Analysis of clinical outcomes of linear vs. deep stop decompression from 3.5 to 6 atmospheres absolute (350 - 600 kpa) in awake rats.

UNLABELLED: Recreational divers are introducing "deep stops" at half the depth (HD-DS) to reduce the risk of spinal DCS with only Doppler evidence to support it. Therefore this research was designed to show the effect of an HD-DS on spinal DCS manifestations by evaluating whether: (1) air diving-induced spinal DCS could be produced in awake, freely moving rats at 3.5-6.0 atm abs (350-600 kPa); and (2) whether the introduction of an HD-DS reduced spinal DCS in such a model. Fifty-one female, Wistar rats (221 to 450 g) underwent one-hour compression at 350 to 600 kPa with seven minutes of decompression with/without a five-minute DS (HD-DS / No-DS). Animals were observed for three hours. Outcomes were classified as: (1) asymptomatic; (2) breathing difficulties; (3) paralysis/weakness; (4) immobility; or (5) death. Eight animals, exposed to 385 kPa air breathing for 60 minutes followed by a three-staged decompression of 7.5 minutes, remained asymptomatic. The profile is known to produce spinal DCS in anesthetized rats. Eleven animals were then used to determine the threshold for DCS: 500 kPa. A total of 14 animals were compressed to 550 kPa (Group 1). Group 1-A (n = 8) No-DS; Group 1-B (n = 6) HD-DS; 18 were compressed to 600 kPa (Group 2). Group 2-A (n = 8) No-DS; Group 2-B (n = 10) HD-DS. RESULTS: (1) 385 kPa protocol did not produce visible DCS manifestations in awake rats. The binomial probability of no DCS in this sample size is 0.002818 for the proportion expected from a published report. The binomial probability of no fatalities is 0.005346). (2) No animals developed spinal DCS when assessed by visible paralysis/weakness or immobility, so no difference could be shown. Group 1-A: two deaths; two breathing abnormalities; four asymptomatic. Group 1-B: all asymptomatic. Difference recorded for breathing difficulties (p = 0.0483); none for fatalities (p = 0.2024). Group 2 mortality was 55% (n = 10). Group 2-A and 2-B: no difference for death (p = 0.6063) or breathing problems (p = 0.2084). CONCLUSIONS: This model could not evaluate HD-DS for the prevention of spinal DCS in rats.

Cardiovascular and endocrine responses to 90 degree tilt during a 35-day saturation dive to 46 and 37 ATA.

INTRODUCTION: Hyperbaria-induced diuresis is accompanied by decreased basal and stimulated release of arginine vasopressin (AVP) and decreased blood volume possibly contributing to the reported orthostatic intolerance. Since hyperosmolality is not a consistent finding, the explanation of blood volume reduction at hyperbaria must involve an osmotic component to the diuresis. Investigations of a possible involvement of atrial natriuretic peptide (ANP) to the hyperbaric diuresis have revealed mixed results. METHODS: Urinary excretion of electrolytes, AVP, and aidosterone were measured in four male subjects studied at 1 atmosphere absolute (ATA) and at 46 and 37 ATA (0.5 atmospheres pressure O2: 5% N2: remainder He) during a 35-d saturation dive. Also, the supine and 90 degrees tilt-stimulated plasma levels of AVP, plasma renin activity (PRA), and aldosterone, and the suppressed responses of ANP and the cardiovascular responses to tilt were determined at these pressures. RESULTS: Tilt-stimulated levels of PRA were increased two- to threefold and the AVP response was eliminated throughout hyperbaria, except in two episodes of tilt-induced syncope where AVP was elevated 10- to 20-fold. This pattern supports most previous reports. Contrary to some reports, both supine and tilt-suppressed levels of ANP were reduced by about 50% at all three tilt experiments conducted at hyperbaria compared to predive control values. DISCUSSION: These results suggest an altered ANP response at pressures of 37 ATA or greater, which is consistent with an appropriate ANP response to blood volume reduction and further suggest that the hyperbaric diuresis is not dependent on increased ANP.