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Effects of indomethacin on systemic and renal haemodynamics during postnatal maturation in conscious lambs
Author(s) -
Kesavarao Kumar Ebenezar,
Ghane Fatemah Sharbaf,
Smith Francine Gabriel
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a763-d
Subject(s) - vascular resistance , hemodynamics , renal blood flow , mean arterial pressure , cyclooxygenase , nitric oxide , medicine , endocrinology , blood pressure , kidney , heart rate , chemistry , anesthesia , enzyme , biochemistry
To investigate the role of endogenously produced prostaglandins in modulating systemic and renal haemodynamics during postnatal maturation, experiments were carried out in conscious, chronically instrumented lambs aged one to two weeks (group I, 10–14 days (n=6)) and six to eight weeks (group II, 40–58 days (n=13)). Mean arterial pressure (MAP), mean venous pressure (MVP) and renal blood flow (RBF) were measured for 5 min before (Control) and for 20 min after I.V. injection of vehicle (experiment one) and after 24–48 h, the non‐selective cyclooxygenase inhibitor, indomethacin (1 mg/kg, experiment two). Heart rate (HR) and renal vascular resistance (RVR) were calculated from the measured variables. MAP increased significantly in both groups by 2 mins after indomethacin, returning to control over the next 7 min. HR significantly decreased to reach a nadir at 3 mins in groups I and II, returning to Control by 7 min. A marked increase in RVR leading to a decrease in RBF also occurred within 2 min of administration of indomethacin in both groups; control levels were reached within 7 min. There were no effects of vehicle on any of the measured or calculated variables. These data provide new evidence to suggest that endogenously produced prostaglandins modulate systemic and renal haemodynamics during postnatal maturation in conscious lambs. These transient responses to indomethacin indicate a buffering effect of other vasoactive factors, such as nitric oxide, in the absence of endogenously produced prostaglandins.