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Atrial natriuretic peptide ameliorates hypoxic pulmonary vasoconstriction without influencing systemic circulation

100%

Hohne C., Drzimalla M., Krebs M. O., Boemke W., Kaczmarczyk G.

Journal of Physiology and Pharmacology

2003

tom 54

nr 4

Hypoxic pulmonary vasoconstriction (HPV) is encountered during ascent to high altitude. Atrial natriuretic peptide (ANP) could be an option to treat HPV because of its natriuretic, diuretic, and vasodilatory properties. Data on effects of ANP on pulmonary and systemic circulation during HVP are conflicting, partly owing to anesthesia, surgical stress or uncontrolled dietary conditions. Therefore, ten conscious, chronically tracheotomized dogs were studied under standardized dietary conditions. The dogs were trained to breathe spontaneously at a ventilator circuit. Protocol: 30min of normoxia [inspiratory oxygen fraction (FiO2)=0.21] were followed by 30min of hypoxia without ANP infusion (Hypoxia I, FiO2=0.1). While maintaining hypoxia an intravenous infusion of atrial natriuretic peptide was started with 50ng·kg body wt-1·min-1 for 30min (Hypoxia+ANP1=low dose), followed by 1000ng·kg body wt-1·min-1 for 30min (Hypoxia+ANP2=high dose). Thereafter, ANP infusion was stopped and hypoxia maintained for a final 30min (Hypoxia II). Compared to normoxia, mean pulmonary arterial pressure (MPAP) (16±0.7 vs. 26±1.3mmHg) and pulmonary vascular resistance (PVR) (448±28 vs. 764±89dyn·s-1·cm-5) increased during Hypoxia I and decreased during Hypoxia+ANP 1 (MPAP 20±1mmHg, PVR 542±55dyn·s-1·cm-5) (P<0.05). The higher dose of ANP did not further decrease MPAP or PVR, but started to have a tendency to decrease mean arterial pressure and cardiac output. We conclude that low dose ANP is able to reduce HPV without affecting systemic circulation during acute hypoxia.

Selective inhibition of guanylate cyclase prevents impairment of hypoxic pulmonary vasoconstriction in endotoxemic mice

84%

Spohr F., Busch C. J., Teschendorf P., Weimann J.

Journal of Physiology and Pharmacology

2009

tom 60

nr 2

107-112

Nitric oxide (NO) may cause sepsis-induced impairment of hypoxic pulmonary vasoconstriction (HPV). Although NO exerts many of its actions by activating soluble guanylate cyclase (sGC), there are several cGC-independent mechanisms that may lead to NO-induced vasodilation during endotoxemia. We investigated the role of sGC for the regulation of HPV during lipopolysaccharide (LPS) induced endotoxemia using 1H-(1,2,4)oxadiazole(4,3-)quinoxaline-1-one (ODQ), a specific inhibitor of sGC, in isolated, perfused, and ventilated mouse lungs. Without ODQ, lungs from LPS-challenged mice constricted significantly less in response to hypoxia as compared to lungs from mice not treated with LPS (26 ± 27% vs. 134 ± 37%, respectively, p < 0.05). 20 mg/kg ODQ, but not 2 mg/kg or 10 mg/kg, restored the blunted HPV response in LPS-challenged mice as compared to mice not challenged with LPS (80±14 % vs. 98±21 %). ODQ had no effect on baseline perfusion pressures under normoxic conditions. Analysis of pulmonary vascular P-Q relationships suggested that the restoration of pulmonary vascular response to hypoxia by ODQ is associated with a restoration of pulmonary vascular properties during normoxia. Our data show in a murine model that specific inhibition of sGC may be a new approach to restore HPV during endotoxemia.

Ograniczanie wyników

2 Journal of Physiology and Pharmacology

1 Boemke W.

1 Busch C. J.

1 Drzimalla M.

1 Hohne C.

1 Kaczmarczyk G.

1 Krebs M. O.

1 Spohr F.

1 Teschendorf P.

1 Weimann J.

1 2009

1 2003

Wyniki wyszukiwania

Atrial natriuretic peptide ameliorates hypoxic pulmonary vasoconstriction without influencing systemic circulation

Selective inhibition of guanylate cyclase prevents impairment of hypoxic pulmonary vasoconstriction in endotoxemic mice