Microvascular response to compartment syndrome-like external pressure elevation: An in vivo fluorescence microscopic study in the hamster striated muscle

Objective: To quantitatively assess the nature and the magnitude of the microvascular response of striated muscle tissue upon elevation of external pressure, as in compartment syndrome. Methods: Using the skinfold chamber model in Syrian golden hamsters and intravital fluorescence microscopy, we studied the individual response of the different segments of the microcirculation, i.e., the arterioles, capillaries, and postcapillary venules, in terms of vasomotor control (change of vessel diameter) and cessation of blood flow upon defined changes in external tissue pressure. Results: The unique findings of our study are that (1) arteriolar flow ceased at mean external pressures of 25.6 +/- 2.4, 28.3 +/- 2.8, 34.5 +/- 4.6, and 44.4 +/- 6.8 mm Hg in vessels with diameters of less than 20, 20 to 40, 40 to 60, and greater than 60 mu m, respectively, without signs of spasm or collapse even at a pressure maximum of 70 mm Hg, whereas (2) in venules the increase of external pressure was associated with a diameter reduction ranging from 5 to 25%,vith cessation of blood flow at mean external pressures between 27 and 33 mm Hg. blood flow ceased in 50% of the muscle capillaries already at an external pressure of 12 mm Hg. Thus, at distinct external pressure levels venous and capillary blood flow ceased, but arterioles were still capable of carrying flow, which was directed along arteriolo-arteriolar "thoroughfare" channels. To restart blood flow, external pressure had to be decreased by 9, 11, 15, and 17 mm Hg in arterioles with diameters of less than 20, 20 to 40, 40 to 60, and greater than 60 mu m, and by approximately 9 mm Hg in venules regardless of vessel diameter. Capillary blood flow was found to be restored at a mean reduction of external tissue pressure of approximately 4 mm Hg. Conclusion: Our study disproves the critical closing theory but complies-in particular because of the supposed constriction-induced increase of venular resistance-with the hypothesis of reduced arteriovenous pressure gradients as the cause of flow cessation in compartment syndrome. The necessity of a substantially increased perfusion pressure gradient to restart blood flow in arterioles, capillaries, and venules confirms the existence of yield stress in these microvessels. The high susceptibility of capillaries to elevated external pressure indicates the necessity of early fasciotomy to restore impaired nutritive circulation in cases of compartment syndrome.