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Seventeen male physical education students performed three types of treadmill exercise: (1) progressive exercise to exhaustion, (2) prolonged exercise of 50 min duration at the anaerobic threshold of 4 mmol . l-1 blood lactate (AE), (3) a single bout of short-term high-intensity exercise at 156% of maximal exercise capacity in the progressive test, leading to exhaustion within 1.5 min (ANE). Immediately before and after ANE and before, during, and after AE adrenaline, noradrenaline, growth hormone, cortisol, insulin, testosterone, and oestradiol were determined in venous blood, and glucose and lactate were determined in arterialized blood from the earlobe. Adrenaline and noradrenaline increased 15 fold during ANE and 3--4 fold and 6--9 fold respectively during AE. The adrenaline/noradrenaline ratio was 1 : 3 during ANE and 1 : 10 during AE. Cortisol increased by 35% in ANE (12% of which appeared in the postexercise period) and 54% in AE. Insulin increased during ANE but decreased during AE. Testosterone and oestradiol increased by 14% and 16% during ANE and by 22% and 28% during AE. The results point to a markedly higher emotional stress and higher sympatho-adrenal activity in anaerobic exercise. Growth hormone and cortisol appear to be the more affected by intense prolonged exercise. Taking plasma volume changes and changes of metabolic clearance rates into consideration, neither of the exercise tests appeared to affect secretion of testosterone and oestradiol.

Oxidized-raffinose cross-linked hemoglobin, Hemolink, at doses < or =0.6 g/kg were well tolerated in healthy volunteers with no evidence of organ dysfunction. Further investigation of its potential use in surgical and trauma settings appears warranted.

The effects of intravenous practolol 0.4 mg/kg were studied in 12 hypertensive patients during halothane/nitrous oxide anaesthesia. Practolol decreased heart rate (HR) and cardiac output (Q) from the elevated levels following atropine administration during anaesthesia, but values of arterial pressure (AP), HR and Q after the combination of atropine and practolol were not significantly different from those during anaesthesia prior to blockade. The effects of a similar anaesthetic sequence were studied in a further 11 treated hypertensive patients given practolol by mouth 1.5 mg/kg/6 hours for at least 48 hours preoperatively in addition to current anti-hypertensive therapy. By comparison with treated hypertensive patients previously studied, those pretreated with practolol had similar AP awake, but higher AP throughout anaesthesia with either spontaneous or artificial ventilation. Cardiac output was higher and systemic vascular resistance was lower both before and during anaesthesia. Both the present groups of patients showed significantly attenuated responses of tachycardia and hypertension following laryngoscopy and intubation compared with previous studies. The incidence of dysrhythmia and e.c.g. evidence of myocardial ischaemia was significantly lower (4%) in beta-blocked patients compared with those who had not received practolol (38%).

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To examine the metabolic and hormonal responses to non-exhaustive steady-state exercise at the individual anaerobic threshold (IAT), 12 male physical education students performed treadmill exercise of 50 min duration. The treadmill speed equaled that at the IAT as assessed in a standardized progressive exercise test (75 +/- 2% of maximal oxygen uptake). Heart rate averaged 177.0 +/- 12.2 min-1 at 15 min and 184.5 +/- 11.5 min-1 at 50 min. After the initial adjustment, arterial lactate stabilized at individually different levels between 2.70 and 6.00 mmol/l without any substantial trend in the individual curves. Arterial glucose was unchanged throughout the test. Glycerol increased continuously to 157% above the preexercise value (P less than 0.001). The FFA blood level was not depressed but rather showed an increasing tendency between 25 and 50 min (P less than 0.05). Between 0 and 25 min, insulin decreased (P less than 0.01), growth hormone increased to 8 times its pre-exercise value (P less than 0.001), and cortisol did not show any significant changes. Between 25 and 50 min, no significant additional changes were detected for these hormones. At 15 min epinephrine and norepinephrine had increased 2.8- and 7-fold above the respective pre-exercise values (P less than 0.001); both catecholamines continued to increase until 50 min (P less than 0.001 and P less than 0.01). It is concluded that prolonged exercise at the IAT is associated with a steady-state condition in carbohydrate supply and turnover, as is suggested by the stable blood levels of glucose and lactate. The stably elevated blood level of lactate did not result in depression of the FFA blood level, suggesting unimpaired supply of FFA from extramuscular sources. Exercise at the IAT places a high load on aerobic metabolism without encountering progressive lactate accumulation and the associated metabolic effects.

Sarcolemmal and mitochondrial phospholipids were extracted from normally perfused and ischemic regions of the dog heart and the composition of these extracts was analyzed. Relatively pure sarcolemmal fraction obtained from myocardium subjected to 3 h of ischemia exhibited a significantly lower concentration of phospholipids than that obtained from normal myocardium. In particular, phosphatidylcholine and phosphatidylethanolamine were reduced by approximately 33%. The fatty acid content in the sarcolemmal phospholipid fraction was also reduced by approximately 30% without any change in the relative composition. In the mitochondrial fraction, the relative phospholipid composition was also altered by ischemia; the major components (phosphatidylcholine, phosphatidylethanolamine, and cardiolipin) being reduced by approximately 15-20%. An attempt was made to correlate these biochemical changes with ultrastructural lesions observed electron microscopically. These observations revealed extensive regional variability and a wide heterogeneity in the extent of ultrastructural damage evident in the different organelles even in a single cell. This may suggest that ischemic damage, in the early stages, may advance at widely varying rates in different regions. Our findings demonstrate that significant biochemical and structural disorganization occurs during 3 h of ischemia in the myocardium and raise the possibility that one of the initiating events is the activation of sarcolemmal and mitochondrial phospholipases.