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.

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.

scholarly journals The Reduced Uterine Perfusion Pressure (RUPP) Model of Preeclampsia Causes Decreased Capillary Perfusion in Skeletal Muscle

2015 ◽  
Vol 29 (S1) ◽  
Author(s):  
Graham Fraser ◽  
Jude Morton ◽  
Sydney Schmidt ◽  
Stephane Bourque ◽  
Sandra Davidge ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Perfusion Pressure ◽  
Capillary Perfusion ◽  
Uterine Perfusion

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.

Abstract P208: Imaging The Longitudinal Reduction In Placental Ischemia In Response To Therapeutic Intervention For Preeclampsia

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Dylan J Lawrence ◽  
Carolyn Bayer
Keyword(s):  
Vascular Remodeling ◽  
Therapeutic Response ◽  
Perfusion Pressure ◽  
Sprague Dawley ◽  
Placental Function ◽  
Sprague Dawley Rats ◽  
Uterine Perfusion ◽  
Placental Ischemia ◽  
Phosphodiesterase 5

Preeclampsia is believed to be induced by abnormal vascular remodeling and the resulting placental ischemia during early development. Sildenafil, a phosphodiesterase-5 inhibitor, reduces the maternal symptoms of preeclampsia by promoting angiogenesis and enhancing NO-mediated vasodilation. However, the effect of sildenafil on in vivo placental function has not been demonstrated. We performed longitudinal spectral photoacoustic (sPA) imaging of placental therapeutic response to sildenafil in the reduced uterine perfusion pressure (RUPP) model of preeclampsia. Sprague Dawley rats were administered sildenafil (S) via drinking water beginning on gestational day (GD) 11. Imaging was performed on GD14, 16, and 18 with the RUPP procedure implemented after the first imaging session. sPA images of oxygenation show that the placental ischemia induced by the RUPP surgery (RUPP, n=8, 48%; NP, n=8, 54%), was effectively eliminated by treatment with sildenafil (RUPP+S, n=8, 53%, p<0.05). In addition to improved placental oxygenation, sildenafil was also found to reduce mean arterial pressure in RUPP animals by GD18 (RUPP, 110 mmHg; RUPP+S, 98 mmHg; p<0.05), consistent with prior reports. Our studies demonstrate that sPA imaging can detect changes in placental oxygenation which could be used to indicate in vivo placental therapeutic response. Figure 1: Placental hypoxia in the RUPP is improved by treatment with sildenafil on GD16. B-mode US images (a, c) of anatomy were used to manually select the placenta (p) and average placental oxygenation was calculated. A custom red-blue oxygenation colormap was then overlaid for visualization (b, d). Scale bars = 3mm.

Regional transcapillary albumin exchange in rodent endotoxaemia: effects of fluid resuscitation and inhibition of nitric oxide synthase

2000 ◽  
Vol 100 (1) ◽  
pp. 81-89 ◽  
Author(s):  
Suveer SINGH ◽  
Peter B. ANNING ◽  
C. Peter WINLOVE ◽  
Timothy W. EVANS
Keyword(s):  
Nitric Oxide ◽  
Skeletal Muscle ◽  
Surface Area ◽  
Blood Volume ◽  
Fluid Resuscitation ◽  
Volume Ratio ◽  
Capillary Density ◽  
Microvascular Permeability ◽  
Capillary Perfusion ◽  
Dual Isotope

Sepsis is characterized by increased microvascular permeability and regional variations in capillary perfusion, which may be modulated by nitric oxide (NO) and reversed by fluid resuscitation (FR). The effects of saline FR and NO synthase blockade [by NG-nitro-L-arginine methyl ester (L-NAME)] on microvascular albumin transport and perfused capillary density were assessed in anaesthetized Wistar rats with acute normodynamic endotoxaemia. Separate dual-isotope techniques were employed to measure the permeability index (PIA) and the permeability×surface area product index (PIB), which provide different and complementary information regarding blood–tissue albumin exchange. PIA represents the tissue/blood distribution volume ratio of albumin. PIB is a composite measure of endothelial permeability and the vascular surface area available for albumin exchange, and therefore takes into account the effect of altered blood volume. Capillary density was quantified by fluorescence microscopy following circulation of Evans Blue-labelled albumin. Compared with controls, PIA was reduced significantly in lipopolysaccharide (LPS)-treated animals in skeletal muscle and skin, probably due to blood volume redistribution rather than to changes in permeability. PIB was increased significantly in LPS-treated animals in the kidney, mesentery, skeletal muscle, skin and lung, and in the small bowel following FR. FR also improved the LPS-induced metabolic base deficit, but did not alter capillary density. L-NAME significantly attenuated the LPS-induced rise in PIB in the lung. In conclusion, acute endotoxaemia induces tissue-dependent variations in microvascular albumin exchange. FR improves acid–base disturbance in endotoxaemia, through mechanisms other than microvascular recruitment. NO appears to increase microvascular permeability in endotoxaemia, an effect that may be attenuated by L-NAME, particularly in the lung.

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.

Skeletal muscle microvascular and tissue injury after varying durations of ischemia

1996 ◽  
Vol 271 (6) ◽  
pp. H2388-H2398 ◽  
Author(s):  
A. G. Harris ◽  
R. Leiderer ◽  
F. Peer ◽  
K. Messmer
Keyword(s):  
Skeletal Muscle ◽  
Tissue Injury ◽  
Capillary Density ◽  
Vessel Diameter ◽  
Functional Capillary Density ◽  
Cell Nuclei ◽  
Microvascular Damage ◽  
Significant Difference ◽  
Red Blood Cell Velocity ◽  
Adherent Leukocytes

The purpose of this study was to examine the effect of varying durations of ischemia on several microvascular parameters in the awake hamster chamber model. The goal was to characterize the microvascular damage that occurs in skeletal muscle as a result of ischemia and reperfusion. The chamber tissues were subjected to 1-5 h of ischemia, and then the following parameters were measured: vessel diameter, endothelial thickness, macromolecular leakage, red blood cell velocity, adherent leukocytes, rolling leukocytes, freely flowing leukocytes, functional capillary density, and propidium iodide-positive cell nuclei. In control animals there was no significant difference in any parameters over the entire observation period. After 1 or 2 h of ischemia an increase in rolling and adherent leukocytes was measured. After 3 h of ischemia there was a significant increase in the mean endothelial thickness and in the number of nonviable cells. After 4 h of ischemia a significant difference in the extent of macromolecular leakage and the functional capillary density was additionally observed. After 5 h of ischemia this damage was more pronounced and often so severe that approximately 50% of the vessels demonstrated no reflow.

ACE2 and ANG-(1-7) in the rat uterus during early and late gestation

2008 ◽  
Vol 294 (1) ◽  
pp. R151-R161 ◽  
Author(s):  
Liomar A. A. Neves ◽  
Kathryn Stovall ◽  
JaNae Joyner ◽  
Gloria Valdés ◽  
Patricia E. Gallagher ◽  
...  
Keyword(s):  
Early Pregnancy ◽  
Perfusion Pressure ◽  
Late Pregnancy ◽  
Late Gestation ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Induced Hypertension ◽  
Uteroplacental Blood Flow ◽  
Uterine Perfusion

The present study was designed to determine ANG peptide content [ANG I, ANG II, ANG-(1-7)], ACE2 mRNA, and the immunocytochemical distribution of ANG-(1-7) and ACE2 in the uteroembryonic unit during early and late gestation in Sprague-Dawley rats and in a rat model of pregnancy-induced hypertension, the reduced uterine perfusion pressure (RUPP) model. At early pregnancy ANG-(1-7) and ACE2 staining were localized in the primary and secondary decidual zone and luminal and glandular epithelial cells. During late gestation, ANG-(1-7) and ACE2 staining was visualized in the labyrinth placenta and amniotic and yolk sac epithelium. Uterine ANG II concentration at early pregnancy was significantly decreased by 21–55% in the implantation and interimplantation sites compared with virgin rats, whereas ANG-(1-7) levels were maintained at prepregnancy levels. At late gestation, uterine concentrations of ANG I and ANG II were significantly increased (30% and 25%, respectively). In RUPP animals, ANG-(1-7) concentration is significantly reduced in the uterus (181 ± 16 vs. 372 ± 74 fmol/g of tissue) and placenta (143 ± 26 vs. 197 ± 20 fmol/g of tissue). ACE2 mRNA increased in the uterus of early pregnant compared with virgin rats, yet within the implantation site it was downregulated. At late pregnancy, ACE2 mRNA is elevated by 58% in the uterus and decreased by 59% in RUPP animals. The regulation of ANG-(1-7) and ACE2 in early and late pregnancy supports the hypothesis that ANG-(1-7) and ACE2 may act as a local autocrine/paracrine regulator throughout pregnancy, participating in the early (angiogenesis, apoptosis, and growth) and late (uteroplacental blood flow) events of pregnancy.

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