Six male subjects exercised for 50 min at 25% (light exercise) and 55% (moderate exercise) of their estimated aerobic capacities in environments of 42 degrees C db, 35 degrees C wb and 30 degrees C db, 24 degrees C wb, respectively. Alterations in the hematocrit, hemoglobin, and plasma protein concentrations, and in the activity of an injected aliquot of isotopically labeled albumin were each used to calculate the percentage change in plasma volume occurring during exercise and recovery. Changes in each measure were consistent with a reduction in plasma volume during exercise and a return to preexercise levels during recovery. There was no significant difference between the measures when exercising in the heat, but during the more severe exercise in the cooler environment disproportional changes in protein, hematocrit, and hemoglobin were observed. Disproportional changes were also seen during the recovery phase, when the hematocrit and hemoglobin concentration indicated a more rapid return of the plasma volume to preexercise levels than did either the plasma protein concentration or albumin activity. During moderate exercise and recovery there was a 1% decrease in red cell volume. It is concluded that exercise accelerates the rate of protein movement from extravascular compartments to the intravascular compartment, leading to elevated plasma protein levels during recovery which favor the return of water to the intravascular space. Hemoglobin concentration is considered to be the most reliable measure of plasma volume change during exercise.

Forty-five conditioned male mongrel dogs were exposed to multifocal ischemia sufficient to maintain suppression for 60 minutes of the P1-N1 amplitude of the cortical sensory evoked response (CSER), a quantifiable index of neuronal function. Ischemia was induced and regulated by successive embolization of 20 to 50 microliters increments of air via the right internal carotid artery. Subsequently, the P1-N1 amplitude recovery of the CSER was followed for an additional 15, 60, or 120 minutes while the dogs were treated or left untreated. The combination of prostaglandin I2 (PGI2), indomethacin, and heparin promoted a statistically significant augmentation of return of CSER amplitude relative to no treatment, PGI2 alone, indomethacin alone, PGI2 and heparin, indomethacin and heparin, or PGI2 and indomethacin. After 60 minutes of recovery, animals receiving combined PGI2, indomethacin, and heparin achieved a 57% recovery of P1-N1 amplitude relative to baseline, while the corresponding recoveries in all other groups clustered around 20%. By 120 minutes of postischemic follow-up, the CSER recovery induced by PGI2, indomethacin, and heparin was 80% compared to 17% in untreated animals. By 15 minutes into the recovery period, the combination of the three agents had eliminated very low flows in the "neuron-disabling" range (defined as 0 to 15 ml/100 gm/min for gray matter and 0 to 6 ml/100 gm/min for white matter) in contrast to the relative inefficacy of no treatment or treatment with other than the triple combination of drugs. The study lends some support to a planned clinical trial of PGI2, indomethacin, and heparin in acute occlusive stroke in humans.

The experience of 458 man-dives with 731 excursions between 50 m and 300 m carried out by Royal Navy saturation divers is summarized. During saturation decompression there were 6 treated bends and 33 reported niggles. Two bends occurred in dives deeper than 249 m and the remaining 4 bends occurred in dives where decompression began in much less than the saturation stop time after completion of downward excursions. There was one case of vestibular system decompression sickness after an excursion to 300 m. It is concluded that the decompression table is effective in use shallower than 150 m but that the risk increases with greater depth. There is, however, only limited experience in the deeper range. There is no evidence that chamber compression with air to 10 m adversely affects decompression from deeper than 50 m. An account of the medical and physiological conditions affecting divers in these dives is given.

No abstract

Ischaemia is a major mechanism underlying central nervous system (c.n.s.) damage in decompression sickness. Some recent experimental observations on the effect of bubble-induced ischaemia on c.n.s. tissue sharpen and extend our understanding of the pathophysiology of decompression sickness. After bubble-induced brain ischaemia, a measurable increase in 111In-labelled leucocytes occurs in the injured hemisphere. By 4 h into the recovery period the cells are concentrated in zones of low blood flow, as measured by the [14C]iodoantipyrine technique. The presence of these cells during the critical early hours of c.n.s. ischaemia suggests that they may contribute to the evolution of neuronal damage. Oedema is often cited as the cause of clinical deterioration after c.n.s. ischaemia or trauma. Recent evidence indicates that the presence and degree of circumscribed brain oedema is not a good predictor of the amount of nerve cell recovery (by using cortical sensory evoked response) after bubble-induced brain ischaemia. This brings into question the role of circumscribed oedema of the c.n.s. in dysfunction of post-ischemic nerve cells.