Morphological and physiological responses of the lungs of dogs to acute decompression

Catron, PW; Flynn, ET; Yaffe, L.; Bradley, Michael E.; Thomas, LB; Hinman, Donald J.; Survanshi, SS; Johnson, J. T.; Harrington, Jennifer

doi:10.1152/jappl.1984.57.2.467

Cited by 19 publications

(14 citation statements)

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“…These facts, combined with their ease of handling, make them very useful in DCS experimentation. The pathological findings of livid skin DCS, multiple punctate spinal and cerebral hemorrhages, and profuse pulmonary congestion after no-stop decompression are consistent with previous observations in other animal models of DCS, as well as human results (7,8,14,30).…”

Section: Discussionsupporting

confidence: 90%

Natural history of severe decompression sickness after rapid ascent from air saturation in a porcine model

Dromsky

Toner

Survanshi

et al. 2000

Journal of Applied Physiology

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Weathersby. Natural history of severe decompression sickness after rapid ascent from air saturation in a porcine model. J Appl Physiol 89: 791-798, 2000.-We developed a swine model to describe the untreated natural history of severe decompression sickness (DCS) after direct ascent from saturation conditions. In a recompression chamber, neutered male Yorkshire swine were pressurized to a predetermined depth from 50-150 feet of seawater [fsw; 2.52-5.55 atmospheres absolute (ATA)]. After 22 h, they returned to the surface (1 ATA) at 30 fsw/min (0.91 ATA/min) without decompression stops and were observed. Depth was the primary predictor of DCS incidence (R ϭ 0.52, P Ͻ 0.0001) and death (R ϭ 0.54, P Ͻ 0.0001). Severe DCS, defined as neurological or cardiopulmonary impairment, occurred in 78 of 128 animals, and 42 of 51 animals with cardiopulmonary DCS died within 1 h after surfacing. Within 24 h, 29 of 30 survivors with neurological DCS completely resolved their deficits without intervention. Pretrial Monte Carlo analysis decreased subject requirement without sacrificing power. This model provides a useful platform for investigating the pathophysiology of severe DCS and testing therapeutic interventions. The results raise important questions about present models of human responses to similar decompressive insults.

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Section: Discussionsupporting

confidence: 90%

Natural history of severe decompression sickness after rapid ascent from air saturation in a porcine model

Dromsky

Toner

Survanshi

et al. 2000

Journal of Applied Physiology

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“…This is attributed to an increase in microvascular permeability caused by the formation of gaps between the endothelial cell lining and disruptions of the underlying basal lamina [7]. Repetitive compression±decompression cycles until right ventricular systolic pressure has doubled [26] and altitude decompression performed in addition to simple compression±decom-pression [6] produced interstitial pulmonary edema in experimental dogs and sheep. However, compared with the present experiments conducted in a porcine model sharing important features of human DCS, the dogs and sheep were exposed to a different dive profile with an even more severe decompression stress.…”

Section: Discussionmentioning

confidence: 99%

Computed chest tomography in an animal model for decompression sickness: radiologic, physiologic, and pathologic findings

et al. 2000

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This study was conducted to investigate the early pulmonary effects of acute decompression in an animal model for human decompression sickness by CT and light microscopy. Ten test pigs were exposed to severe decompression stress in a chamber dive. Three pigs were kept at ambient pressure to serve as controls. Decompression stress was monitored by measurement of pulmonary artery pressure and arterial and venous Doppler recording of bubbles of inert gas. Chest CT was performed pre- and postdive and in addition the inflated lungs were examined after resection. Each lung was investigated by light microscopy. Hemodynamic data and bubble recordings reflected severe decompression stress in the ten test pigs. Computed tomography revealed large quantities of ectopic gas, predominantly intravascular, in three of ten pigs. These findings corresponded to maximum bubble counts in the Doppler study. The remaining test pigs showed lower bubble grades and no ectopic gas by CT. Sporadic interstitial edema was demonstrated in all animals--both test and control pigs--by CT of resected lungs and on histologic examination. A severe compression-decompression schedule can liberate large volumes of inert gas which are detectable by CT. Despite this severe decompression stress, which led to venous microembolism, CT and light microscopy did not demonstrate changes in lung structure related to the experimental dive. Increased extravascular lung water found in all animals may be due to infusion therapy.

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“…Venous gas bubbles formed during decompression may cause increased microvascular permeability, leading to pulmonary oedema and haemorrhage. Furthermore, obstruction of pulmonary vasculature by gas emboli may lead to pulmonary hypertension with systemic hypotension and hypoxaemia [105][106][107].…”

Section: Arterial Gas Embolismmentioning

confidence: 99%

“…Clinically, the diver presents with cough, chest pain, wheezing, dyspnoea and pharyngeal irritation (the chokes) [87]. Obstruction of right ventricular outflow with acute right-sided cardiac failure (air lock), circulatory collapse and death may ensue [87,[101][102][103][104][105][106][107][108].…”

Section: Arterial Gas Embolismmentioning

confidence: 99%

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Lung injury related to extreme environments

Adir

Bové

2014

Eur Respir Rev

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@ERSpublications Lung injury is a well understood and preventable consequence of water immersion while swimming and diving http://ow.ly/AOdvgAs extreme sports become more popular, related respiratory injury may compromise the athlete's performance and result in morbidity and even mortality. In this article we will discuss different lung injuries in relation to performing different activities in an extreme environment. Hydrostatic lung injuriesThe evolution of fish to amphibians, reptiles to endothermic birds and mammals has been accompanied by a progressively thinner pulmonary blood gas barrier, to accommodate the constraint of increased oxygen uptake and carbon dioxide output [1]. Accordingly, pulmonary circulation has evolved as a separate high flow-low pressure system. In humans, mean pulmonary artery pressures (PAP) are 8-20 mmHg, pulmonary wedge pressures are 5-14 mmHg and pulmonary capillary pressures are 8-12 mmHg [2]. A low-pressure regimen preserves the integrity of an alveolar capillary membrane only 0.3 mm thick. However, this structure is vulnerable to increased pressures during strenuous exercise or environmental hypoxic exposure as a cause of stress failure of the pulmonary capillaries and accumulation of extravascular lung water [3]. Reports of lung injury related to extremes of exercise and variations in ambient pressure and altitude confirm this vulnerability. The resulting lung injury takes the form of noncardiogenic pulmonary oedema.The occurrence of noncardiogenic pulmonary oedema and pulmonary haemorrhage has been described in relation to a variety of disorders related to auto-and exogenous immunological reactions, infections and certain inhalants. However, numerous reports of lung injury manifesting as pulmonary oedema with associated haemorrhage have been described more recently in relation to immersion underwater, swimming, extreme exercise and exposure to altitude. In addition, pulmonary oedema resulting from negative intra-alveolar pressure has been described in the anaesthesia literature and may play a role in exercise-and immersion-induced pulmonary oedema. Haemodynamically induced pulmonary oedemaA single mechanism responsible for production of noncardiogenic pulmonary oedema related to immersion, altitude and exercise has not been identified. However, a combination of haemodynamically related factors, alterations in capillary integrity, increased blood volume and increased cardiac output may all contribute to the syndrome. WEST et al.[4] described exercise-induced pulmonary haemorrhage in race For editorial comments see page 401.

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Morphological and physiological responses of the lungs of dogs to acute decompression

Cited by 19 publications

References 0 publications

Natural history of severe decompression sickness after rapid ascent from air saturation in a porcine model

Natural history of severe decompression sickness after rapid ascent from air saturation in a porcine model

Computed chest tomography in an animal model for decompression sickness: radiologic, physiologic, and pathologic findings

Lung injury related to extreme environments

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