Effects of hypoxia on isolated intrapulmonary arteries from the sheep

• Published in: Pulmonary pharmacology (Edinburgh) Vol. 4; no. 3; pp. 158 - 164
• Main Authors: Demiryurek, A.T., Wadsworth, R.M., Kane, K.A.
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 1991
• Subjects: Acetylcholine - pharmacology; Animals; Endothelium, Vascular - drug effects; Endothelium, Vascular - physiology; In Vitro Techniques; Muscle Contraction - drug effects; Muscle Relaxation - drug effects; Muscle, Smooth, Vascular - drug effects; Oxygen - toxicity; Potassium Chloride - pharmacology; Pulmonary Artery - drug effects; Sheep - physiology
• ISSN: 0952-0600; 1522-9637
• DOI: 10.1016/0952-0600(91)90006-O

The effects of hypoxia on contraction of sheep pulmonary artery rings (large= 2.2–4.1 mm diameter, small = 0.32–0.64 mm diameter) has been investigated following precontraction or with the artery rings set at their optimal resting force. Hypoxia (PO 2 4 mmHg) caused a marked contraction of pulmonary artery rings precontracted with 5-HT at its EC 85 (small arteries 40 ± 8 g cm −2) but not when precontracted with KCI. At optimal resting force hypoxia caused a small contraction (small arteries 11 ± 2 g cm −2). Large artery rings gave a smaller contraction in response to hypoxia at optimal resting force than did small artery rings (2 ± 0.2 g cm −2 at PO 2 = 4 mmHg). Large, unlike the small, artery rings did not contract in response to hypoxia when precontracted with 5-HT at its EC 35. Lowering the PO 2 to 40 mmHg caused contraction in arteries precontracted with 5-HT at its EC 85 but not in arteries at their optimal resting force. Removal of the endothelium abolished all hypoxia-induced contractile responses in sheep pulmonary artery rings. Hypoxia reversibly abolished acetylcholine-induced relaxation and augmented the 5-HT contraction (206 ± 28 to 255 ± 34 g cm −2) in small rings. It is concluded that hypoxia may produce contraction in sheep pulmonary artery rings at least, in part, by reducing the output of vasodilator mediators from the endothelium.