A Simple “Streak Length Method” for Quantifying and Characterizing Red Blood Cell Velocity Profiles and Blood Flow in Rat Skeletal Muscle Arterioles

2012 ◽  
Vol 19 (4) ◽  
pp. 327-335 ◽  
Author(s):  
BARAA K. AL-KHAZRAJI ◽  
NICOLE M. NOVIELLI ◽  
DANIEL GOLDMAN ◽  
PHILIP J. MEDEIROS ◽  
DWAYNE N. JACKSON
1998 ◽  
Vol 274 (2) ◽  
pp. H430-H440 ◽  
Author(s):  
Miklós Pál ◽  
András Tóth ◽  
Peipei Ping ◽  
Paul C. Johnson

NADH fluorescence at tissue sites 15–20 μm in diameter and red blood cell velocity in adjacent capillaries were measured in resting sartorius muscle of the anesthetized cat during a 3-min period of sympathetic trunk stimulation. At stimulation frequencies of 2 and 4 Hz, red blood cell velocity fell briefly to 30–40% of control and then returned to ∼75% of control values (vascular escape). No change in NADH fluorescence was observed. With stimulus frequencies of 6–12 Hz, flow reduction was greater and led to an increase in fluorescence when the flow reduction was >50% and was sustained for >30 s. NADH changes were more pronounced at tissue sites near venous capillaries than at sites near arterial capillaries. Hyperemia ensued after the end of sympathetic stimulation only when NADH fluorescence rose during stimulation. Resting blood flow in this muscle appears to be well above the minimum required to support oxidative metabolism. A shift to anaerobic metabolism does not appear to cause vascular escape during sympathetic stimulation but appears to be required for poststimulation hyperemia. These observations suggest that two separate oxygen-dependent mechanisms elicit vasodilation during and after sympathetic trunk stimulation.


1993 ◽  
Vol 265 (5) ◽  
pp. H1510-H1515 ◽  
Author(s):  
G. E. Kuhnle ◽  
A. R. Pries ◽  
A. E. Goetz

We have developed a new in vivo microscopic technique for comprehensive measurements of vessel diameter, segment length, and red blood cell velocity in discrete arteriolar vessel trees of the lung. In anesthetized and mechanically ventilated rabbits, a transparent window was implanted into the right thoracic wall. We injected fluorescently labeled red cells to visualize blood flow and to measure red blood cell velocity. The distribution of microvascular pressures was simulated in a computer model based on morphometric and microhemodynamic data. Of the total pulmonary vascular pressure drop from pulmonary artery to left atrium, on average 2.5% occurred in distal arteriolar vessel trees with main trunk diameters of 73-111 microns. Along the pathlength from main trunk to terminal arterioles (0.18-2.79 mm), the pressure drop ranged between 0.06 and 0.94 mmHg. The pressure drop along individual pathways correlated significantly with pathlength of terminal arterioles, whereas red blood cell velocity did not. The results indicate that in terminal arteriolar vessel trees of the ventilated rabbit lung the resistance to blood flow is low, and the heterogeneity of microvascular pressures in arterioles feeding capillary networks is high.


1990 ◽  
Vol 258 (6) ◽  
pp. H1918-H1924 ◽  
Author(s):  
R. L. Hester

During increases in blood flow, both the terminal and the proximal arterioles dilate. The mechanism behind the dilation of the proximal arterioles is not known but may be the result of the diffusion of a vasoactive metabolite from adjacent venules. To determine whether an increase in venous adenosine (ADO) concentration could affect an adjacent arteriole, venules were perfused using a micropipette containing 10(-7)-10(-4) M ADO. During the venular perfusion, arteriolar diameter and red blood cell velocity were measured at a site 0.5 to 6 mm from the micropipette tip. The adjacent arteriole of the venular arteriolar pair dilated 29 +/- 3% with a 5-s 10(-4) M ADO perfusion, 32 +/- 4% with a 10-s 10(-4) M ADO perfusion, and 85 +/- 22% with a 60-s 10(-4) M ADO perfusion. One and 2-min perfusions with 10(-5) M ADO resulted in a 36 +/- 6% and 33 +/- 4% increase in diameter of the paired arteriole, respectively. The red blood cell velocity responses were variable, yet, on average, calculated blood flow increased in each group of experiments. Venular perfusions with saline resulted in a 2% change in arteriolar diameter. To rule out nondiffusional effects, venular perfusions were performed when the arteriole was not paired with the venule but crossed the venule. Venular perfusion with 10(-6) and 10(-7) M ADO resulted in a significant increase in diameter of the crossing arteriole of 19 +/- 3% and 6 +/- 2%, respectively. Therefore, the diffusion of a vasoactive metabolite from a venule to an arteriole may provide a mechanism by which the tissue can send a signal to cause a dilation of the more proximal arterioles.


1988 ◽  
Vol 254 (2) ◽  
pp. H331-H339 ◽  
Author(s):  
L. Kuo ◽  
R. N. Pittman

Experiments were performed on the hamster cheek pouch retractor muscle to investigate the influence of isovolemic hemodilution on microcirculatory hemodynamics and the rate of oxygen transport to striated muscle. In 23 hamsters, measurements of red blood cell velocity, hematocrit, vessel diameter, segment length (L), hemoglobin oxygen saturation (SO2), and longitudinal SO2 gradient (delta SO2/L) were made in four branching orders of arterioles before and after isovolemic exchange with plasma. Hemodilution decreased systemic hematocrit from 52 to 33%. In first- through fourth-order arterioles, this degree of hemodilution resulted in an average decrease in microcirculatory hematocrit from 42 to 28% and average increases in red blood cell velocity, computed blood flow, and systemic arterial PO2 of 50, 30, and 10%, respectively. In addition, delta SO2/L was significantly smaller in second-, third-, and fourth order arterioles compared with control values. It was estimated that approximately 84% of the oxygen that diffused across the arteriolar network was transferred by diffusion to nearby venules and capillaries; the remaining oxygen was consumed by the surrounding tissue. Following hemodilution, the magnitude of diffusional transfer declined to 73%. Oxygen flow remained at its control level in the first-order arterioles and progressively increased above control with increasing branching order. The increased oxygen delivery to the capillary network after limited hemodilution can be attributed to a compensatory increase in blood flow, an increase in systemic arterial blood oxygenation, and a decrease in precapillary oxygen loss.


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