Hemorrhagic hypotension induces arteriolar vasomotion and intermittent capillary perfusion in rat pancreas

1994 ◽  
Vol 267 (5) ◽  
pp. H1936-H1940 ◽  
Author(s):  
B. Vollmar ◽  
G. Preissler ◽  
M. D. Menger
Keyword(s):  
Blood Cell ◽  
Microscopic Analysis ◽  
Capillary Density ◽  
Functional Capillary Density ◽  
Intravital Fluorescence Microscopy ◽  
Capillary Perfusion ◽  
Induced Hypotension ◽  
Rat Pancreas ◽  
Hemorrhagic Hypotension ◽  
Acinar Tissue

Hemorrhage-induced intermittent capillary perfusion and its relation to arteriolar vasomotion was studied in rat pancreatic acinar tissue using intravital fluorescence microscopy. During prehemorrhage conditions, microscopic analysis of the pancreatic microcirculation displayed neither arteriolar vasomotion nor intermittency of capillary perfusion (n = 22 animals). Hemorrhage-induced hypotension of 40 mmHg provoked arteriolar vasomotion in 18 of 22 animals and 59 of 115 arterioles studied. The maximum relative amplitude of arteriolar vasomotion was 44 +/- 8% (range 12–81%), and vasomotion frequency averaged 4.73 +/- 0.11 cycles/min. Hemorrhagic hypotension was further accompanied by 1) a decrease of functional capillary density [length of red blood cell-perfused capillaries per area of tissue under investigation (cm/cm2)] from 515 +/- 3 cm-1 at baseline to 386 +/- 3 cm-1 (P < 0.05) and 2) the instantaneous occurrence of intermittency of capillary perfusion in all observation areas (N = 220) of the 22 animals studied. The frequency of intermittency of capillary perfusion (4.72 +/- 0.14 cycles/min) did not differ from the frequency of arteriolar vasomotion, which implies a causal relationship between these two hemorrhage-induced microvascular mechanisms with the probable aim to counteract the decrease of functional capillary density.

Evolution of a “falx lunatica” in demarcation of critically ischemic myocutaneous tissue

2005 ◽  
Vol 288 (3) ◽  
pp. H1224-H1232 ◽  
Author(s):  
Yves Harder ◽  
Michaela Amon ◽  
Mirko Georgi ◽  
Andrej Banic ◽  
Dominique Erni ◽  
...  
Keyword(s):  
Capillary Density ◽  
Functional Capillary Density ◽  
Tissue Necrosis ◽  
Capillary Perfusion ◽  
Edema Formation ◽  
Perfusion Failure ◽  
Ischemic Tissue ◽  
Flap Elevation ◽  
Observation Period

Using intravital microscopy in a chronic in vivo mouse model, we studied the demarcation of myocutaneous flaps and evaluated microvascular determinants for tissue survival and necrosis. Chronic ischemia resulted in a transition zone, characterized by a red fringe and a distally adjacent white falx, which defined the demarcation by dividing the proximally normal from the distally necrotic tissue. Tissue survival in the red zone was determined by hyperemia, as indicated by recovery of the transiently reduced functional capillary density, and capillary remodeling, including dilation, hyperperfusion, and increased tortuosity. Angiogenesis and neovascularization were not observed over the 10-day observation period. The white rim distal to the red zone, appearing as “falx lunatica,” showed a progressive decrease of functional capillary density similar to that of the necrotic distal area but without desiccation, and thus transparency, of the tissue. Development of the distinct zones of the critically ischemic tissue could be predicted by partial tissue oxygen tension (Pt[Formula: see text]) analysis by the time of flap elevation. The falx lunatica evolved at a Pt[Formula: see text] between 6.2 ± 1.3 and 3.8 ± 0.7 mmHg, whereas tissue necrosis developed at <3.8 ± 0.7 mmHg. Histological analysis within the falx lunatica revealed interstitial edema formation and muscle fiber nuclear rarefaction but an absence of necrosis. We have thus demonstrated that ischemia-induced necrosis does not demarcate sharply from normal tissue but develops beside a fringe of tissue with capillary remodeling an adjacent falx lunatica that survives despite nutritive capillary perfusion failure, probably by direct oxygen diffusion.

Argatroban administration reduces leukocyte adhesion and improves capillary perfusion within the intestinal microcirculation in experimental sepsis

2010 ◽  
Vol 104 (11) ◽  
pp. 1022-1028 ◽  
Author(s):  
Christian Fuchs ◽  
Elena Ladwig ◽  
Juan Zhou ◽  
Dragan Pavlovic ◽  
Kristina Behrend ◽  
...  
Keyword(s):  
Leukocyte Adhesion ◽  
Capillary Density ◽  
Functional Capillary Density ◽  
Experimental Sepsis ◽  
Capillary Perfusion ◽  
Vascular Contractility ◽  
Intestinal Microcirculation ◽  
Sham Surgery ◽  
The Impact

SummaryCo-activation of pro-coagulatory pathways in sepsis may result in disseminated intravascular coagulation and contributes to microvascular dysfunction. We investigated the effects of the direct thrombin inhibitor, argatroban (ARG), on the sepsis-induced impairment of the intestinal microcirculation (capillary perfusion, leukocyte adhesion) and the vascular contractility in rats. Forty male Lewis rats were randomly assigned to one of four groups: sham surgery (SHAM), experimental sepsis (colon ascendens stent peritonitis – CASP), CASP+ARG, and SHAM+ARG. At 16 hours after colon stent insertion (or sham surgery), 2 mg/kg argatroban or buffer were given intravenously, and 1 hour thereafter, intravital microscopy was performed. In addition, experiments to study the impact of ARG on vascular contractility were conducted in vitro. ARG administration in CASP rats significantly increased functional capillary density in mucosal (+128%) and muscular layers (longitudinal: +42%; circular: +64%) and decreased the number of firmly adhering leukocytes in the intestinal submucosa compared to untreated animals. In vitro findings indicated a vasodilating effect of ARG. ARG administration during experimental sepsis improved intestinal microcirculation by preserving functional capillary density, an indicator of microvascular perfusion, and by reducing leukocyte adherence to the endothelium in submucosal venules.

scholarly journals Reduced uterine perfusion pressure decreases functional capillary density in skeletal muscle

2015 ◽  
Vol 309 (12) ◽  
pp. H2002-H2007 ◽  
Author(s):  
Graham M. Fraser ◽  
Jude S. Morton ◽  
Sydney M. Schmidt ◽  
Stephane Bourque ◽  
Sandra T. Davidge ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Continuous Flow ◽  
Perfusion Pressure ◽  
Capillary Density ◽  
Functional Capillary Density ◽  
Stopped Flow ◽  
Sprague Dawley ◽  
Capillary Perfusion ◽  
Pregnant State ◽  
Uterine Perfusion

The purpose of this study was to examine the functional and structural capillary density in the reduced uterine perfusion pressure (RUPP) model, which when performed during pregnancy is an established animal model of preeclampsia. We hypothesized that the RUPP model would be associated with capillary rarefaction and impaired capillary perfusion, which would be more pronounced in the pregnant state. Female Sprague-Dawley rats ( n = 32) were randomized to nonpregnancy (Nonpregnant) or breeding (Pregnant) at 12 wk of age and again to RUPP or SHAM surgeries on gestational day (GD) 14 (or equivalent age in nonpregnant rats). On GD 20 (or equivalent), capillary structure and perfusion of the extensor digitorum longus were imaged using digital intravital video microscopy. Functional videos were analyzed by a blinded observer to measure capillary density, expressed as capillaries per millimeter intersecting three staggered reference lines (200 μm). Flow was scored as the percentage of capillaries having 1) continuous, 2) intermittent, or 3) stopped flow. Total capillary density was not different between groups. There was a main effect of RUPP surgery resulting in decreased continuous flow vessels ( P < 0.01) and increased stopped flow ( P < 0.01), which was driven by differences between pregnant animals (Continuous flow: pregnant SHAM 80.1 ± 7.8% vs. pregnant RUPP 67.8 ± 11.2%, P < 0.05) (Stopped flow: pregnant SHAM 8.7 ± 3.2% vs. pregnant RUPP 17.9 ± 5.7%, P < 0.01). Our results demonstrate that the RUPP surgery is associated with a decrease in functional capillary density in skeletal muscle that is more pronounced in the pregnant state, which may contribute to the vascular pathophysiology observed in preeclampsia.

Effect of erythrocyte aggregation at normal human levels on functional capillary density in rat spinotrapezius muscle

2006 ◽  
Vol 290 (3) ◽  
pp. H941-H947 ◽  
Author(s):  
Sangho Kim ◽  
Aleksander S. Popel ◽  
Marcos Intaglietta ◽  
Paul C. Johnson
Keyword(s):  
Arterial Pressure ◽  
Blood Cell ◽  
Red Blood Cell ◽  
High Speed ◽  
Capillary Density ◽  
Functional Capillary Density ◽  
Erythrocyte Aggregation ◽  
Reduced Pressure ◽  
Healthy Humans ◽  
Plasma Skimming

Previous studies have shown that functional capillary density (FCD) is substantially reduced by erythrocyte aggregation. However, only supranormal levels of aggregability were studied. To investigate the effect of erythrocyte aggregability at the level seen in healthy humans, the FCD of selected capillary fields in rat spinotrapezius muscle was determined with high-speed video microscopy under normal (nonaggregating) conditions and after induction of erythrocyte aggregation with Dextran 500 (200 mg/kg). To examine shear rate dependence, the effect was studied both at normal and reduced arterial pressures (50 and 25 mmHg), the latter achieved by short periods of hemorrhage. In a separate study, volume flow was determined in arterioles (52.1 ± 3.7 μm) under the same conditions. Before Dextran 500 infusion, FCD fell to 91% and 76% of control values, respectively, when arterial pressure was reduced to 50 and 25 mmHg. After Dextran 500 infusion, FCD was 96% at normal arterial pressure and fell to 79% and 37% of normal control values at 50 and 25 mmHg. All FCD values were significantly lower after dextran infusion. FCD reduction after lowering arterial pressure or dextran infusion appeared to be due to plasma skimming rather than capillary plugging. Reduction of FCD by dextran at reduced pressure was compensated by increased red blood cell flux in capillaries with red blood cell flow. We conclude that the level of aggregability seen in healthy humans is an important determinant of FCD only at reduced arterial pressure.

Vasomotion in critically perfused muscle protects adjacent tissues from capillary perfusion failure

2000 ◽  
Vol 279 (2) ◽  
pp. H550-H558 ◽  
Author(s):  
M. Rücker ◽  
O. Strobel ◽  
B. Vollmar ◽  
F. Roesken ◽  
M. D. Menger
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Capillary Flow ◽  
Capillary Density ◽  
Functional Capillary Density ◽  
Sprague Dawley ◽  
Capillary Perfusion ◽  
Peripheral Tissues ◽  
Flow Motion ◽  
Stepwise Reduction

We analyzed the incidence and interaction of arteriolar vasomotion and capillary flow motion during critical perfusion conditions in neighboring peripheral tissues using intravital fluorescence microscopy. The gracilis and semitendinosus muscles and adjacent periosteum, subcutis, and skin of the left hindlimb of Sprague-Dawley rats were isolated at the femoral vessels. Critical perfusion conditions, achieved by stepwise reduction of femoral artery blood flow, induced capillary flow motion in muscle, but not in the periosteum, subcutis, and skin. Strikingly, blood flow within individual capillaries was decreased ( P < 0.05) in muscle but was not affected in the periosteum, subcutis, and skin. However, despite the flow motion-induced reduction of muscle capillary blood flow during the critical perfusion conditions, functional capillary density remained preserved in all tissues analyzed, including the skeletal muscle. Abrogation of vasomotion in the muscle arterioles by the calcium channel blocker felodipine resulted in a redistribution of blood flow within individual capillaries from cutaneous, subcutaneous, and periosteal tissues toward skeletal muscle. As a consequence, shutdown of perfusion of individual capillaries was observed that resulted in a significant reduction ( P < 0.05) of capillary density not only in the neighboring tissues but also in the muscle itself. We conclude that during critical perfusion conditions, vasomotion and flow motion in skeletal muscle preserve nutritive perfusion (functional capillary density) not only in the muscle itself but also in the neighboring tissues, which are not capable of developing this protective regulatory mechanism by themselves.

Microvascular and capillary perfusion following glycocalyx degradation

2007 ◽  
Vol 102 (6) ◽  
pp. 2251-2259 ◽  
Author(s):  
Pedro Cabrales ◽  
Beatriz Y. Salazar Vázquez ◽  
Amy G. Tsai ◽  
Marcos Intaglietta
Keyword(s):  
Blood Gases ◽  
Molecular Size ◽  
Capillary Density ◽  
Functional Capillary Density ◽  
Capillary Perfusion ◽  
Fluorescent Marker ◽  
Fluorescent Markers ◽  
Margin Of Error ◽  
Before And After ◽  
Chamber Model

Systemic parameters and microvascular and capillary hemodynamics were studied in the hamster window chamber model before and after hyaluronan degradation by intravenous injection of Streptomyces hyaluronidase (100 units, 40–50 U/ml plasma). Glycocalyx permeation was estimated using fluorescent markers of different molecular size (40, 70, and 2,000 kDa), and electrical charge. Systemic parameters (blood pressure, heart rate, blood gases) and microhemodynamics (vascular tone, velocity, and blood flow) remained statistically unchanged after injection of hyaluronidase, compared with inactivated hyaluronidase. Conversely, capillary hemodynamics were drastically affected. Functional capillary density, the capillaries perfused with red blood cells (RBCs), decreased by 35%, capillary Hct of the remaining functional capillaries increased from 16 to 27%, and penetration of 70-kDa fluorescent marker increased. Furthermore, plasma-only perfused capillaries statistically increased 30 min after hyaluronidase. The decrease in functional capillary density accounted for an increased RBC flux in the remainder of the capillaries, since the same number of RBCs had to traverse a reduced number of capillaries. Flux balances showed a reduction from baseline of 11% for the RBC flux and 20% for the plasma flux after treatment. These discrepancies are within the margin of error of the techniques used and could be explained by accounting for RBC over-velocity compared with plasma. These findings suggest that the decrease in the glycocalyx leads to capillary perfusion impairments.

Dexmedetomidine Attenuates the Microcirculatory Derangements Evoked by Experimental Sepsis

2015 ◽  
Vol 122 (3) ◽  
pp. 619-630 ◽  
Author(s):  
Marcos L. Miranda ◽  
Michelle M. Balarini ◽  
Eliete Bouskela
Keyword(s):  
Blood Gases ◽  
Capillary Density ◽  
Sepsis Syndrome ◽  
In Vivo Studies ◽  
Experimental Sepsis ◽  
Leukocyte Rolling ◽  
Capillary Perfusion ◽  
Arterial Blood ◽  
Baseline Values

Abstract Background: Dexmedetomidine, an α-2 adrenergic receptor agonist, has already been used in septic patients although few studies have examined its effects on microcirculatory dysfunction, which may play an important role in perpetuating sepsis syndrome. Therefore, the authors have designed a controlled experimental study to characterize the microcirculatory effects of dexmedetomidine in an endotoxemia rodent model that allows in vivo studies of microcirculation. Methods: After skinfold chamber implantation, 49 golden Syrian hamsters were randomly allocated in five groups: (1) control animals; (2) nonendotoxemic animals treated with saline; (3) nonendotoxemic animals treated with dexmedetomidine (5.0 μg kg−1 h−1); (4) endotoxemic (lipopolysaccharide 1.0 mg/kg) animals treated with saline; and (5) endotoxemic animals treated with dexmedetomidine. Intravital microscopy of skinfold chamber preparations allowed quantitative analysis of microvascular variables and venular leukocyte rolling and adhesion. Mean arterial blood pressure, heart rate, arterial blood gases, and lactate concentrations were also documented. Results: Lipopolysaccharide administration increased leukocyte rolling and adhesion and decreased capillary perfusion. Dexmedetomidine significantly attenuated these responses: compared with endotoxemic animals treated with saline, those treated with dexmedetomidine had less leukocyte rolling (11.8 ± 7.2% vs. 24.3 ± 15.0%; P &lt; 0.05) and adhesion (237 ± 185 vs. 510 ± 363; P &lt; 0.05) and greater functional capillary density (57.4 ± 11.2% of baseline values vs. 45.9 ± 11.2%; P &lt; 0.05) and erythrocyte velocity (68.7 ± 17.6% of baseline values vs. 54.4 ± 14.8%; P &lt; 0.05) at the end of the experiment. Conclusions: Dexmedetomidine decreased lipopolysaccharide-induced leukocyte–endothelial interactions in the hamster skinfold chamber microcirculation. This was accompanied by a significant attenuation of capillary perfusion deficits, suggesting that dexmedetomidine yields beneficial effects on endotoxemic animals’ microcirculation.

Microvascular ischemia-reperfusion injury in striated muscle: significance of "no reflow"

1992 ◽  
Vol 263 (6) ◽  
pp. H1892-H1900 ◽  
Author(s):  
M. D. Menger ◽  
D. Steiner ◽  
K. Messmer
Keyword(s):  
Shear Rate ◽  
Striated Muscle ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Capillary Density ◽  
Wall Shear Rate ◽  
Reactive Oxygen Metabolites ◽  
Capillary Perfusion ◽  
No Reflow ◽  
Oxygen Metabolites

“No reflow” has been implicated as prominent phenomenon in microvascular injury associated with ischemia-reperfusion (I/R). The objectives of this study were 1) to elucidate the significance of no reflow in microvascular I/R injury of striated muscle and 2) to determine whether reactive oxygen metabolites play a role in the development of postischemic no reflow. By use of the hamster dorsal skinfold preparation and intravital microscopy, microvascular perfusion of capillaries and postcapillary venules of striated muscle was quantitatively assessed before and 30 min, 2 h, and 24 h after 4 h of tourniquet-induced ischemia. I/R was characterized by a significant reduction (P < 0.01) in functional capillary density to 35% of baseline values during initial reperfusion, with incomplete recovery after 24 h (n = 9). In addition, capillary perfusion was found to be extremely heterogeneous, and wall shear rate in postcapillary venules was significantly decreased (P < 0.01). Treatment with either superoxide dismutase (SOD; n = 9) or allopurinol (n = 9) resulted in maintenance of capillary density of 60% of baseline (P < 0.05). Furthermore, I/R-induced capillary perfusion inhomogeneities and decrease of wall shear rate in venules were attenuated significantly (P < 0.01) by SOD and allopurinol. Thus part of capillary perfusion disturbances during I/R in striated muscle may be caused by increased postcapillary vascular resistance, probably mediated by reactive oxygen metabolites. However, the fact that in SOD- and allopurinol-treated animals 40% of the capillaries were still found to be nonperfused indicates that mechanisms other than oxygen radicals play an important role in the development of postischemic no reflow.

Plasma viscosity regulates systemic and microvascular perfusion during acute extreme anemic conditions

2006 ◽  
Vol 291 (5) ◽  
pp. H2445-H2452 ◽  
Author(s):  
Pedro Cabrales ◽  
Amy G. Tsai
Keyword(s):  
Flow Distribution ◽  
Capillary Density ◽  
High Viscosity ◽  
Plasma Viscosity ◽  
Functional Capillary Density ◽  
Microvascular Perfusion ◽  
Arterial Blood ◽  
Chamber Model ◽  
Kidney Liver ◽  
Window Chamber

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.

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