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The precise mechanism of erythropoietin (ESF) production and release from the kidney still remains obscure although it is well known that many forms of hypoxia, e.g., anemic, hypoxic, ischemic, and histotoxic, are capable of increasing erythropoietin production by the kidney (1). Recent observations (2, 3) indicate that following renal artery constriction in the dog, there is a release of prostaglandins (PG) into the renal venous blood. We have reported recently (4-6) that both hypoxic and ischemic hypoxia are capable of producing a significant increase in prostaglandin E (PGE) release into the renal venous effluent, which was blocked by the potent prostaglandin synthetase inhibitor, indomethacin. We have also demonstrated (7, 8) that indomethacin is capable of blocking erythropoietin production as well.Thus, the present studies were carried out to assess the relationship between PGE release and erythropoietin production by the kidney during a 12-hr ischemic hypoxic stimulus induced by means of renal artery constriction as well as the effects of indomethacin on these changes.Materials and methods. Twelve female mongrel dogs (six control and six indomethacin-treated) weighing 14.5-21 kg were used in this study. The animals were anesthetized with sodium pentobarbital (30 mg/ kg iv), and the left femoral arteries were cannulated for monitoring systemic arterial blood pressure (Statham P23AC pressure transducer) and the collection of arterial blood samples for erythropoietin bioassay. The animals were subjected to retroperitoneal laparotomies permitting extirpation of the right kidney and the exposure of the left kidney through a flank incision. A branch of the left ovarian vein was isolated and a cannula was inserted through this vein into the left renal vein to collect renal venous blood samples for PGE assay. Utilizing a squarewave electromagnetic blood flowmeter (Carolina Medical Electronics, Model 501) and either an 8-or 10-mm circumference flow probe, renal blood flow (RBF) was monitored with the probe placed around the left renal artery. Systemic arterial blood pressure (BP) and RBF were recorded continuously throughout the experimental period on a Grass oscillographic recorder (Model 7PCPA).After the initial zero time parameters (BP, RBF) and blood samples for PGE and erythropoietin were collected, a vascular occluder (Model OC12, IN VIVO Metric Systems) was placed around the left renal artery between the flow probe and the kidney. Renal blood flow was reduced to 30% of normal and sustained throughout the 12-hr experimental period with minor adjustments as needed. Six of the 12 dogs in the experimental group were pretreated with indomethacin (5 mg/kg orally) 18 and 2 hr prior to the application of the vascular occluder. Anesthesia was maintained throughout the experiments by administration of sodium pentobarbital as required via a cannula in the femoral vein.Blood samples for erythropoietin and 498

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In the long run a programmed physical exercise does not lead to oxidative stress, but an excessive physical load may cause its occurrence.

Ejection fraction of 30-40% is an indication for hyperbaric oxygenation therapy. The decision about the treatment is made by the physician based on his experience, general condition of the patient, frequency and severity of hypoxic episodes. If EF% is 30% or below, HBO is not recommended, because antioxidative defense mechanisms are exhausted under hyypoxia and the balance of the organism should not be changed. An increase in average EF% by 11% demonstrates that combined use of HBO and Erythropoietin gives good results.

Regular training has been claimed to increase the activity of antioxidant enzymes and, consequently, augments the resistance to oxidative stress; however, large volumes of training performed by elite sportsmen could lead to a chronic oxidative stress state. The aim of our study was to assess the oxidative status of elite athletes at the beginning of the preparatory and the beginning of the competition training phases, so that the influence of three months of programmed physical activity on redox status could be determined. The chronic effects of exercise on the redox state of the athletes were compared to the effects of a single bout of karate training. Thirty elite karate athletes, 16-30 years old, were subjected to maximal graded exercise test to estimate their aerobic capacity; blood sampling was also performed to measure levels of superoxide anion radical (O₂⁻), hydrogen peroxide (H₂O₂), superoxide dismutase activity (SOD) and catalase activity (CAT). The only significant change after the three-month training process was found in the significantly decreased CAT activity (X ± SE: 7.95 ± 0.13 U/g Hb × 10³ in the preparatory period, 6.65 ± 0.28 U/g Hb × 10³ in the competition stage; P < 0.01). After a single karate training session, there was statistically significant decrease of O₂⁻(X ± SE: 32.7 ± 4.9 nmol/ml in the preparatory period, 24.5 ± 2.5 nmol/ml in the competition stage; P < 0.05) and increase of H₂O₂(X ± SE: 11.8 ± 1.0 nmol/ml in the preparatory period, 14.2 ± 0.9 nmol/ml in the competition stage; P < 0.01), as well as significant CAT increase (X ± SE: 6.6 ± 0.6 U/g Hb × 10³ in the preparatory period, 8.5 ± 0.5 U/g Hb × 10³ in the competition stage; P < 0.05). Although the three-month training process induced, at the first sight, negative changes in the redox state, expressed through the decrease in CAT activity, adequate response of the antioxidant system of our athletes to acute exercise was preserved.

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