What is the clinical evidence from this study?

Study design: Other. Population: Ischemia/reperfusion injury. Intervention: Xamoterol vs. Control (I/R without XA) and XA with various kinase inhibitors. Primary outcome: Mean coronary flow, left ventricular end-diastolic pressure, rate-pressure product, and creatine kinase release.

March 11, 2005Cardiovascular Research

PI 3-kinase, protein kinase C, and protein kinase A are involved in the trigger phase of β1-adrenergic preconditioning

View Full Paper

Ask AI

Bookmark

Key result

Transient preischemic exposure to the beta1-AR agonist xamoterol protected isolated rat hearts against ischemia/reperfusion injury, an effect blocked by PI3K, PKC, and PKA inhibitors.

Population

Isolated non-working rat heart model pretreated with 6-hydroxydopamine

Comparison

Transient beta1-adrenoreceptor stimulation with… vs Control group subjected to 40 min of global…

Design

Preclinical

Authors

ARArnaud RobinetCentre Hospitalier Universitaire de Reims GHGuillaume HoizeyLaboratoire de Spectrométrie Ionique et Moléculaire HMHervé MillartUniversité de Reims Champagne-Ardenne

Discussion

Member takes

Implication

Preischemic beta1-AR agonism protects isolated rat hearts; hypothesis-generating for translation to in vivo or clinical ischemia/reperfusion injury.

Structured PICO

Population

Isolated non-working rat hearts subjected to global ischemia and reperfusion to study pharmacological preconditioning.

Intervention

Transient beta1-adrenoreceptor stimulation with xamoterol (0.01 microM for 5 min) with or without inhibitors (atenolol, LY-294002, wortmannin, GF-109203X, H89)

Comparator

Control group subjected to 40 min of global ischemia and 30 min of reperfusion without xamoterol preconditioning

Outcome

Mean coronary flow (MCF), left ventricular end-diastolic pressure (LVEDP), rate-pressure product (RPP), and creatine kinase (CK) releasesurrogate

Transient preischemic exposure to a beta1-AR agonist protects against ischemia/reperfusion injury via pathways involving PI 3-kinase, PKC, and PKA.

Cite This Study

Robinet et al. (2005) studied Ischemia/reperfusion injury. Xamoterol vs. Control (I/R without XA) and XA with various kinase inhibitors was evaluated on Mean coronary flow, left ventricular end-diastolic pressure, rate-pressure product, and creatine kinase release. Transient preischemic exposure to the beta1-AR agonist xamoterol protected isolated rat hearts against ischemia/reperfusion injury, an effect blocked by PI3K, PKC, and PKA inhibitors.

synapsesocial.com/papers/6a91584ab18f518eae4643fe https://doi.org/10.1016/j.cardiores.2005.02.010

View Full Paper

Ask AI

Bookmark

Implication

Preischemic beta1-AR agonism protects isolated rat hearts; hypothesis-generating for translation to in vivo or clinical ischemia/reperfusion injury.

PI 3-kinase, protein kinase C, and protein kinase A are involved in the trigger phase of β1-adrenergic preconditioning

Discussion

Member takes

Implication

Structured PICO

Cite This Study

PI 3-kinase, protein kinase C, and protein kinase A are involved in the trigger phase of β1-adrenergic preconditioning

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider