Holm I E, Ewald H, Bülow J, Bünger C
Institute of Experimental Clinical Research, University of Aarhus, Denmark.
J Orthop Res. 1990 Mar;8(2):205-12. doi: 10.1002/jor.1100080208.
The purpose of the present study was to investigate regulatory mechanisms for subchondral bone blood flow. A model including elevation of joint cavity pressure in the immature dog knee was applied. The role of prostaglandins in bone blood flow regulation was indirectly examined by indomethacin blockade. In six puppies, both venous tamponade of the joint cavity [50% of the mean arterial blood pressure (MAP)] and arterial tamponade (150% of MAP) resulted in a significant increase in the intraosseous pressure of the distal femoral epiphyses (p less than 0.05). During venous tamponade no changes were registered in pO2, pCO2, pH, potassium, and lactate in blood withdrawn from the distal femoral epiphyses. Arterial tamponade resulted in hypoxia, a decrease in pH, and increased lactate. Inhibition of the prostaglandin synthesis did not alter this response pattern. Thus, the present study suggests the presence of a regulatory mechanism for subchondral bone blood flow since venous tamponade did not significantly alter intraosseous gas tensions, pH, lactate, or potassium in spite of elevated venous outlet resistance. The study does not allow any conclusion as to the exact nature of the regulatory mechanism, but local metabolic regulation is likely to be involved as indicated by accumulation of vasoactive substances at higher tamponade levels. Prostaglandins are probably of minor importance in this regulation.
本研究的目的是探讨软骨下骨血流的调节机制。应用了一个包括幼龄犬膝关节腔压力升高的模型。通过吲哚美辛阻断间接研究前列腺素在骨血流调节中的作用。在六只幼犬中，关节腔静脉压迫（平均动脉血压（MAP）的50%）和动脉压迫（MAP的150%）均导致股骨远端骨骺骨内压显著升高（p<0.05）。在静脉压迫期间，从股骨远端骨骺抽取的血液中的pO2、pCO2、pH、钾和乳酸没有变化。动脉压迫导致缺氧、pH值降低和乳酸增加。前列腺素合成的抑制并未改变这种反应模式。因此，本研究表明存在软骨下骨血流的调节机制，因为尽管静脉流出阻力升高，但静脉压迫并未显著改变骨内气体张力、pH值、乳酸或钾。该研究无法就调节机制的确切性质得出任何结论，但如在较高压迫水平下血管活性物质的积累所示，局部代谢调节可能参与其中。前列腺素在这种调节中可能不太重要。
