Feline left ventricular oxygen consumption is not affected by volume expansion, ejection or redevelopment of pressure during relaxation

Abstract

We studied the dependency of myocardial oxygen consumption on the mechanical events during left ventricular relaxation in isolated supported cat hearts. The volume of the left ventricle was controlled by means of a balloon connected to a membrane pump. Oxygen consumption (MVO2 in cm3.min-1.100 g-1) for three protocols (PROT) performed at peak isovolumic pressure, was studied: (1) rapid ejection to zero pressure, (2) partial rapid ejection followed by redevelopment of pressure, (3) volume expansion during relaxation, and compared with oxygen consumption of isovolumic (ISOV) beats. We found (mean +/- SD): (table; see text) In the protocols 1 and 3 the differences were not significant (paired Student's t-test, p greater than 0.05). In protocols 1 and 2 left ventricular volume was decreased up to 2.15 cm3 (i.e. stroke volume, SV) during the pressure release. We studied the specific effect of ejection (i.e., wall muscle shortening) in a fourth protocol in which the ventricle ejected up to 2.7 cm3 under nearly zero pressure load (isobaric contraction). There was a small amount of oxygen consumption associable with this unloaded ejection i.e. MVO2 = 3.38 (+/- 0.47) + 0.30 (+/- 0.16) SV, but it was too small to compensate for a decrease in MVO2 expected from the pressure release according to the tension time index. These findings suggest that oxygen consumption does not depend on the mechanical events during ventricular relaxation.

Left Ventricular Mechanoenergetics in Small Animals

“…Our recent finding is that freely shortening myocardial slices under mechanically unloaded conditions do not require a significant additional VO 2 for cross-bridge cycling [109,125,126]. This finding is further supported by the result showing that a specific cross-bridge cycling inhibitor, 5 mM BDM, does not affect the slice VO 2 , though 5 mM BDM markedly reduced the slice motility [109].…”

Increased O2 consumption in excitation–contraction coupling in hypertrophied rat heart slices related to increased Na+–Ca2+ exchange activity

“…The expression levels of cardiac sarcoplasmic reticulum (SR) Ca 2? -ATPase (SERCA2), phospholamban (PLB) and phosphorylated Ser 16 (phospho-ser 16 ) PLB (p-PLB) in this model were also decreased, suggesting that the Ca 2? -handling of the cardiac myocyte was already altered [10,11].…”

“…The same amounts of membrane proteins (10 lg/lane) were separated on SDS-polyacrylamide gels (10% for SERCA2 and NKA, 15% for PLB, p-PLB and PLM, and 7.5% for NCX1) in a minigel apparatus (Mini-PROTEAN II, Bio-Rad) and transferred to polyvinyliodene difluoride membranes. The membranes were blocked (4% Block Ace, Dainippon Pharmaceutical Co., Osaka) and then incubated with anti-SERCA2 antibody (1:1,000 dilution, Affinity Bio Reagents), anti-PLB antibody (1:2,000 dilution, Upstate Biotechnology), anti-p-PLB (Ser 16 ) antibody (1:1,000 dilution, Upstate Biotechnology), anti-NCX1 antibody (1:200 dilution, a generous gift from Dr. Iwamoto, Fukuoka University), anti-PLM antibody (1:100 dilution, ABGENT), or anti-NKA antibody (1:10,000 dilution, Upstate Biotechnology). The antigens were detected by the luminescence method (ECL Western blotting detection kit, Amersham) with peroxidase-linked anti-mouse IgG (1:2,000 dilution) or peroxidase-linked anti-rabbit IgG (1:2,000 or 1:5,000 dilution).…”

“…exchange (NCX) coupling was increased by 100%. The depressed mVO 2 consumption by SERCA2 was supported by lower protein expressions of phosphorylated-Ser 16 phospholamban and SERCA2. The increase in NKA-NCX coupling mVO 2 was supported by marked augmentation of NCX current.…”

“…handling in excitation-contraction (E-C) coupling (E-C coupling mVO 2 ) [12][13][14][15]. Previous reports have reported that freely shortening myocardial slices under mechanically unloaded conditions do not require a significant additional VO 2 for crossbridge cycling [16,17]. This finding is further supported by our results showing that 5 mmol/l 2,3-butanedione monoxime (BDM: a specific cross-bridge cycling inhibitor) does not affect the rat LV myocardial slice VO 2 , although 5 mmol/l BDM markedly reduces the slice motility [14,15].…”