TY - JOUR
T1 - Variability of hypoxic pulmonary vasoconstriction in sheep. Role of prostaglandins
AU - Ahmed, Tahir
AU - Oliver, W.
AU - Wanner, A.
PY - 1983/1/1
Y1 - 1983/1/1
N2 - In a minority of conscious sheep, the hypoxic pulmonary vasoconstrictor response is blunted ('nonresponders'). The purpose of this investigation was to determine if this blunted response is related to an increased activity of H2-histamine receptors, beta-adrenergic receptors, or the generation of inhibitory prostaglandins. We measured pulmonary arterial pressure, pulmonary arterial wedge pressure, and pulmonary blood flow for the calculation of pulmonary vascular resistance (PVR) in 2 'nonresponders' and 5 sheep with a typical hypoxic pulmonary vasoconstrictor response ('responders') while breathing room air and 13% O2 (balance, N2). Arterial oxygen tension (Pa(O2)) was also determined as a measure of the severity of hypoxia. During hypoxia, mean PVR increased by 6% (p = NS) in the 'nonresponders' (Pa(O2), 49 ± 4 mmHg) and by 70% (p < 0.01) in the 'responders' (mean Pa(O2), 46 ± 4 mmHg). Metiamide (H2-blocker) and propranolol (beta-adrenergic blocker) pretreatments did not restore the hypoxic pulmonary vascular response in the 'nonresponders' whereas pretreatment with indomethacin (prostaglandin synthetase inhibitor) caused mean PVR to increase by 48% (p < 0.01) during hypoxia, indicating a partial restoration of hypoxic pulmonary vasoconstriction. In the 'responders' the hypoxic pulmonary vascular response was not potentiated by indomethacin pretreatment (68% increase in mean PVR). We conclude that some sheep exhibit a blunted hypoxic pulmonary vasoconstrictor response caused by enhanced production of inhibitory prostaglandins.
AB - In a minority of conscious sheep, the hypoxic pulmonary vasoconstrictor response is blunted ('nonresponders'). The purpose of this investigation was to determine if this blunted response is related to an increased activity of H2-histamine receptors, beta-adrenergic receptors, or the generation of inhibitory prostaglandins. We measured pulmonary arterial pressure, pulmonary arterial wedge pressure, and pulmonary blood flow for the calculation of pulmonary vascular resistance (PVR) in 2 'nonresponders' and 5 sheep with a typical hypoxic pulmonary vasoconstrictor response ('responders') while breathing room air and 13% O2 (balance, N2). Arterial oxygen tension (Pa(O2)) was also determined as a measure of the severity of hypoxia. During hypoxia, mean PVR increased by 6% (p = NS) in the 'nonresponders' (Pa(O2), 49 ± 4 mmHg) and by 70% (p < 0.01) in the 'responders' (mean Pa(O2), 46 ± 4 mmHg). Metiamide (H2-blocker) and propranolol (beta-adrenergic blocker) pretreatments did not restore the hypoxic pulmonary vascular response in the 'nonresponders' whereas pretreatment with indomethacin (prostaglandin synthetase inhibitor) caused mean PVR to increase by 48% (p < 0.01) during hypoxia, indicating a partial restoration of hypoxic pulmonary vasoconstriction. In the 'responders' the hypoxic pulmonary vascular response was not potentiated by indomethacin pretreatment (68% increase in mean PVR). We conclude that some sheep exhibit a blunted hypoxic pulmonary vasoconstrictor response caused by enhanced production of inhibitory prostaglandins.
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U2 - 10.1164/arrd.1983.127.1.59
DO - 10.1164/arrd.1983.127.1.59
M3 - Article
C2 - 6849552
AN - SCOPUS:0020675835
VL - 127
SP - 59
EP - 62
JO - American Journal of Respiratory and Critical Care Medicine
JF - American Journal of Respiratory and Critical Care Medicine
SN - 1073-449X
IS - 1
ER -