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ENDOTOXIN‐INDUCED ACUTE LUNG INJURY IS ENHANCED IN RATS WITH SPONTANEOUS HYPERTENSION

Identifieur interne : 003B84 ( Main/Merge ); précédent : 003B83; suivant : 003B85

ENDOTOXIN‐INDUCED ACUTE LUNG INJURY IS ENHANCED IN RATS WITH SPONTANEOUS HYPERTENSION

Auteurs : Demeral D. Liu [Taïwan] ; Yung Hsiang Hsu ; Hsing I. Chen

Source :

Clinical and Experimental Pharmacology and Physiology [ 0305-1870 ] ; 2007-01.

RBID : ISTEX:6F7AE8437A2EB3FB91283C2D246B4ED8C199429E

English descriptors

Teeft :
- Acute lung injury, Arterial pressure, Authors journal compilation, Basal, Blackwell publishing asia, Bronchoalveolar lavage, Cgmp, Conscious rats, Corresponding values, Crit, Cytokine, Distress syndrome, Endotoxaemia, Endotoxin, Endotoxin lung injury, Endotoxin shock, Enos, Enos mrna expression, Ester, Free radicals, Guanidine, Heart rate, Hypertension, Hypertensive, Hypertensive rats, Hypotension, Inducible, Inducible nitric oxide synthase, Inos, Inos expression, Lavage, Lipopolysaccharide, Lung injury, Lung tissue, Lung weight gain, Methyl, Methyl ester, Methyl guanidine, Mrna, Mrna expression, Nitric, Nitric oxide, Normotensive, Oedema, Oxide, Pcbal, Plasma methyl guanidine, Present study, Pretreatment, Protein concentration, Rat, Rats vehicle, Synthase, Systemic hypotension, Vehicle lipopolysaccharide.

Abstract

1 Acute lung injury (ALI), or acute respiratory distress syndrome, is a major cause of mortality in endotoxaemia. The present study tested whether the endotoxaemia‐induced changes and associated ALI were enhanced in rats with established hypertension and to examine the possible mechanisms involved. 2 Fifty spontaneously hypertensive rats (SHR) and the same number of normotensive Wistar Kyoto (WKY) rats, aged 12–15 weeks, were used. The experiments were performed in conscious, unanaesthetized rats. Endotoxaemia was produced by intravenous lipopolysaccharide (LPS; 10 mg/kg). NG‐Nitro‐l‐arginine methyl ester (l‐NAME; 10 mg/kg, i.v.), l‐N6‐(1‐iminoethyl)‐lysine (l‐Nil; 5 mg/kg, i.v.) and 3‐morpholinosydnonimine (SIN‐1; 5 mg/kg, i.v.) were given 5 min before LPS to observe the effects of nitric oxide synthase (NOS) inhibition and nitric oxide (NO) donation. 3 We monitored arterial pressure and heart rate and evaluated ALI by determining the lung weight/bodyweight ratio, lung weight gain, leakage of Evans blue dye, the protein concentration in bronchoalveolar lavage and histopathological examination. Plasma nitrate/nitrite, methyl guanidine, pro‐inflammatory cytokines, including tumour necrosis factor‐α and interleukin‐1β, and lung tissue cGMP were determined. Expression of mRNA for inducible and endothelial NOS was examined using reverse transcription–polymerase chain reaction. 4 Lipopolysaccharide caused systemic hypotension, ALI and increases in plasma nitrate/nitrite, methyl guanidine, pro‐inflammatory cytokines and lung cGMP content. The LPS‐induced changes were greater in SHR than in WKY rats. Pretreatment with l‐NAME or l‐Nil attenuated, whereas the NO donor SIN‐1 aggravated, the endotoxin‐induced changes. 5 In conclusion, rats with genetic hypertension are more susceptible to endotoxaemia and this results in a greater extent of ALI compared with normotensive WKY rats.

Url:

https://api.istex.fr/ark:/67375/WNG-2R3R8ZBX-1/fulltext.pdf

DOI: 10.1111/j.1440-1681.2007.04526.x

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<term>Inducible</term>
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<front><div type="abstract" xml:lang="en">1 Acute lung injury (ALI), or acute respiratory distress syndrome, is a major cause of mortality in endotoxaemia. The present study tested whether the endotoxaemia‐induced changes and associated ALI were enhanced in rats with established hypertension and to examine the possible mechanisms involved. 2 Fifty spontaneously hypertensive rats (SHR) and the same number of normotensive Wistar Kyoto (WKY) rats, aged 12–15 weeks, were used. The experiments were performed in conscious, unanaesthetized rats. Endotoxaemia was produced by intravenous lipopolysaccharide (LPS; 10 mg/kg). NG‐Nitro‐l‐arginine methyl ester (l‐NAME; 10 mg/kg, i.v.), l‐N6‐(1‐iminoethyl)‐lysine (l‐Nil; 5 mg/kg, i.v.) and 3‐morpholinosydnonimine (SIN‐1; 5 mg/kg, i.v.) were given 5 min before LPS to observe the effects of nitric oxide synthase (NOS) inhibition and nitric oxide (NO) donation. 3 We monitored arterial pressure and heart rate and evaluated ALI by determining the lung weight/bodyweight ratio, lung weight gain, leakage of Evans blue dye, the protein concentration in bronchoalveolar lavage and histopathological examination. Plasma nitrate/nitrite, methyl guanidine, pro‐inflammatory cytokines, including tumour necrosis factor‐α and interleukin‐1β, and lung tissue cGMP were determined. Expression of mRNA for inducible and endothelial NOS was examined using reverse transcription–polymerase chain reaction. 4 Lipopolysaccharide caused systemic hypotension, ALI and increases in plasma nitrate/nitrite, methyl guanidine, pro‐inflammatory cytokines and lung cGMP content. The LPS‐induced changes were greater in SHR than in WKY rats. Pretreatment with l‐NAME or l‐Nil attenuated, whereas the NO donor SIN‐1 aggravated, the endotoxin‐induced changes. 5 In conclusion, rats with genetic hypertension are more susceptible to endotoxaemia and this results in a greater extent of ALI compared with normotensive WKY rats.</div>
</front>
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ENDOTOXIN‐INDUCED ACUTE LUNG INJURY IS ENHANCED IN RATS WITH SPONTANEOUS HYPERTENSION

ENDOTOXIN‐INDUCED ACUTE LUNG INJURY IS ENHANCED IN RATS WITH SPONTANEOUS HYPERTENSION

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Abstract

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