Altered NADH and improved function by anesthetic and ischemic preconditioning in guinea pig intact hearts.

Abstract

NADH increases during ischemia because O(2) shortage limits NADH oxidation at the electron transport chain. Ischemic (IPC) and anesthetic preconditioning (APC) attenuate cardiac reperfusion injury. We examined whether IPC and APC similarly alter NADH, i.e., mitochondrial metabolism. NADH fluorescence was measured at the left ventricular wall of 40 Langendorff-prepared guinea pig hearts. IPC was achieved by two 5-min periods of ischemia and APC by exposure to 0.5 or 1.3 mM sevoflurane for 15 min, each ending 30 min before 30 min of global ischemia. During ischemia, NADH initially increased in nonpreconditioned control hearts and then gradually declined below baseline levels. This increase in NADH was lower after APC but not after IPC. The subsequent decline was slower after IPC and APC. On reperfusion, NADH was less decreased after IPC or APC, mechanical and metabolic functions were improved, and infarct size was lower compared with controls. Our results indicate that IPC and APC cause distinctive changes in mitochondrial metabolism during ischemia and thus lead to improved function and tissue viability on reperfusion.

• Authors: Matthias L Riess, Amadou K S Camara, Qun Chen, Enis Novalija, Samhita S Rhodes, David F Stowe
• Journal: American journal of physiology. Heart and circulatory physiology (Am J Physiol Heart Circ Physiol) Vol. 283 Issue 1 Pg. H53-60 (Jul 2002) ISSN: 0363-6135 [Print] United States
• PMID: 12063274 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• Anesthetics
• Methyl Ethers
• Troponin I
• NAD
• Sevoflurane
• Creatine Kinase

Topics

• Anesthetics (pharmacology)
• Animals
• Creatine Kinase (metabolism)
• Dose-Response Relationship, Drug
• Guinea Pigs
• Heart (physiopathology)
• Heart Ventricles (metabolism)
• In Vitro Techniques
• Ischemic Preconditioning, Myocardial (methods)
• Methyl Ethers (pharmacology)
• Mitochondria (drug effects, metabolism)
• Myocardial Ischemia (physiopathology)
• Myocardium (metabolism)
• NAD (metabolism)
• Sevoflurane
• Troponin I (metabolism)
• Ventricular Function, Left (drug effects, physiology)