Blood flow is essential for normal bone growth and bone repair. Like other organs, the regulation of blood flow to bone is complex and involves numerous physiologic mechanisms including the sympathetic nervous system, circulating hormones, and local metabolic factors. Our studies addressed the following questions: (1) Which endogenous vasoconstrictor agents regulate in vivo blood flow to bone? (2) Does a decrease in bone vascular reactivity to vasoconstrictor hormones account for the increase in blood flow during bone healing? (3) Does the endothelium influence bone arteriolar function? An intact bone model was developed in the rat to assess hormonal regulation of in vivo bone blood flow and in vivo bone vascular reactivity. An isolated, perfused bone arteriole preparation was employed to characterize the responsiveness of small resistance-size arterioles (diameter < 100 µm) to vasoconstrictor hormones and to evaluate the role of the vascular endothelium to modulate vascular smooth muscle reactivity. Our results indicate that: (1) though exogenous endothelin is a potent constrictor of the in vivo bone vasculature, endogenous endothelin does not actively regulate in vivo blood flow; (2) the increase in blood flow to a bone injury site is not due to a decrease in bone vascular sensitivity to norepinephrine, and (3) isolated bone arterioles of young rats are very sensitive to vasoconstrictor hormones but exhibit only modest endothelium-mediated vasodilation.

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The most dramatic improvements in the stability of hybrid frames used for proximal tibial fractures result from addition of an anterior, proximal half-pin.

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Purpose: Because the protean biological effects of ethanol include acute alterations in both cortical function and circulatory control, we investigated the effect of acute alcohol consumption on retrobulbar hemodynamics and contrast sensitivity in healthy human volunteers. Subjects and Methods: Twelve young adults received orange juice with and without ethanol in a double-masked fashion. The ethanol dose was sufficient to raise blood alcohol to 0.07 ± 0.003 g/dl. Retrobulbar hemodynamics were assessed at baseline and twice at elevated blood alcohol by color Doppler imaging. Results: Acute elevation of blood alcohol lowered intraocular pressure from 13.0 ± 0.7 to 10.7 ± 0.7 mm Hg (p < 0.05). In contrast, elevated blood alcohol left peak systolic velocity, end diastolic velocity and the resistance index constant in three retrobulbar arteries (ophthalmic, central retinal and posterior ciliary). For example, in the central retinal artery, peak systolic velocity, end diastolic velocity and the resistance index averaged 11.0 ± 1.3 cm/s, 2.8 ± 0.4 cm/s and 0.75 ± 0.03 before ethanol, as compared with 10.5 ± 1.0 cm/s, 2.9 ± 0.3 cm/s and 0.72 ± 0.03 after ethanol (all p = NS). Alcohol ingestion also failed to alter either visual acuity or contrast sensitivity, as assessed under both photopic and mesopic conditions. Conclusions: Although ethanol has widespread cognitive and cardiovascular effects, at blood levels near legal definitions of intoxication we found it ineffective in altering either retrobulbar hemodynamics or contrast sensitivity.

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