Energy expenditure by Ba(2+) contracture in rat ventricular slices derives from cross-bridge cycling.
Am J Physiol
; 277(1): H74-9, 1999 07.
Article
in En
| MEDLINE
| ID: mdl-10409184
To clarify the energy-expenditure mechanism during Ba(2+) contracture of mechanically unloaded rat left ventricular (LV) slices, we measured myocardial O(2) consumption (VO(2)) of quiescent slices in Ca(2+)-free Tyrode solution and VO(2) during Ba(2+) contracture by substituting Ca(2+) with Ba(2+). We then investigated the effects of cyclopiazonic acid (CPA) and 2,3-butanedione monoxime (BDM) on the Ba(2+) contracture VO(2). The Ca(2+)-free VO(2) corresponds to that of basal metabolism (2.32 +/- 0.53 ml O(2). min(-1). 100 g LV(-1)). Ba(2+) increased the VO(2) in a dose-dependent manner (from 0.3 to 3.0 mmol/l) from 110 to 150% of basal metabolic VO(2). Blockade of the sarcoplasmic reticulum (SR) Ca(2+) pump by CPA (10 micromol/l) did not at all decrease the Ba(2+)-activated VO(2). BDM (5 mmol/l), which specifically inhibits cross-bridge cycling, reduced the Ba(2+)activated VO(2) almost to basal metabolic VO(2). These energetic results revealed that the Ba(2+)-activated VO(2) was used for the cross-bridge cycling but not for the Ca(2+) handling by the SR Ca(2+) pump.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Sarcoplasmic Reticulum
/
Barium
/
Ventricular Function
/
Energy Metabolism
/
Myocardial Contraction
Type of study:
Health_economic_evaluation
Limits:
Animals
Language:
En
Journal:
Am J Physiol
Year:
1999
Document type:
Article
Affiliation country:
Japan
Country of publication:
United States