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August 1, 1997Circulation Research

Hemodynamic pressure overloading in adult feline myocardium induced de novo TNF-alpha mRNA expression within 30 minutes and protein production within 60 minutes, depressing myocyte cell motion.

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Population

Adult feline myocardium (ex vivo and in vivo), papillary muscles, and isolated contracting cardiac myocytes

Comparison

Hemodynamic pressure overloading and myocardial… vs Normal perfusion pressures and unstretched…

Design

Preclinical

Follow-up

up to 60 minutes

Key result

Hemodynamic pressure overloading in adult feline myocardium induced de novo TNF-alpha mRNA expression within 30 minutes and protein production within 60 minutes, depressing myocyte cell motion.

Authors

SKSamir KapadiaHOHakan OralJLJoseph Lee

Discussion

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Overview

May implicate TNF-α in load-induced contractile impairment; leaves open its role and targetability in human HF.

Key Points

  • This study aims to investigate how hemodynamic pressure affects TNF-alpha expression in adult feline myocardium.
  • Examined TNF-alpha mRNA and protein biosynthesis in myocardium under normal and pressure-overloading conditions.
  • Analyzed effects of myocardial stretch on TNF-alpha mRNA expression in papillary muscles.
  • Assessed cell motion in cardiac myocytes treated with superfusates from pressure-overloaded and control hearts.
  • De novo TNF-alpha mRNA expression observed within 30 minutes and protein production within 60 minutes during pressure overload.
  • Cell motion was depressed in myocytes treated with superfusates from pressure-overloaded hearts compared to controls.
  • TNF-alpha mRNA biosynthesis also occurred in vivo under physiological hemodynamic conditions.

Structured PICO

P
Population
Adult feline myocardium (ex vivo and in vivo), papillary muscles, and isolated contracting cardiac myocytes
I
Intervention
Hemodynamic pressure overloading and myocardial stretch
C
Comparator
Normal perfusion pressures and unstretched myocardium
O
Outcome
TNF-alpha mRNA and protein biosynthesissurrogate

This study provides initial evidence that adult mammalian myocardium produces biologically active TNF-alpha in response to hemodynamic pressure overloading, contributing to depressed myocyte contractility.

Cite This Study

Kapadia et al. (1997) studied Hemodynamic pressure overloading. Hemodynamic pressure overloading vs. Normal perfusion pressures / unstretched myocardium was evaluated on TNF-alpha mRNA and protein biosynthesis. Hemodynamic pressure overloading in adult feline myocardium induced de novo TNF-alpha mRNA expression within 30 minutes and protein production within 60 minutes, depressing myocyte cell motion.

synapsesocial.com/papers/6a0a0fc141a1eeaa0645ade1https://doi.org/10.1161/01.res.81.2.187
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