scholarly journals Intravital microscopic observation of the microvasculature during hemodialysis in healthy rats

2022 ◽  
Vol 12 (1) ◽  
Author(s):  
B. G. H. Janssen ◽  
Y. M. Zhang ◽  
I. Kosik ◽  
A. Akbari ◽  
C. W. McIntyre
Keyword(s):  
Cardiovascular Disease ◽  
Blood Flow ◽  
Microscopic Observation ◽  
Physiological Stress ◽  
Small Animal ◽  
Organ Injury ◽  
Microvascular Blood Flow ◽  
Systemic Hemodynamic ◽  
Direct Demonstration ◽  
Wistar Kyoto

AbstractHemodialysis (HD) provides life-saving treatment for kidney failure. Patient mortality is extremely high, with cardiovascular disease (CVD) being the leading cause of death. This results from both a high underlying burden of cardiovascular disease, as well as additional physiological stress from the HD procedure itself. Clinical observations indicate that HD is associated with microvascular dysfunction (MD), underlining the need for a fundamental pathophysiological assessment of the microcirculatory consequences of HD. We therefore successfully developed an experimental small animal model, that allows for a simultaneous real-time assessment of the microvasculature. Using in-house built ultra-low surface area dialyzers and miniaturized extracorporeal circuit, we successfully dialyzed male Wistar Kyoto rats and combined this with a simultaneous intravital microscopic observation of the EDL microvasculature. Our results show that even in healthy animals, a euvolemic HD procedure can induce a significant systemic hemodynamic disturbance and induce disruption of microvascular perfusion (as evidence by a reduction in the proportion of the observed microcirculation receiving blood flow). This study, using a new small animal hemodialysis model, has allowed direct demonstration that microvascular blood flow in tissue in skeletal muscle is acutely reduced during HD, potentially in concert with other microvascular beds. It shows that preclinical small animal models can be used to further investigate HD-induced ischemic organ injury and allow rapid throughput of putative interventions directed at reducing HD-induced multi-organ ischemic injury.

Effect of a maldistribution of microvascular blood flow on capillary O2 extraction in sepsis

2002 ◽  
Vol 282 (1) ◽  
pp. H156-H164 ◽  
Author(s):  
Christopher G. Ellis ◽  
Ryon M. Bateman ◽  
Michael D. Sharpe ◽  
William J. Sibbald ◽  
Ravi Gill
Keyword(s):  
Blood Flow ◽  
Imaging System ◽  
Early Stage ◽  
Cecal Ligation ◽  
Organ Injury ◽  
Microvascular Blood Flow ◽  
Stopped Flow ◽  
O2 Extraction ◽  
Remote Organ Injury ◽  
Fast Flow

Inherent in the remote organ injury caused by sepsis is a profound maldistribution of microvascular blood flow. Using a 24-h rat cecal ligation and perforation model of sepsis, we studied O2 transport in individual capillaries of the extensor digitorum longus (EDL) skeletal muscle. We hypothesized that erythrocyte O2 saturation (So 2) levels within normally flowing capillaries would provide evidence of either a mitochondrial failure (increased So 2) or an O2 transport derangement (decreased So 2). Using a spectrophotometric functional imaging system, we found that sepsis caused 1) an increase in stopped flow capillaries (from 10 to 38%, P < 0.05), 2) an increase in the proportion of fast-flow to normal-flow capillaries ( P< 0.05), and 3) a decrease in capillary venular-end So 2 levels from 58.4 ± 20.0 to 38.5 ± 21.2%, whereas capillary arteriolar-end So 2levels remained unchanged compared with the sham group. Capillary O2 extraction increased threefold ( P < 0.05) and was directly related to the degree of stopped flow in the EDL. Thus impaired O2 transport in early stage sepsis is likely the result of a microcirculatory dysfunction.

Laser-Doppler perfusion imaging of microvascular blood flow in rabbit tenuissimus muscle

1995 ◽  
Vol 269 (4) ◽  
pp. H1496-H1500 ◽  
Author(s):  
M. Linden ◽  
A. Sirsjo ◽  
L. Lindbom ◽  
G. Nilsson ◽  
A. Gidlof
Keyword(s):  
Blood Flow ◽  
Microscopic Observation ◽  
Atmospheric Oxygen ◽  
Tissue Perfusion ◽  
Laser Doppler ◽  
Microvascular Blood Flow ◽  
Flow Measurements ◽  
Flow Changes ◽  
Blood Flow Measurements

To evaluate a newly developed high-resolution laser-Doppler perfusion imager (HR-LDPI) for analysis of local tissue perfusion, blood flow measurements in the rabbit tenuissimus muscle were carried out in combination with intravital microscopic observation. The principle of the LDPI method is based on a low-power laser beam scan of the exposed tissue from which a two-dimensional color-coded perfusion map is created through computerized signal analysis. The perfusion of the tenuissimus muscle prepared for microscopic observation was analyzed in a 5 mm x 8 mm area as the muscle was exposed to atmospheric oxygen tension (Po2; 20 kPa), a low Po2 (approximately 3 kPa), and after vasodilatation induced by topical application of prostaglandin E2 (PGE2). In selected areas free from larger vessels, a significantly lower perfusion average reading was demonstrated under high Po2 conditions compared with low Po2 conditions (P < 0.05, n = 5 animals), and application of PGE2 gave rise to an average reading significantly higher than that at low Po2 (P < 0.01, n = 6 animals). The results were in good agreement with the flow changes observed microscopically, and the architecture of the microvascular network, as depicted by in vivo micrographs, was clearly recognizable in the perfusion images. In conclusion, blood flow changes in the rabbit tenuissimus muscle induced by various stimuli were quantitated with the HR-LDPI method and could be spatially resolved in great detail, illustrating the potential of using HR-LDPI for analysis of local blood flow and to reveal spatial perfusion heterogeneity in tissues.

1715-P: Impaired Postprandial Adipose Tissue Microvascular Blood Flow in Healthy People with a Family History of Type 2 Diabetes

Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1715-P
Author(s):  
KATHERINE ROBERTS-THOMSON ◽  
RYAN D. RUSSELL ◽  
DONGHUA HU ◽  
TIMOTHY M. GREENAWAY ◽  
ANDREW C. BETIK ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Blood Flow ◽  
Adipose Tissue ◽  
Family History ◽  
Healthy People ◽  
Microvascular Blood Flow ◽  
History Of

Excess oxygen delivery during muscle contractions in spontaneously hypertensive rats

1995 ◽  
Vol 78 (1) ◽  
pp. 101-111 ◽  
Author(s):  
J. M. Lash ◽  
H. G. Bohlen
Keyword(s):  
Blood Flow ◽  
Oxygen Saturation ◽  
Oxygen Delivery ◽  
Spontaneously Hypertensive Rats ◽  
Muscle Contractions ◽  
Hypertensive Rats ◽  
Hemoglobin Oxygen Saturation ◽  
Spontaneously Hypertensive ◽  
Tissue Po2 ◽  
Wistar Kyoto

These experiments determined whether a deficit in oxygen supply relative to demand could account for the sustained decrease in tissue PO2 observed during contractions of the spinotrapezius muscle in spontaneously hypertensive rats (SHR). Relative changes in blood flow were determined from measurements of vessel diameter and red blood cell velocity. Venular hemoglobin oxygen saturation measurements were performed by using in vivo spectrophotometric techniques. The relative dilation [times control (xCT)] of arteriolar vessels during contractions was as large or greater in SHR than in normotensive rats (Wistar-Kyoto), as were the increases in blood flow (2 Hz, 3.50 +/- 0.69 vs. 3.00 +/- 1.05 xCT; 4 Hz, 10.20 +/- 3.06 vs. 9.00 +/- 1.48 xCT; 8 Hz, 16.40 +/- 3.95 vs. 10.70 +/- 2.48 xCT). Venular hemoglobin oxygen saturation was lower in the resting muscle of SHR than of Wistar-Kyoto rats (31.0 +/= 3.0 vs. 43.0 +/- 1.9%) but was higher in SHR after 4- and 8-Hz contractions (4 Hz, 52.0 +/- 4.8 vs. 43.0 +/- 3.6%; 8 Hz, 51.0 +/- 4.6 vs. 41.0 +/- 3.6%). Therefore, an excess in oxygen delivery occurs relative to oxygen use during muscle contractions in SHR. The previous and current results can be reconciled by considering the possibility that oxygen exchange is limited in SHR by a decrease in anatomic or perfused capillary density, arteriovenular shunting of blood, or decreased transit time of red blood cells through exchange vessels.

Nitric oxide release in rat skeletal muscle capillary

1996 ◽  
Vol 270 (5) ◽  
pp. H1696-H1703 ◽  
Author(s):  
D. Mitchell ◽  
K. Tyml
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Leukocyte Adhesion ◽  
Microvascular Blood Flow ◽  
Capillary Length ◽  
Nitric Oxide Release ◽  
Longus Muscle ◽  
Potent Vasodilator ◽  
Capillary Bed ◽  
Synthase Inhibitor

Nitric oxide (NO) has been shown to be a potent vasodilator released from endothelial cells (EC) in large blood vessels, but NO release has not been examined in the capillary bed. Because the capillary bed represents the largest source of EC, it may be the largest source of vascular NO. In the present study, we used intravital microscopy to examine the effect of the NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), on the microvasculature of the rat extensor digitorum longus muscle. L-NAME (30 mM) applied locally to a capillary (300 micron(s) from the feeding arteriole) reduced red blood cell (RBC) velocity [VRBC; control VRBC = 238 +/- 58 (SE) micron/s; delta VRBC = -76 +/- 8%] and RBC flux (4.4 +/- 0.7 to 2.8 +/- 0.7 RBC/s) significantly in the capillary, but did not change feeding arteriole diameter (Dcon = 6.3 +/- 0.7 micron, delta D = 5 +/- 7%) or draining venule diameter (Dcon = 10.1 +/- 0.6 micron, delta D = 4 +/- 2%). Because of the VRBC change, the flux reduction was equivalent to an increased local hemoconcentration from 1.8 to 5 RBCs per 100 micron capillary length. L-NAME also caused an increase in the number of adhering leukocytes in the venule from 0.29 to 1.43 cells/100 micron. L-NAME (30 mM) applied either to arterioles or to venules did not change capillary VRBC. Bradykinin (BK) locally applied to the capillary caused significant increases in VRBC (delta VRBC = 111 +/- 23%) and in arteriolar diameter (delta D = 40 +/- 5%). This BK response was blocked by capillary pretreatment with 30 mM L-NAME (delta VRBC = -4 +/- 27%; delta D = 5 +/- 9% after BK). We concluded that NO may be released from capillary EC both basally and in response to the vasodilator BK. We hypothesize that 1) low basal levels of NO affect capillary blood flow by modulating local hemoconcentration and leukocyte adhesion, and 2) higher levels of NO (stimulated by BK) may cause a remote vasodilation to increase microvascular blood flow.

scholarly journals Two-step machine learning method for the rapid analysis of microvascular flow in intravital video microscopy

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ossama Mahmoud ◽  
Mahmoud El-Sakka ◽  
Barry G. H. Janssen
Keyword(s):  
Machine Learning ◽  
Blood Flow ◽  
Human Error ◽  
Image Data ◽  
Video Microscopy ◽  
Microvascular Blood Flow ◽  
Image Processing Algorithm ◽  
Step Algorithm ◽  
3D Cnn

AbstractMicrovascular blood flow is crucial for tissue and organ function and is often severely affected by diseases. Therefore, investigating the microvasculature under different pathological circumstances is essential to understand the role of the microcirculation in health and sickness. Microvascular blood flow is generally investigated with Intravital Video Microscopy (IVM), and the captured images are stored on a computer for later off-line analysis. The analysis of these images is a manual and challenging process, evaluating experiments very time consuming and susceptible to human error. Since more advanced digital cameras are used in IVM, the experimental data volume will also increase significantly. This study presents a new two-step image processing algorithm that uses a trained Convolutional Neural Network (CNN) to functionally analyze IVM microscopic images without the need for manual analysis. While the first step uses a modified vessel segmentation algorithm to extract the location of vessel-like structures, the second step uses a 3D-CNN to assess whether the vessel-like structures have blood flowing in it or not. We demonstrate that our two-step algorithm can efficiently analyze IVM image data with high accuracy (83%). To our knowledge, this is the first application of machine learning for the functional analysis of microvascular blood flow in vivo.

On the poro-elastic models for microvascular blood flow resistance: An in vitro validation

2021 ◽  
Vol 117 ◽  
pp. 110241
Author(s):  
Alberto Coccarelli ◽  
Supratim Saha ◽  
Tanjeri Purushotham ◽  
K. Arul Prakash ◽  
Perumal Nithiarasu
Keyword(s):  
Blood Flow ◽  
Flow Resistance ◽  
Microvascular Blood Flow
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