoscopy and tracheal intubation in patients with coronary artery disease

Anaesthesia ◽  
1988 ◽  
Vol 43 (6) ◽  
pp. 495-497 ◽  
Author(s):  
S.C. Kale ◽  
R.P. Mahajan ◽  
T.S. Jayalakshami ◽  
V. Raghavan ◽  
B. Das
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Tracheal Intubation ◽  
Pressor Response ◽  
Artery Disease

scholarly journals Supraspinal fatigue impedes recovery from a low-intensity sustained contraction in old adults

2012 ◽  
Vol 112 (5) ◽  
pp. 849-858 ◽  
Author(s):  
Tejin Yoon ◽  
Bonnie Schlinder-Delap ◽  
Manda L. Keller ◽  
Sandra K. Hunter
Keyword(s):  
Young Adults ◽  
Pressor Response ◽  
Motor Evoked Potential ◽  
Silent Period ◽  
Voluntary Activation ◽  
Age Difference ◽  
Task Failure ◽  
Old Adults ◽  
Sustained Contraction ◽  
Low Intensity

This study determined the contribution of supraspinal fatigue and contractile properties to the age difference in neuromuscular fatigue during and recovery from a low-intensity sustained contraction. Cortical stimulation was used to evoke measures of voluntary activation and muscle relaxation during and after a contraction sustained at 20% of maximal voluntary contraction (MVC) until task failure with elbow flexor muscles in 14 young adults (20.9 ± 3.6 yr, 7 men) and 14 old adults (71.6 ± 5.4 yr, 7 men). Old adults exhibited a longer time to task failure than the young adults (23.8 ± 9.0 vs. 11.5 ± 3.9 min, respectively, P < 0.001). The time to failure was associated with initial peak rates of relaxation of muscle fibers and pressor response ( P < 0.05). Increments in torque (superimposed twitch; SIT) generated by transcranial magnetic stimulation (TMS) during brief MVCs, increased during the fatiguing contraction ( P < 0.001) and then decreased during recovery ( P = 0.02). The increase in the SIT was greater for the old adults than the young adults during the fatiguing contraction and recovery ( P < 0.05). Recovery of MVC torque was less for old than young adults at 10 min post-fatiguing contraction (75.1 ± 8.7 vs. 83.6 ± 7.8% of control MVC, respectively, P = 0.01) and was associated with the recovery of the SIT ( r = −0.59, r2 = 0.35, P < 0.001). Motor evoked potential (MEP) amplitude and the silent period elicited during the fatiguing contraction increased less for old adults than young adults ( P < 0.05). The greater fatigue resistance with age during a low-intensity sustained contraction was attributable to mechanisms located within the muscle. Recovery of maximal strength after the low-intensity fatiguing contraction however, was impeded more for old adults than young because of greater supraspinal fatigue. Recovery of strength could be an important variable to consider in exercise prescription of old populations.

Verapamil blockade of pressor and uterine responses to AVP-OT analogue, oxypressin

1988 ◽  
Vol 254 (1) ◽  
pp. R75-R77
Author(s):  
D. Gazis ◽  
G. Gonzalez ◽  
M. Mendlowitz
Keyword(s):  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Channel Blocker ◽  
Pressor Response ◽  
Pressor Responses ◽  
Significant Difference

The effects of the calcium channel blocker verapamil on simultaneously recorded uterine and pressor responses to the equipotent (in eliciting these responses) oxytocin-vasopressin analogue, oxypressin, were studied in urethan-anesthetized and pentolinium- and indomethacin-treated rats during injections and infusions of this analogue. Doses of verapamil that almost completely blocked the pressor response to infused oxypressin had no effect on a pressor response to injected oxypressin of equal magnitude. Larger doses of verapamil blocked the pressor response to injected oxypressin somewhat. Uterine responses were only marginally affected by these doses of verapamil, and there was no significant difference between infusion and injection or between estrus and diestrus.

Regional pulmonary blood flow during 96 hours of hypoxia in conscious sheep

1986 ◽  
Vol 61 (6) ◽  
pp. 2136-2143 ◽  
Author(s):  
D. C. Curran-Everett ◽  
K. McAndrews ◽  
J. A. Krasney
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Pulmonary Blood Flow ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
Superior Vena ◽  
Acute Hypoxia ◽  
Vena Cava ◽  
Normobaric Hypoxia ◽  
Pulmonary Arterial

The effects of acute hypoxia on regional pulmonary perfusion have been studied previously in anesthetized, artificially ventilated sheep (J. Appl. Physiol. 56: 338–342, 1984). That study indicated that a rise in pulmonary arterial pressure was associated with a shift of pulmonary blood flow toward dorsal (nondependent) areas of the lung. This study examined the relationship between the pulmonary arterial pressor response and regional pulmonary blood flow in five conscious, standing ewes during 96 h of normobaric hypoxia. The sheep were made hypoxic by N2 dilution in an environmental chamber [arterial O2 tension (PaO2) = 37–42 Torr, arterial CO2 tension (PaCO2) = 25–30 Torr]. Regional pulmonary blood flow was calculated by injecting 15-micron radiolabeled microspheres into the superior vena cava during normoxia and at 24-h intervals of hypoxia. Pulmonary arterial pressure increased from 12 Torr during normoxia to 19–22 Torr throughout hypoxia (alpha less than 0.049). Pulmonary blood flow, expressed as %QCO or ml X min-1 X g-1, did not shift among dorsal and ventral regions during hypoxia (alpha greater than 0.25); nor were there interlobar shifts of blood flow (alpha greater than 0.10). These data suggest that conscious, standing sheep do not demonstrate a shift in pulmonary blood flow during 96 h of normobaric hypoxia even though pulmonary arterial pressure rises 7–10 Torr. We question whether global hypoxic pulmonary vasoconstriction is, by itself, beneficial to the sheep.

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