January 1, 1996Circulation

Arrhythmogenic Action of Thrombin During Myocardial Reperfusion via Release of Inositol 1,4,5-Triphosphate

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Population

Buffer-perfused rat hearts subjected to 20 minutes of global ischemia

Comparison

Thrombin or thrombin receptor agonist peptide… vs Control hearts or hearts treated with inactive…

Design

Preclinical

Follow-up

2 minutes of reperfusion

Authors

AJAlexander JacobsenMax Planck Institute for Evolutionary Biology XDXiao‐Jun DuBaker Heart and Diabetes Institute KLKim A. LambertBaker Heart and Diabetes Institute

Discussion

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Implication

May identify a catecholamine-independent pathway for reperfusion VF; leaves open thrombin or InsP3 as therapeutic targets.

Structured PICO

Population

Buffer-perfused rat hearts (including catecholamine-depleted models) subjected to 20 minutes of global ischemia

Intervention

Thrombin (5 IU/mL) or thrombin receptor agonist peptide (TRAP(1-6), 50 micromol/L) administered during reperfusion, with or without inhibitors (gentamicin, U-73122)

Comparator

Control hearts (no thrombin/TRAP) or hearts treated with inactive isomer U-73343

Outcome

Release of inositol 1,4,5-triphosphate [Ins(1,4,5)P3] and duration of ventricular arrhythmias (ventricular tachycardia and ventricular fibrillation) during reperfusionsurrogate

Thrombin induces reperfusion arrhythmias in rat hearts via the release of inositol 1,4,5-triphosphate, suggesting a mechanism for arrhythmogenesis independent of catecholamines.

Cite This Study

Jacobsen et al. (1996) studied this question.

synapsesocial.com/papers/6a82a3596416d6fbd1239d9e https://doi.org/10.1161/01.cir.93.1.23

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Arrhythmogenic Action of Thrombin During Myocardial Reperfusion via Release of Inositol 1,4,5-Triphosphate

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Arrhythmogenic Action of Thrombin During Myocardial Reperfusion via Release of Inositol 1,4,5-Triphosphate

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider