Cardiac formation of prostacyclin during cardioplegia in man
| Autor: | Lennart Kaijser, Carlo Patrono, A. Edlund, Åke Wennmalm, C. Olin, E. Pinca, W. Bomfin |
|---|---|
| Rok vydání: | 1982 |
| Předmět: |
Adult
Male medicine.medical_specialty Cellular respiration Prostacyclin Stimulation 6-Ketoprostaglandin F1 alpha Biochemistry Endocrinology Oxygen Consumption Internal medicine medicine Humans Lactic Acid Coronary sinus Aged business.industry Myocardium Hypoxia (medical) Hypothermia Middle Aged Epoprostenol Anaerobic glycolysis cardiovascular system Cardiology Heart Arrest Induced Lactates Prostaglandins Liberation lipids (amino acids peptides and proteins) Female medicine.symptom business medicine.drug |
| Zdroj: | Prostaglandins. 24(1) |
| ISSN: | 0090-6980 |
| Popis: | In patients undergoing aortic valve surgery during cardioplegia (a condition characterized by extra-corporal circulation, potassium-induced cardiac arrest and cardiac hypothermia) cardiac release or uptake of 6-keto-PGF 1α , and in some cases also of 6,15-diketo-13,14-dihydro-PGF 1α were determined, using radioimmunoassay with specific antibodies for determination of the arterial and coronary sinus plasma levels of these PGI 2 metabolites. The aim of the study was to find out whether cardiac hypoxia, as evidenced by anaerobic glycolysis in the heart, resulted in stimulation of it PGI 2 production. Before cardioplegia the uptake of oxygen (23 ml/min) and the arterio-coronary sinus concentration difference (a-cs) of lactate (0.3 mM) were within the normal range, indicating that the O 2 supply to the heart was sufficient for aerobic metabolism. During cardioplegia the oxygen uptake fell, to less than 3 % of the basal value. The uptake of lactate was significantly reversed into a small release inicating that myocardial hypoxia developed. No release of 6-keto-PGF 1α took place before cardioplegia, implying that the hearts' PGI 2 productino was low or absent when its O 2 supply was sufficient. During cardioplegia a significant (a-cs) of 6-keto-PGF 1α developed, amounting to −75 pg/ml. Since no evidence of a hypoxia-induced decrease in the metabolic breakdown of PGI 2 or 6-keto-PGF 1α in the heart could be demonstrated - as shown by a continued, or even augmented liberation of 6,15-diketo-13,14-dihydro-PGF 1α during cardioplegia - the cardiac release of 6-keto-PGF 1α indicated that the PGI 2 production in the heart was stimulated during the cardioplegia/hypoxia. From these data we suggest that human cardiac formation of PGI 2 is low or absent when the O 2 supply is sufficient. Furthermore, cardiac hypoxia, as evidenced by release of lactate, results in stimulation of cardiac PGI 2 formation. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|