Air embolism-induced lung injury in isolated rat lungs

Wang, David; Li, Min-Hui; Hsu, Kang; Shen, Chao‐Yu; Chen, H. I.; Lin, Yixin

doi:10.1152/jappl.1992.72.4.1235

Cited by 70 publications

(76 citation statements)

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“…Changes in body weight (BW) were considered to be the result of changes in lung weight (LW). Our earlier examinations of isolated lung preparations in which Evans blue dye was added to the perfusate revealed that the dye was confined to the lungs after exposure to either low (2.5 mm Hg) or high (10 mm Hg) PVP for 30 min [18,22]. Although the hematocrit was reduced in the perfusate, the perfusate osmolarity (285 mosm) was not significantly altered compared to that of whole blood.…”

Section: Isolation and Perfusion Of Rat Lungsmentioning

confidence: 97%

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Nitric Oxide Mediates Lung Injury Induced by Ischemia-Reperfusion in Rats

et al. 2003

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Nitric oxide (NO) has been reported to play a role in lung injury (LI) induced by ischemia-reperfusion (I/R). However, controversy exists as to the potential beneficial or detrimental effect of NO. In the present study, an in situ, perfused rat lung model was used to study the possible role of NO in the LI induced by I/R. The filtration coefficient (K_fc), lung weight gain (LWG), protein concentration in the bronchoalveolar lavage (PCBAL), and pulmonary arterial pressure (PAP) were measured to evaluate the degree of pulmonary hypertension and LI. I/R resulted in increased K_fc, LWG, and PCBAL. These changes were exacerbated by inhalation of NO (20–30 ppm) or 4 mML-arginine, an NO precursor. The permeability increase and LI caused by I/R could be blocked by exposure to 5 mM N^ω-nitro-L-arginine methyl ester (L-NAME; a nonspecific NO synthase inhibitor), and this protective effect of L-NAME was reversed with NO inhalation.Inhaled NO prevented the increase in PAP caused by I/R, while L-arginine had no such effect. L-NAME tended to diminish the I/R-induced elevation in PAP, but the suppression was not statistically significant when compared to the values in the I/R group.These results indicate that I/R increases K_fc and promotes alveolar edema by stimulating endogenous NO synthesis. Exogenous NO, either generated from L-arginine or delivered into the airway, is apparently also injurious to the lung following I/R.

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Section: Isolation and Perfusion Of Rat Lungsmentioning

confidence: 97%

“…The procedure used to prepare isolated, perfused lungs was similar to that described previously [6,18,22]. Rats were tracheotomized under pentobarbital anesthesia (30 mg/kg i.p.…”

Section: Isolation and Perfusion Of Rat Lungsmentioning

confidence: 99%

Nitric Oxide Mediates Lung Injury Induced by Ischemia-Reperfusion in Rats

et al. 2003

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“…Thus, the decreased diameter may indicate that the vessels were in a partially constricted state. Vasoconstrictors such as thromboxane A2 (Fukushima & Kobayashi, 1986) and endothelin-1 (Wang et al, 1992) are released during air embolization and their effects may be maintained after the vessels are removed from the lung.…”

Section: Passive Vessel Propertiesmentioning

confidence: 99%

Endothelium‐dependent relaxations in sheep pulmonary arteries and veins: resistance to block by N^G‐nitro‐L‐arginine in pulmonary hypertension

Kemp¹,

Smolich²,

Ritchie³

et al. 1995

British J Pharmacology

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1 The effect of the nitric oxide synthase inhibitor, NG-nitro-L-arginine (L-NOARG), on endotheliumdependent relaxation to a receptor-independent agent, ionomycin, was examined in isolated pulmonary arteries and veins from control, short-term and chronic pulmonary hypertensive sheep. All vessel segments were contracted to optimal levels of active force with endothelin-I to record endotheliumdependent relaxation. 2 Pulmonary hypertension was induced by continuous pulmonary artery air embolization for 1 day (short-term) and 14 days (chronic) and was associated with a 2 and 3 fold increase in pulmonary vascular resistance respectively.3 L-NOARG (0.1 mM) reduced the maximum relaxation (Rm,) to ionomycin in large and mediumsized pulmonary arteries from control sheep by approximately 70%. By contrast, L-NOARG (0.1 mM) did not inhibit the Rmax to ionomycin in matched vessels from short-term and chronic pulmonary hypertensive sheep. 4 Resistance of ionomycin-induced relaxations to inhibition by L-NOARG, was confined to the arterial vasculature in chronic pulmonary hypertensive animals, as relaxations to ionomycin in large and medium-sized chronic pulmonary hypertensive veins were, like those in control veins, abolished by L-NOARG. Both large and medium-sized pulmonary veins from short-term pulmonary hypertensive sheep, however, were resistant to block by L-NOARG.5 Neither sensitivity (pEC5o) nor RmS, to ionomycin in large, short-term pulmonary hypertensive arteries was affected when the extracellular concentration of K+ was increased isotonically to 30 mm. Nifedipine (0.3 gM) was present throughout to prevent high K+-induced smooth muscle contraction. In the presence of this high extracellular K+, however, L-NOARG (0.1 mM) caused complete inhibition of the relaxation to ionomycin, whereas in normal extracellular K+ (4.7 mM), L-NOARG only weakly inhibited ionomycin relaxations. 6 In conclusion, the onset of pulmonary hypertension in sheep following air embolization, is associated with the development of resistance of endothelium-dependent relaxations to block by L-NOARG. The mechanism of L-NOARG resistance appears to be due to the up-regulation of a K+ channel-mediated backup vasodilator mechanism which can compensate for the loss of nitric oxide (NO)-mediated relaxation. Although this mechanism remains functionally 'silent' in the presence of NO it is able to maintain adequate endothelium-dependent vasodilatation during pulmonary hypertension if NO synthesis is compromised.

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“…LUNG DISEASES, SUCH AS ASTHMA (10), chronic obstructive pulmonary disease (12), endotoxin shock (33), and vascular microembolism (50), or inhalation of oxidant irritants, such as toxic smoke (35), cigarette smoke (35), and ozone (45), may cause increased pulmonary production of reactive oxygen species from endogenous and/or exogenous sources. The major reactive oxygen species are the superoxide anion radical, hydrogen peroxide (H 2 O 2 ), and the hydroxyl radical (⅐ OH) (5).…”

mentioning

confidence: 99%

Afferent vagal pathways mediating respiratory reflexes evoked by ROS in the lungs of anesthetized rats

Ruan

Kou

2003

Journal of Applied Physiology

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vagal pathways mediating respiratory reflexes evoked by ROS in the lungs of anesthetized rats. J Appl Physiol 94: 1987, 2003. First published January 10, 2003 10.1152/ japplphysiol.01047.2002We investigated the afferent vagal pathways mediating respiratory reflexes evoked by reactive oxygen species (ROS) in the lungs of anesthetized rats. Spontaneous inhalation of 0.2% aerosolized H 2O2 acutely evoked initial bradypnea followed by delayed tachypnea, which was frequently mixed with delayed augmented inspiration. The initial response was abolished after perivagal capsaicin treatment (PCT), but was prolonged during vagal cooling (VC) to 7°C; PCT and VC are known to differentially block the conduction of unmyelinated C and myelinated fibers, respectively. The delayed responses were eliminated during VC but emerged earlier after PCT. Vagotomy, catalase (an antioxidant for H 2O2), dimethylthiourea (an antioxidant for ⅐ OH), or deferoxamine (an antioxidant for ⅐ OH) largely or totally suppressed these reflexive responses, whereas sham nerve treatment, heat-inactivated catalase, saline vehicle, or iron-saturated deferoxamine failed to do so. These results suggest that 1) the H 2O2-evoked initial and delayed airway reflexes are antagonistic and may result from stimulation of lung C fibers and rapidly adapting receptors, respectively, and 2) the reflex effects of H 2O2 are, in part, due to the action of ⅐ OH on these afferents. vagal sensory receptors; oxygen radicals; reactive oxygen species; hydrogen peroxide LUNG DISEASES, SUCH AS ASTHMA (10), chronic obstructive pulmonary disease (12), endotoxin shock (33), and vascular microembolism (50), or inhalation of oxidant irritants, such as toxic smoke (35), cigarette smoke (35), and ozone (45), may cause increased pulmonary production of reactive oxygen species from endogenous and/or exogenous sources. The major reactive oxygen species are the superoxide anion radical, hydrogen peroxide (H 2 O 2 ), and the hydroxyl radical (⅐ OH) (5). The superoxide anion radical dismutates to form H 2 O 2 , which, in the presence of iron, can further react to form ⅐ OH, a more reactive oxygen radical, via the Fenton reaction (5). Vagal sensory receptors are known to play an important role in detecting the onset of pathophysiological conditions and are responsible for triggering defensive or protective airway reflexes (8, 29, 39).While abundant information suggests the importance of reactive oxygen species in producing pulmonary pathophysiological consequences (4), very few studies have investigated their role and mechanism in eliciting airway reflexes.The concept that reactive oxygen species may stimulate pulmonary sensory receptors and play a vital role in eliciting airway reflexes is considerably new (29). This concept is indirectly supported from findings that vagally mediated airway reflexes evoked by inhaled cigarette smoke (27), inhaled wood smoke (22), or pulmonary air embolism (6) and responses of vagal sensory receptors to the latter two insults (7,24,25) are greatly attenuated b...

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Air embolism-induced lung injury in isolated rat lungs

Cited by 70 publications

References 0 publications

Nitric Oxide Mediates Lung Injury Induced by Ischemia-Reperfusion in Rats

Nitric Oxide Mediates Lung Injury Induced by Ischemia-Reperfusion in Rats

Endothelium‐dependent relaxations in sheep pulmonary arteries and veins: resistance to block by N^G‐nitro‐L‐arginine in pulmonary hypertension

Afferent vagal pathways mediating respiratory reflexes evoked by ROS in the lungs of anesthetized rats

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Air embolism-induced lung injury in isolated rat lungs

Cited by 70 publications

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Nitric Oxide Mediates Lung Injury Induced by Ischemia-Reperfusion in Rats

Nitric Oxide Mediates Lung Injury Induced by Ischemia-Reperfusion in Rats

Endothelium‐dependent relaxations in sheep pulmonary arteries and veins: resistance to block by NG‐nitro‐L‐arginine in pulmonary hypertension

Afferent vagal pathways mediating respiratory reflexes evoked by ROS in the lungs of anesthetized rats

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Endothelium‐dependent relaxations in sheep pulmonary arteries and veins: resistance to block by N^G‐nitro‐L‐arginine in pulmonary hypertension