Venular oscillatory flow during hemorrhagic shock and NO inhibition in hamster cheek pouch microcirculation

Blood flow oscillations (flowmotion) during hemorrhagic shock (HS) were recorded with laser Doppler perfusion monitoring (LDPM) and red blood cell (RBC) velocimetry in arterioles and venules in hamster cheek pouch microcirculation. Experiments were carried out after baroceptor denervation or inhibition of nitric oxide (NO) synthesis with NG-monomethyl-L-arginine prior to and during HS. Flowmotion was characterized by spectral analysis with fast Fourier transform and autoregressive modeling. Low frequency flowmotion was detected in LDPM and RBC velocity tracings derived from arterioles while high frequency oscillations dominated in venules under baseline conditions. Venular blood flow was significantly higher compared with arteriolar flow during HS, while large amplitude low frequency flowmotion was found in venules but not in arterioles where dominated small amplitude high frequency oscillations coincident with respiratory or heart rates. Baroceptor denervation did not affect venular blood flow and low frequency flowmotion during HS. NO inhibition reduced significantly venular blood flow compared with control and abolished low frequency flowmotion in venules. High frequency oscillations remained in arterioles during HS. In conclusion, LDPM low frequency flowmotion was not originated by variations in the diameter of vessels, but corresponded to RBC velocity changes. A compensatory higher blood flow and concomitant low frequency flowmotion in venules appeared to be related to NO production during HS, independently of neural mechanism.