| First Author | Merx MW | Year | 2005 |
| Journal | FASEB J | Volume | 19 |
| Issue | 8 | Pages | 1015-7 |
| PubMed ID | 15817640 | Mgi Jnum | J:136939 |
| Mgi Id | MGI:3797360 | Doi | 10.1096/fj.04-2886fje |
| Citation | Merx MW, et al. (2005) Oxygen supply and nitric oxide scavenging by myoglobin contribute to exercise endurance and cardiac function. FASEB J 19(8):1015-7 |
| abstractText | Recent studies of myoglobin (Mb) knockout (myo-/-) mice have extended our understanding of Mb's diverse functions and have demonstrated a complex array of compensatory mechanisms. The present study was aimed at detailed analysis of cardiac function and exercise endurance in myo-/- mice and at providing evidence for Mb's functional relevance. Myo-/- isolated working hearts display decreased contractility (dP/dtmax 3883+/-351 vs. 4618+/-268 mmHg/sec, myo-/- vs. WT, P<0.005). Due to a shift in sympathetic/parasympathetic tone, heart rate is reduced in conscious myo mice-/- (615+/-33 vs. 645+/-27 bpm, myo-/- vs. WT, P<0.001). Oxygen consumption (VO2) under resting conditions (3082+/-413 vs. 4452+/-552 ml x kg(-1) x h(-1), myo-/- vs. WT, P<0.001) and exercise endurance, as determined by spiroergometry, are decreased (466+/-113 vs. 585+/-153 m, myo-/- vs. WT, P<0.01). Conscious myo-/- mice evaluated by echocardiography display lowered cardiac output (0.64+/-0.06 vs. 0.75+/-0.09 ml x min(-1) x g(-1), myo-/- vs. WT, P<0.001), impaired systolic shortening (60+/-3.5 vs. 65+/-4%, myo-/- vs. WT, P<0.001) and fail to respond to beta1-stimulation. Strikingly, the latter cardiac effects of Mb deficiency can be partially attenuated by NOS inhibition. Loss of Mb results in a distinct phenotype, even under resting conditions, and the importance of oxygen supply and nitric oxide scavenging by Mb is clearly demonstrated at the conscious animal level. |
