Vasoreactions to acute hypoxia, whole lungs and isolated vessels compared: modulation by NO.
We aimed to explain diverse pulmonary vascular responses to hypoxia in different preparations and their modulation by NO. In rats we compared isolated perfused lungs (IPL), small vessels in vitro (PRVs) and in vivo preparations. In IPL and in vivo, acute and chronic nitric oxide synthase (NOS) blockade with L-NAME left normoxic pulmonary artery pressure unchanged but enhanced hypoxic vasoconstriction, hypoxia-induced pulmonary vasoconstriction (HPV). PRVs in vitro, precontracted with PGF(2alpha), showed four tension changes in acute hypoxia: dilatation, contraction, dilatation, contraction. Acute and chronic NOS blockade reduced the first two phases. In non-precontracted PRVs (from other laboratories), NOS inhibition enhanced HPV as in vivo and IPL; attenuation of HPV seems associated with precontraction. Thus reduced NOS activity does not cause pulmonary hypertension but exaggerates HPV. In IPL, prolonged severe hypoxia caused biphasic vasoconstriction separated by dilatation; the time course resembled that seen in PRVs. We suggest that the sequence of events during hypoxia in PRVs can be detected in whole lung preparations.
Emery
C J
CJ
Respiratory Medicine, Medical School, Beech Hill Road, Sheffield S10 2RX, UK.
Teng
G-Q
GQ
Liu
X
X
Barer
G R
GR
D000818:Animals; D000860:Hypoxia / Q000503:physiopathology*; D066298:In Vitro Techniques; D008168:Lung / Q000098:blood supply* / Q000503:physiopathology; D008297:Male; D009213:Myography; D019331:NG-Nitroarginine Methyl Ester; D009569:Nitric Oxide / Q000494:pharmacology; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D026902:Potassium Channel Blockers; D011652:Pulmonary Circulation / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors; D014661:Vasoconstriction / Q000502:physiology*
D026902:Potassium Channel Blockers; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D019331:NG-Nitroarginine Methyl Ester