Desmopressin improves intestinal functional capillary density and decreases leukocyte activation in experimental endotoxemia

2015 ◽  
Vol 97 ◽  
pp. 98-104 ◽  
Author(s):  
K Wafa ◽  
C Lehmann ◽  
L Wagner ◽  
I Drzymulski ◽  
A Wegner ◽  
...  
Critical Care ◽  
2011 ◽  
Vol 15 (S1) ◽  
Author(s):  
L Wagner ◽  
I Drzymulski ◽  
D Pavlovic ◽  
D Henzlers ◽  
M Wendt ◽  
...  

2006 ◽  
Vol 291 (5) ◽  
pp. H2445-H2452 ◽  
Author(s):  
Pedro Cabrales ◽  
Amy G. Tsai

The hamster window chamber model was used to study systemic and microvascular hemodynamic responses to extreme hemodilution with low- and high-viscosity plasma expanders (LVPE and HVPE, respectively) to determine whether plasma viscosity is a factor in homeostasis during extreme anemic conditions. Moderated hemodilution was induced by two isovolemic steps performed with 6% 70-kDa dextran until systemic hematocrit (Hct) was reduced to 18% ( level 2). In a third isovolemic step, hemodilution with LVPE (6% 70-kDa dextran, 2.8 cP) or HVPE (6% 500-kDa dextran, 5.9 cP) reduced Hct to 11%. Systemic parameters, cardiac output (CO), organ flow distribution, microhemodynamics, and functional capillary density, were measured after each exchange dilution. Fluorescent-labeled microspheres were used to measure organ (brain, heart, kidney, liver, lung, and spleen) and window chamber blood flow. Final blood and plasma viscosities after the entire protocol were 2.1 and 1.4 cP, respectively, for LVPE and 2.8 and 2.2 cP, respectively, for HVPE (baseline = 4.2 and 1.2 cP, respectively). HVPE significantly elevated mean arterial pressure and CO compared with LVPE but did not increase vascular resistance. Functional capillary density was significantly higher for HVPE [87% (SD 7) of baseline] than for LVPE [42% (SD 11) of baseline]. Increases in mean arterial blood pressure, CO, and shear stress-mediated factors could be responsible for maintaining organ and microvascular perfusion after exchange with HVPE compared with LVPE. Microhemodynamic data corresponded to microsphere-measured perfusion data in vital organs.


1990 ◽  
Vol 10 (3) ◽  
pp. 317-326 ◽  
Author(s):  
Albert Gjedde ◽  
Hiroto Kuwabara ◽  
Antoine M. Hakim

The blood flow of brain tissue often returns to normal after an ischemic episode. As “luxury” rather than “reactive” reperfusion, this hyperemia is associated with low metabolism. It is not known to what extent the high blood flow accompanies a high, normal, or low density of capillaries. The resolution of this question may indicate whether the functional capillary density is variable and, if so, whether it is coupled to blood flow or metabolism. To answer these questions, we defined functional capillaries as capillaries that transport glucose. We then calculated the density of functional capillaries ( Dcap) and the mean time of transit of blood through the capillaries ( tcap) from hemodynamic variables obtained in vivo by positron tomography of five patients afflicted by cerebral ischemic stroke. Each patient was studied twice, within 36 h of the insult and 1 week later. We identified nominally “ischemic” regions in the first study as cortical gray matter regions, contiguous with the ischemic focus, in which the magnitude of blood flow did not exceed 20 ml 100 g−1 min−1. In these regions, values of metabolism and functional capillary density were proportionately low compared with normal values obtained in the contralateral hemisphere. The studies revealed a reduction of the functional density of exchange vessels in postischemic brain tissue as soon as 36 h after the insult. In “ischemic” regions, within 36 h of the insult, the net extraction of oxygen was inversely related to the capillary transit time and appeared to be limited mainly by the low functional density of the capillaries. Contrary to expectations, the reduced density persisted, even when more than adequate perfusion of the tissue returned. For these reasons, we concluded that changes of the capillary density were associated with changes of the metabolism of the tissue rather than with blood flow.


2005 ◽  
Vol 58 (2) ◽  
pp. 425-425 ◽  
Author(s):  
J Kroth ◽  
K Weidlich ◽  
S Hiedl ◽  
A Bauer ◽  
F Christ ◽  
...  

2007 ◽  
Vol 112 (8) ◽  
pp. 429-440 ◽  
Author(s):  
Yves Harder ◽  
Michaela Amon ◽  
Mirko Georgi ◽  
Claudia Scheuer ◽  
Rene Schramm ◽  
...  

In the present study in a murine model of chronic ischaemia, we analysed: (i) whether aging was associated with an increased susceptibility to ischaemic necrosis, and (ii) whether this was based on microvascular dysfunction or reduced ischaemic tolerance. An ischaemic pedicled skin flap was created in the ear of homozygous hairless mice. The animals were assigned to three age groups, including adolescent (2±1 months), adult (10±2 months) and senescent (19±3 months). Microvascular perfusion of the ischaemic flap was assessed over 5 days by intravital microscopy, evaluating FCD (functional capillary density), capillary dilation response and the area of tissue necrosis. Expression of the stress-protein HO (haem oxygenase)-1 was determined by immunohistochemistry and Western blotting. Induction of chronic ischaemia stimulated a significant expression of HO-1 without a significant difference between the three age groups. This was associated with capillary dilation, which, however, was more pronounced in adolescent (10.5±2.8 μm compared with 3.95±0.79 μm at baseline) and adult (12.1±3.1 μm compared with 3.36±0.45 μm at baseline) animals compared with senescent animals (8.5±1.7 μm compared with 3.28±0.69 μm at baseline; P value not significant). In senescent animals, flap creation further resulted in complete cessation of capillary flow in the distal area of the flap (FCD, 0±0 cm/cm2), whereas adult (11.9±13.5 cm/cm2) and, in particular, adolescent animals (58.4±33.6 cm/cm2; P<0.05) were capable of maintaining residual capillary perfusion. The age-associated microcirculatory dysfunction resulted in a significantly increased flap necrosis of 49±8% (P<0.05) and 42±8% (P<0.05) in senescent and adult animals respectively, compared with 31±6% in adolescent mice. Of interest, functional inhibition of HO-1 by SnPP-IX (tin protoporphyrin-IX) in adolescent mice abrogated capillary dilation, decreased functional capillary density and aggravated tissue necrosis comparably with that observed in senescent mice. Thus aging is associated with an increased susceptibility to tissue necrosis, which is due to a loss of vascular reactivity to endogenous HO-1 expression, rather than a reduction in ischaemic tolerance.


Neonatology ◽  
2011 ◽  
Vol 99 (1) ◽  
pp. 73-77 ◽  
Author(s):  
A.P.C. Top ◽  
M. van Dijk ◽  
J.E. van Velzen ◽  
C. Ince ◽  
D. Tibboel

1997 ◽  
Vol 272 (4) ◽  
pp. H1710-H1716 ◽  
Author(s):  
M. Steinbauer ◽  
A. G. Harris ◽  
K. Messmer

The objectives of this study were 1) to elucidate the effects of dextran (Dx) at a nonhemodiluting dose of 5 mg/kg on ischemia-reperfusion injury in striated muscle and 2) to investigate whether the effects are dependent on the molecular weight of Dx. We used the model of a 4-h pressure-induced ischemia in the hamster skinfold chamber. By means of intravital microscopy the following parameters were assessed: vessel diameter, red blood cell velocity, rolling and adherent leukocytes, macromolecular extravasation, and functional capillary density. The animals received a continuous infusion (total dose 5 mg/kg) of dextran of different molecular weights or equivalent volumes of saline. Seven groups were studied: NaCl (control, n = 6), Dx 1 (n = 6), Dx 40 (n = 7), Dx 60 (n = 6), Dx 70 (n = 7), Dx 110 (n = 7), and Dx 150 (n = 7). Leukocyte rolling was reduced by all Dx fractions, the difference from the control reaching significance 0.5 h after reperfusion in the Dx 60, Dx 70, and Dx 110 group, whereas leukocyte adherence was attenuated by > 40,000-mol-wt Dx at 0.5 h after reperfusion. Concomitantly, functional capillary density tended to improve after treatment with > or = 40,000-mol-wt Dx. However, all Dx fractions studied failed to reduce postischemic macromolecular extravasation. These results provide evidence that Dx at 5 mg/kg attenuates postischemic microvascular disturbances; this effect is molecular weight dependent.


Sign in / Sign up

Export Citation Format

Share Document