Exhaled Nitric Oxide is Decreased by Exposure to the Hyperbaric Oxygen Therapy Environment

نویسندگان

  • Zudin A. Puthucheary
  • Jia Liu
  • Michael Bennett
  • Barbara Trytko
  • Sharron Chow
  • Paul S. Thomas
چکیده

UNLABELLED Exhaled nitric oxide (eNO) detects airway inflammation. Hyperbaric oxygen therapy (HBOT) is used for tissue hypoxia, but can cause lung damage. We measured eNO following inhalation of oxygen at different tensions and pressures. METHODS Part 1, eNO was measured before and after HBOT. Part 2, normal subjects breathed 40% oxygen. RESULTS Baseline eNO levels in patients prior to HBOT exposure were significantly higher than in normal subjects (P < .05). After HBOT, eNO significantly decreased in patients (15.4 +/- 2.0 versus 4.4 +/- 0.5 ppb, P < .001), but not in normal subjects, after either 100% O2 at increased pressure or 40% oxygen, 1 ATA. In an in vitro study, nitrate/nitrite release decreased after 90 minutes HBOT in airway epithelial (A549) cells. CONCLUSION HBO exposure causes a fall in eNO. Inducible nitric oxide synthase (iNOS) may cause elevated eNO in patients secondary to inflammation, and inhibition of iNOS may be the mechanism of the reduction of eNO seen with HBOT.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Reduced nitric oxide concentration in exhaled gas after exposure to hyperbaric hyperoxia.

The objective of this study was to evaluate exhaled nitric oxide concentration (FENO) and exhaled breath condensate (EBC) pH and H2O2 as biochemical markers of pulmonary oxygen toxicity in association with hyperbaric oxygen (HBO2) therapy. FENO, EBC pH and H2O2 were measured during the course of a 4 week HBO, treatment period, and the responses to a single HBO2 exposure at the start and end of ...

متن کامل

Nitric oxide and cerebral blood flow responses to hyperbaric oxygen.

We have tested the hypothesis that cerebral nitric oxide (NO) production is involved in hyperbaric O(2) (HBO(2)) neurotoxicity. Regional cerebral blood flow (rCBF) and electroencephalogram (EEG) were measured in anesthetized rats during O(2) exposure to 1, 3, 4, and 5 ATA with or without administration of the NO synthase inhibitor (N(omega)-nitro-L-arginine methyl ester), L-arginine, NO donors,...

متن کامل

Reduction of Ischemic and Oxidative Damage to the Hypothalamus by Hyperbaric Oxygen in Heatstroke Mice

The aims of the present paper were to ascertain whether the heat-induced ischemia and oxidative damage to the hypothalamus and lethality in mice could be ameliorated by hyperbaric oxygen therapy. When normobaric air-treated mice underwent heat treatment, the fractional survival and core temperature at 4 hours after heat stress were found to be 0 of 12 and 34 degrees C +/- 0.3 degrees C, respect...

متن کامل

Cardioprotective Effects of Combined Therapy with Hyperbaric Oxygen and Diltiazem Pretreatment on Myocardial Ischemia-Reperfusion Injury in Rats.

BACKGROUND/AIMS In this study, we examined whether the combination of hyperbaric oxygen (HBO) and diltiazem therapy provided a cardioprotective effect on myocardial ischemia-reperfusion injury (MIRI) rat model. METHODS Sixty healthy Sprague-Dawley rats were randomly divided into sham, IR, diltiazem (5 mg/kg), HBO (0.25 MPa, 60 min) and combination therapy (HBO plus diltiazem) groups. MIRI mod...

متن کامل

Evaluation of nitric oxide involvement in effect of lead on dependency to morphine in mice

In the present study, interactions between lead exposure with nitric oxide precursor (L-arginine) or nitric oxide synthase (NOS) inhibitor (L-NAME) on naloxone-induced jumping and diarrhea in morphine-dependent mice were examined. Chronic lead acetate (0.05%) exposure altered naloxone-induced jumping and diarrhea in mice. Jumping was decreased after 7 days and was unchanged 14 and 28 days after...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:
  • Mediators of Inflammation

دوره 2006  شماره 

صفحات  -

تاریخ انتشار 2006