EurekaMag.com logo
+ Site Statistics
References:
52,725,316
Abstracts:
28,411,598
+ Search Articles
+ Subscribe to Site Feeds
EurekaMag Most Shared ContentMost Shared
EurekaMag PDF Full Text ContentPDF Full Text
+ PDF Full Text
Request PDF Full TextRequest PDF Full Text
+ Follow Us
Follow on FacebookFollow on Facebook
Follow on TwitterFollow on Twitter
Follow on Google+Follow on Google+
Follow on LinkedInFollow on LinkedIn

+ Translate

Spectrophotometric analysis of myocardial oxygen metabolism in perfused rat hearts


Kokyu to Junkan. Respiration & Circulation 34(12): 1317-1323
Spectrophotometric analysis of myocardial oxygen metabolism in perfused rat hearts
Cardiac muscle contains myoglobin in cytosol and cytochromes in mitochondria, both of which participate in oxygen metabolism of the heart. The change of myoglobin oxygenation and of the oxidation-reduction state of cytochrome aa3 can be measured by spectrophotometric technique and used as optical indicators of both tissue oxygen concentration and energy state. We evaluated effects of 1) perfusion pressure, 2) catecholamines, 3) coronary vasodilators such as Ca-antagonist, prostaglandin (PGI2) on intracellular oxygenation and energy metabolism in perfused rat hearts. Results: 1) With Langendorff perfusion, the cardiac tissue became hypoxic (more than 50% of myoglobin was in deoxygenated state) at perfusion pressure below 30 cm H2O. This result may indicate the functional obstruction in capillary microcirculation at low perfusion pressure. 2) Infusion of epinephrine (5 .mu.g/30 sec.) under normoxic perfusion conditions, increased cardiac work and lactate release. More than 50% of myoglobin was then deoxygenated and cardiac tissue was severely hypoxic. The increase in lactate release was explained by the enhancement of glycolytic flux in tissue hypoxia. On the other hand, dopamine infusion (50 .mu.g/30 sec.) also increased cardiac work at the same degree, but did not alter lactate release. Myoglobin oxygen saturation (MbO 2S) was kept at normoxic level (MbO2S > 80%) and no tissue hypoxia was observed. 3) During mild hypoxic perfusion conditions (MbO-2S .**GRAPHIC**. 55%), diltiazem (Ca-antagonist) infusion cause dose-dependent increases in coronary flow and intracellular oxygen concentration suggesting that diltiazem improved myocardial hypoxia. 4) Under hypoxic perfusion (MbO2S .**GRAPHIC**. 70%), infusion of prostaglandin I2 increased coronary flow and oxygen concentration at the coronary sinus. The myoglobin oxygen level shifted to more oxygenated state (normoxic condition). Thus, PGI2 was concluded to act effectively in delivering oxygen into the cardiac tissue and to improve myocardial oxygen metabolism. Conclusion: Our spectrophotometric technique is quite useful to permit continuous monitoring of oxygen metabolism and biochemical reactions taking place in cytosol and mitochondria.


Accession: 006460184

PMID: 3823645



Related references

Myocardial performance and metabolism in non-ketotic, diabetic rat hearts: myocardial function and metabolism in vivo and in the isolated perfused heart under the influence of insulin and octanoate. Basic Research in Cardiology 81(6): 620-635, 1986

Axial oxygen diffusion in the Krogh model: modifications to account for myocardial oxygen tension in isolated perfused rat hearts measured by EPR oximetry. Advances in Experimental Medicine and Biology 566: 127-134, 2006

Myocardial oxygen tension and relative capillary density in isolated perfused rat hearts. Journal of Molecular and Cellular Cardiology 27(12): 2551-2558, 1995

Ischemic preconditioning and myocardial metabolism in isolated perfused rat hearts. FASEB Journal 9(3): A421, 1995

Oxygen delivery and myocardial function in rabbit hearts perfused with cell-free hemoglobin. Journal of Applied Physiology 72(2): 476-483, 1992

Myocardial oxygen tension in isolated erythrocyte-perfused rat hearts and comparison with crystalloid media. Journal of Molecular and Cellular Cardiology 29(10): 2855-2858, 1997

Effect of repetitive ischemia on myocardial oxygen tension in isolated perfused and hypoperfused rat hearts. Magnetic Resonance in Medicine 35(2): 214-220, 1996

Oxygen supply limits basal metabolism in saline perfused hearts. Journal of Molecular & Cellular Cardiology 18(SUPPL 1), 1986

Oxygen-induced enzyme release after irreversible myocardial injury. Effects of cyanide in perfused rat hearts. American Journal of Pathology 84(2): 327-350, 1976

Effects of vanadate on myocardial energy metabolism and cardiac performance of perfused rat hearts. Japanese Circulation Journal 58(7): 565, 1994