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Knowledge about vascular regulation in bone is central to the understanding of both normal and pathological bone physiology. This article describes a new method for direct assessment of the reactivity of bone blood vessels. Resistance arteries (diameter approximately 250 microns) were isolated from epiphyseal cancellous bone (porcine femoral condyle). Arterial segments (2 mm long) were mounted as ring preparations on a myograph, and isometric force development was measured continuously. Fifty-nine vessels from 31 pigs were investigated. The active force development was maximal at 0.9 x L100 in nine of 12 investigated arteries (L100 corresponds to the circumference the vessel would have if relaxed and exposed to a luminal pressure of 100 mm Hg [13.3 kPa]). In all subsequent experiments, the vessels were stretched to 0.9 x L100. Noradrenaline (2 x 10(-8) to 10(-5) M) induced a concentration-dependent vasoconstriction; mean maximal tension development was 3.69 N/m. This force development would enable the arteries to contract against a pressure of more than 22 kPa (165 mm Hg), indicating preserved function of the media smooth muscle. Response to acetylcholine (10(-7) to 10(-5) M) was observed in only two of 12 arteries. Bradykinin (10(-11) to 10(-6) M) induced a concentration-dependent and reproducible relaxation in all vessels; the relaxation was endothelium-dependent, since no effect of bradykinin was detected after mechanical removal of the endothelium. Sodium nitroprusside (10(-4) M) induced a reproducible and endothelium-independent vasorelaxation. The results demonstrate preserved function of both smooth muscle and endothelium in this preparation. The model allows pharmacological investigations of bone arteries under well defined conditions and enables studies on focal bone lesions and human bone tissue.

Information is sparse concerning the effect of oophorectomy (OOX) on bone vascularization and blood flow of possible significance for altered remodeling. Whether OOX affects functional characteristics of isolated bone resistance arteries was investigated. Ring preparations (diameter -250 pm) of small femoral bone arteries from oophorectomized and sham-operated rabbits were mounted on a myograph six weeks postoperatively. Cumulative concentration-response curves were obtained for various agonists at a normalized lumen diameter. Oophorectomy did not significantly influence lumen diameter, maximal response to high potassium, or maximal response to high potassium and M noradrenaline. However, OOX significantly increased the maximal response to noradrenaline (OOX 2.14 * 0.36 N/m, Sham 1.25 * 0.14 Nlm) and endothelin-1 (OOX 1.76 0.32, Sham 0.95 3~ 0.15) in metaphyseal arteries. Moreover, the corresponding maximal active pressure for the agonists was significantly increased. OOX did not influence endothelial function assessed by the effects of acetylcholine or substance P. The functional responses of diaphyseal arteries were unaffected by OOX. The study demonstrates regional differences in the effects of OOX on small arteries of importance for control of vascular resistance in bone which suggests a relation between altered vascular function after ovarian hormonal withdrawal and the changes in bone turnover associated with osteoporosis.

Many pathological bone conditions are accompanied by changes in bone perfusion. However, no method has yet allowed investigation of vascular reactivity in human bone tissue. In the present study, arterial segments (diameter = 0.25 mm) were isolated from human bone biopsies and mounted as ring preparations in vitro. The viability of the arteries and the effects of adrenoceptor stimulations were investigated. Combined a-and 0-adrenoceptor stimulation (noradrenaline 10-8-10-5 M) and specific cyIadrenoceptor stimulation (phenylephrine, 10-8-10-4.5 M ) induced ' concentration-dependent contractions in all arteries. Selective stimulation of a2-receptors (B-HT 933, 1 O-R-10-'.5 M) only induced contraction in three of eight arteries. Stimulation of 0-receptors with isoprenaline ( M ) resulted in vasorelaxation in 3 of 10 arteries. In all arteries, acetylcholine ( 10-'0-10-5 M ) induced vasorelaxation, demonstrating preserved function of the endothelium. The results suggest that primarily a1 -receptors are responsible for adrenoceptor induced vasoconstriction in human bone while functional a?-and 0-receptors may not be consistently expressed. The model is the first to allow investigations on vascular reactivity in human bone tissue and may become valuable for assessment of both normal and pathological bone physiology.

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