Attenuation of Epinephrine-Induced Dysrhythmias by Bradykinin: Role of Nitric Oxide and Prostaglandins

Rajani, Vinod; Hussain, Yasser; B, Bolla; Guzman, Felix Q de; Montiague, Raul; Igić, Rajko; Rabito, Sara F.

doi:10.1016/s0002-9149(97)00472-4

Cited by 21 publications

(10 citation statements)

References 21 publications

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“…As it has been reported previously [7,16], practically all arrhythmias appeared simultaneously with the increase in blood pressure, during the period between 5 and 60 s after epinephrine injection. The incidence of PVCs and VTs was significantly lower in CBDL rats compared to sham-operated animals (P < 0.05, Fig.…”

Section: Epinephrine-induced Hemodynamic Changes and Arrhythmiassupporting

confidence: 85%

“…As it has been reported previously [7,16], epinephrine injection elicited a wide range of arrhythmias, including 1st, 2nd, and 3rd degree heart block, premature atrial contractions, premature ventricular contractions (PVCs), and runs of ventricular tachycardias (VTs) defined as three or more consecutive premature ventricular contractions following epinephrine injection. The most frequent ventricular arrhythmias were PVCs and runs of VTs which were used for analysis ( Fig.…”

Section: Evaluation Of Arrhythmiasmentioning

confidence: 72%

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Reduced susceptibility to epinephrine-induced arrhythmias in cirrhotic rats: The roles of nitric oxide and endogenous opioid peptides

Tavakoli¹,

Hajrasouliha²,

Maralani³

et al. 2007

Journal of Hepatology

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Section: Epinephrine-induced Hemodynamic Changes and Arrhythmiassupporting

confidence: 85%

Section: Evaluation Of Arrhythmiasmentioning

confidence: 72%

Reduced susceptibility to epinephrine-induced arrhythmias in cirrhotic rats: The roles of nitric oxide and endogenous opioid peptides

Tavakoli¹,

Hajrasouliha²,

Maralani³

et al. 2007

Journal of Hepatology

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“…In animal models, the end products of all three pathways influence ischemia-reperfusion injury arrhythmias. 3–6 In population studies, higher renin levels are associated with increased risk of cardiovascular disease mortality 7. Furthermore, in randomized clinical trials, blocking these pathways with ACE inhibitors, angiotensin receptor blockers, or aldosterone inhibitors decreases risk of SCA 8–10.…”

Section: Introductionmentioning

confidence: 99%

Genetic variation in angiotensin-converting enzyme–related pathways associated with sudden cardiac arrest risk

et al. 2009

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“…A recent study focusing on K + channels by Zhang et al (11) showed I to not I K,ATP might be involved in the mechanism producing halothaneadrenaline arrhythmias, using K + channel openers or blockers in rats. On the other hand, Rajani et al (12) proposed that bradykinin, acting on the B 2 receptor via a mechanism involving the release of nitric oxide and prostaglandins, might attenuate the genesis of halothaneadrenaline arrhythmia. Thus the potential mechanism of sensitization is thought to be multifactorial and further investigation is required to determine the entire mechanism.…”

Section: Role Of Halothane On Adrenaline Arrhythmiamentioning

confidence: 99%

Development of a Halothane-Adrenaline Arrhythmia Model Using In Vivo Guinea Pigs

Noda

Hashimoto

2004

J Pharmacol Sci

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Abstract. In vivo antiarrhythmic effects of diltiazem hydrochloride and nifekalant hydrochloride, a pure class III antiarrhythmic drug (Vaughan Williams' classification), on adrenaline induced ventricular arrhythmias were examined in halothane anesthetized guinea pigs. Continuous adrenaline infusion (12.5 m g / kg per min) induced ventricular arrhythmias. Arrhythmogenicity was significantly increased with vagotomy and higher concentration of halothane. After injection of diltiazem at 0.5 mg / kg, the arrhythmic ratio (the number of ventricular ectopic beats divided by the total heart beats) was significantly reduced compared with the predrug control value (0.69 vs 0.04, P<0.05). No significant change of arrhythmic ratio was observed after injection of nifekalant (0.57 vs 0.61, ns). After administration of nifekalant, the mean minimum adrenaline infusion rate that induced ventricular arrhythmia decreased from 9.29 to 6.43 m g / kg per min. On the other hand, before administration of diltiazem, the mean arrhythmogenic rate of adrenaline was 8.50 mg / kg per min, but ventricular arrhythmias were no longer induced during continuous infusion of diltiazem at 0.5 mg / kg per min. These results were qualitatively consistent with previous experiments using the canine halothane-adrenaline model. In conclusion, the halothaneadrenaline arrhythmia model using the in vivo guinea pig is useful for screening drugs with potential anti-or pro-arrhythmic properties.

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Attenuation of Epinephrine-Induced Dysrhythmias by Bradykinin: Role of Nitric Oxide and Prostaglandins

Cited by 21 publications

References 21 publications

Reduced susceptibility to epinephrine-induced arrhythmias in cirrhotic rats: The roles of nitric oxide and endogenous opioid peptides

Reduced susceptibility to epinephrine-induced arrhythmias in cirrhotic rats: The roles of nitric oxide and endogenous opioid peptides

Genetic variation in angiotensin-converting enzyme–related pathways associated with sudden cardiac arrest risk

Development of a Halothane-Adrenaline Arrhythmia Model Using In Vivo Guinea Pigs

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