scholarly journals Hemodynamic Effects of Naloxone and Nalbuphine Following High-dose Fentanyl Anesthesia in Dogs

1991 ◽  
Vol 24 (3) ◽  
pp. 478
Author(s):  
Young Jae Kim ◽  
Jin Yoo Park ◽  
Ju Yuel Park
2008 ◽  
Vol 109 (6) ◽  
pp. 1155-1164 ◽  
Author(s):  
Amanda M. Murphy ◽  
Anargyros Xenocostas ◽  
Pria Pakkiri ◽  
Ting-Yim Lee

Object The authors investigated the hemodynamic effects of recombinant human erythropoietin (rhEPO) after subarachnoid hemorrhage (SAH) in rabbits. Methods The authors used male New Zealand White rabbits in this study divided into the following groups: SAH plus saline (16 rabbits), SAH plus low-dose rhEPO (16 rabbits; 1500 IU/kg on Day 0 and 500 IU/kg on Days 2 and 4), SAH plus high-dose rhEPO (10 rabbits; 1500 IU/kg on Days 0, 2, 4, and 6), and sham (6 rabbits). Computed tomography perfusion studies and CT angiography were performed for 1 hour after SAH on Day 0, and once each on Days 2, 4, 7, 9, and 16 after SAH. Assessments of neurological function and tissue histology were also performed. Results The mortality rate was significantly lower after rhEPO treatment (12%) than after saline treatment (44%) (p < 0.05). Neurological outcomes in the low-dose and high-dose rhEPO groups were better than in the saline group after SAH (p < 0.05), and the cerebral blood flow in the high-dose rhEPO group was greater than that in the saline group (p < 0.05). The mean transit time was significantly lower on Days 2 and 4 in the low-dose and high-dose rhEPO groups than in the saline group, but increased significantly on Day 7 in both groups (p < 0.05). The hematocrit increased significantly from baseline values in the high-dose and low-dose rhEPO groups on Days 4 and 7, respectively (p < 0.05). Conclusions Treatment with rhEPO after experimental SAH is associated with improved cerebral blood flow and microcirculatory flow as reflected by lower mean transit times. Improved tissue perfusion correlated with reduced mortality and improved neurological outcomes. Further investigation of the impact of increasing hematocrit on hemodynamic changes is needed.


1988 ◽  
Vol 32 (1) ◽  
pp. 20
Author(s):  
M. M. TODD ◽  
J. C. DRUMMOND ◽  
HOI SANG U

2020 ◽  
Vol 9 (21) ◽  
Author(s):  
Kasper M. Petersen ◽  
Søren Bøgevig ◽  
Troels Riis ◽  
Niklas W. Andersson ◽  
Kim P. Dalhoff ◽  
...  

Background Intravenous high‐dose glucagon is a recommended antidote against beta‐blocker poisonings, but clinical effects are unclear. We therefore investigated hemodynamic effects and safety of high‐dose glucagon with and without concomitant beta‐blockade. Methods and Results In a randomized crossover study, 10 healthy men received combinations of esmolol (1.25 mg/kg bolus+0.75 mg/kg/min infusion), glucagon (50 µg/kg), and identical volumes of saline placebo on 5 separate days in random order (saline+saline; esmolol+saline; esmolol+glucagon bolus; saline+glucagon infusion; saline+glucagon bolus). On individual days, esmolol/saline was infused from −15 to 30 minutes. Glucagon/saline was administered from 0 minutes as a 2‐minute intravenous bolus or as a 30‐minute infusion (same total glucagon dose). End points were hemodynamic and adverse effects of glucagon compared with saline. Compared with saline, glucagon bolus increased mean heart rate by 13.0 beats per minute (95% CI, 8.0–18.0; P <0.001), systolic blood pressure by 15.6 mm Hg (95% CI, 8.0–23.2; P =0.002), diastolic blood pressure by 9.4 mm Hg (95% CI, 6.3–12.6; P <0.001), and cardiac output by 18.0 % (95% CI, 9.7–26.9; P =0.003) at the 5‐minute time point on days without beta‐blockade. Similar effects of glucagon bolus occurred on days with beta‐blockade and between 15 and 30 minutes during infusion. Hemodynamic effects of glucagon thus reflected pharmacologic glucagon plasma concentrations. Glucagon‐induced nausea occurred in 80% of participants despite ondansetron pretreatment. Conclusions High‐dose glucagon boluses had significant hemodynamic effects regardless of beta‐blockade. A glucagon infusion had comparable and apparently longer‐lasting effects compared with bolus, indicating that infusion may be preferable to bolus injections. Registration Information URL: https://www.clinicaltrials.gov ; Unique identifier: NCT03533179.


1992 ◽  
Vol 74 (5) ◽  
pp. 703???711 ◽  
Author(s):  
Jean E. de La Coussaye ◽  
Bruno Bassoul ◽  
Josep Brugada ◽  
Bernard Albat ◽  
Pascale A. Peray ◽  
...  

1987 ◽  
Vol 42 (2) ◽  
pp. 201-209 ◽  
Author(s):  
David M Salerno ◽  
Patricia J Sharkey ◽  
Gregory A Granrud ◽  
Richard W Asinger ◽  
Morrison Hodges

Neurosurgery ◽  
1987 ◽  
Vol 20 (4) ◽  
pp. 559-563 ◽  
Author(s):  
Michael M. Todd ◽  
John C. Drummond ◽  
Sang U Hoi

1987 ◽  
Vol 9 (4) ◽  
pp. 858-864 ◽  
Author(s):  
Arie Roth ◽  
Daniel Kulick ◽  
Lindalee Freidenberger ◽  
Robert Hong ◽  
Shahbudin H. Rahimtoola ◽  
...  

1988 ◽  
Vol 255 (5) ◽  
pp. R737-R743
Author(s):  
S. M. Gardiner ◽  
A. M. Compton ◽  
T. Bennett

The regional hemodynamic effects of rat atrial natriuretic peptide (ANP) (1 and 10 nmol) were measured in the same conscious Brattleboro rats in water-replete and in water-deprived states (14 h). In the latter condition, the effects of ANP were compared with those of captopril (3.2 mumol). In rats in the water-replete state, the low dose of ANP had no significant effects on mean arterial pressure (MAP) or renal, superior mesenteric, or hindquarter vascular resistances, although heart rate (HR) showed a transient increase. The high dose of ANP caused a fall in MAP and an increase in HR. Renal and hindquarter vascular beds showed dilatation followed by constriction; there was a mesenteric vasoconstriction only. In rats in the water-deprived state, the low dose of ANP caused a marked fall in MAP but only a transient increase in HR; there was marked hindquarters vasodilation. The high dose of ANP caused dramatic hypotension and bradyarrhythmia; an initial hindquarter vasodilation gave way to vasoconstriction; renal and mesenteric vasoconstrictions also occurred. The initial effects of captopril on MAP were similar to those of the high dose of ANP, but the regional hemodynamic effects of captopril indicated a potent inhibition of both primary and secondary vasoconstrictor mechanisms.


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