Microcirculatory responses in cat sartorius muscle to hemorrhagic hypotension

1989 ◽  
Vol 257 (5) ◽  
pp. H1647-H1655 ◽  
Author(s):  
I. P. Torres Filho ◽  
M. A. Boegehold ◽  
E. Bouskela ◽  
S. D. House ◽  
P. C. Johnson

The purpose of this study was to examine changes in the microcirculation that might explain the rise in vascular resistance during hemorrhagic hypotension. Diameter and red blood cell velocity of microcirculatory vessels in exteriorized cat sartorius muscles were studied during 4 h of hemorrhagic hypotension at 60 mmHg. During hypotension, vascular resistance of the muscles rose approximately 70% while calculated volume flow in arterioles and venules fell to about the same degree. Average red blood cell velocity for all capillaries showed a comparable decline. Red blood cell flow stopped in approximately 60% of capillaries, but the extent of stoppage varied greatly among capillary fields. Arterioles larger than 45 microns constricted 9-29%, with the largest arterioles showing the greatest constriction. Arterioles smaller than 45 microns dilated 34-56%, with the smallest arterioles showing the greatest dilation. Venular diameter did not change with hemorrhage. The predominance of arteriolar dilation, especially in the later stages of hypotension, should lead to a fall in vascular resistance of the muscle. This effect may be offset by constriction of arteries outside the microcirculatory field observed and blockage of capillaries or venules by formed elements.

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.


2015 ◽  
Vol 3 (S1) ◽  
Author(s):  
VS Kanoore Edul ◽  
C Ince ◽  
A Risso Vazquez ◽  
PN Rubatto ◽  
ED Valenzuela Espinoza ◽  
...  

1996 ◽  
Vol 31 (4) ◽  
pp. 512-515 ◽  
Author(s):  
Roland J. Beuk ◽  
Mirjam G.A. oude Egbrink ◽  
Harrie A.J.M. Kurvers ◽  
Harm-Jan Bonke ◽  
Geert-Jan Tangelder ◽  
...  

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