Effect of Hyperbaric Oxygen on Endotoxin-Induced Lung Injury in Rats

Abstract

Oxygen therapy remains the main component of the ventilation strategy for treatment of patients with acute lung injury. Hyperbaric oxygen therapy (HBO(2)) is the intermittent administration of 100% oxygen at pressure greater than sea level and has been applied widely to alleviate a variety of hypoxia-related tissue injuries. The purpose of this study was to evaluate the effect of hyperbaric oxygen on acute lung injury induced by intratracheal spraying of lipopolysaccharide (LPS) in rats. Male Sprague-Dawley rats underwent implantation of a carotid artery catheter under general anesthesia. Aerosolized LPS was delivered twice into the lungs via intratracheal puncture. Animals were either breathing room air (n = 27) or subjected to hyperbaric oxygen (HBO(2)) exposure (n = 27) 1 h after LPS spraying. Acute lung injury was evaluated 5 h and 24 h later. Compared with the control group, intratracheal spraying of LPS caused profound hypoxemia, greater wet/dry weight ratio (W/D) of the lung (5.67 +/- 0.22 vs. 4.98 +/- 0.19), and higher protein concentration (1706 +/- 168 vs. 200 +/- 90 mg/L) and LDH activity (129 +/- 30 vs. 46 +/- 15, mAbs/min) in bronchoalveolar lavage (BAL) fluid. Intratracheal spraying of LPS also caused significant WBC sequestration in the lung tissue. HBO2 treatment significantly reverted hypoxemia, reduced lung injury measures evaluated at 5 and 24 h, and enhanced 24-h animal survival rate (chi = 5.08, P = 0.024). The malondialdehyde (MDA) concentrations in lung tissue and serum were both increased after LPS spraying. Neither single HBO(2) therapy nor five sequential daily treatments enhanced MDA production in lung tissue or serum. Our results suggested that hyperbaric oxygen might reduce acute lung injury caused by intratracheal spraying of LPS in rats. This treatment modality is not associated with enhancement of oxidative stress to the lung.

A novel method in the treatment of pulmonary contusion: hyperbaric oxygen, an experimental study

“…Hiperbarik hiperoksinin in vivo oksijenin toksititesini artırdığı ve bu etkinin reaktif oksijen radikalleri ile ilişkili olduğu düşünülmektedir. [15] Perng ve ark.nın [8] akut akciğer hasarı çalışmaları kan ve akciğer dokusunda MDA artışını ve HBO'nun akciğer dokusunda MDA miktarını düşürdüğünü göstermektedir. Lakin bu düşüş serum düzeylerinde istatistiksel olarak anlamlı bulunmamıştır.…”

“…[10] Hiperbarik oksijenin akciğer hasarı sonrasında akciğer dokusundaki lökosit infiltrasyonunu ve alveoler septa kalınlaşmasını azalttığı gös-terilmiştir. [8] Çalışmamızda kontüze sıçan akciğerinde intraalveoler hemoraji, alveol yırtılması, alveoler ödem ve konjesyon gibi her bir parametrenin istatistiksel olarak anlamlı şekilde artış gösterdiği tespit edildi. Lökosit sekestrasyonu için kullandığımız skorlama sistemi de yine kontüzyon grubunda lökostik infiltrasyonun kontrol grubuna oranla anlamlı şekilde artmış olduğunu ortaya koydu.…”

“…[7] Birçok araştırmacı HBO'nun doku oksijenasyonunu düzelterek tedaviyi olumlu etkilediğini anti-inflamatuvar etkisi olduğunu bildirmiştir. [8][9][10] Bu çalışmamızda, pek çok alanda etkinliği ispatlanmış olan HBO'nun PK'daki etkinliği ve tek taraflı PK modeli ile oluşturulan PK'da HBO'nun hangi patofizyolojik mekanizmalar üzerine etkisi olduğu araştırıldı. Raghavendran ve ark.nın [3] tanımladığı izole iki taraflı PK modelinin modifiye edilmesi ile oluşturulan tek taraflı PK modeli ile PK yapıldı.…”

Investigation of airway inflammation and asthma by repeated bronchoalveolar lavage combined with measurements of airway and lung tissue mechanics in individual rats

“…First, unlike the mice in the procedure developed by Walters, the rats were not ventilated with 100% O 2 in the present work, because we intended to test our method by using LPS, and hyperbaric O 2 might have reduced the ALI caused by the intratracheal spraying of LPS in rats [42]. Furthermore, we did not use suction to withdraw the washing fluid from the bronchoalveolar cavity: it was collected only via a positional change of the animal.…”

“…ALI is often induced in animal models by the administration of LPS [29,30,[42][43][44][45]. LPS is a characteristic component of the cell wall of Gram-negative bacteria; it is not found in Gram-positive bacteria.…”