scholarly journals Understanding Vasomotion of Lung Microcirculation by In Vivo Imaging

2019 ◽  
Vol 5 (2) ◽  
pp. 22 ◽  
Author(s):  
Enrico Mazzuca ◽  
Andrea Aliverti ◽  
Giuseppe Miserocchi

The balance of lung extravascular water depends upon the control of blood flow in the alveolar distribution vessels that feed downstream two districts placed in parallel, the corner vessels and the alveolar septal network. The occurrence of an edemagenic condition appears critical as an increase in extravascular water endangers the thinness of the air–blood barrier, thus negatively affecting the diffusive capacity of the lung. We exposed anesthetized rabbits to an edemagenic factor (12% hypoxia) for 120 min and followed by in vivo imaging the micro-vascular morphology through a “pleural window” using a stereo microscope at a magnification of 15× (resolution of 7.2 μm). We measured the change in diameter of distribution vessels (50–200 μm) and corner vessels (<50 μm). On average, hypoxia caused a significant decrease in diameter of both smaller distribution vessels (about ~50%) and corner vessels (about ~25%) at 30 min. After 120 min, reperfusion occurred. Regional differences in perivascular interstitial volume were observed and could be correlated with differences in blood flow control. To understand such difference, we modelled imaged alveolar capillary units, obtained by Voronoi method, integrating microvascular pressure parameters with capillary filtration. Results of the analysis suggested that at 120 min, alveolar blood flow was diverted to the corner vessels in larger alveoli, which were found also to undergo a greater filtration indicating greater proneness to develop lung edema.

2019 ◽  
Vol 42 (8) ◽  
pp. 528-536 ◽  
Author(s):  
Jaime Grutzendler ◽  
Maiken Nedergaard

Ultrasonics ◽  
2009 ◽  
Vol 49 (2) ◽  
pp. 226-230 ◽  
Author(s):  
Chih-Kuang Yeh ◽  
Jia-Jiun Chen ◽  
Meng-Lin Li ◽  
Jer-Junn Luh ◽  
Jia-Jin Jason Chen

NeuroImage ◽  
2010 ◽  
Vol 49 (1) ◽  
pp. 337-344 ◽  
Author(s):  
Ofer Prager ◽  
Yoash Chassidim ◽  
Chen Klein ◽  
Haviv Levi ◽  
Ilan Shelef ◽  
...  

Author(s):  
Marko Jakovljevic ◽  
Lotfi Abou-Elkacem ◽  
Dongwoon Hyun ◽  
Jason Yoon ◽  
You Li ◽  
...  

Author(s):  
David A. Hartmann ◽  
Andrée-Anne Berthiaume ◽  
Roger I. Grant ◽  
Sarah A. Harrill ◽  
Tegan Noonan ◽  
...  

The majority of the brain’s vasculature is comprised of intricate capillary networks lined by capillary pericytes. However, it remains unclear whether capillary pericytes contribute to blood flow control. Using two-photon microscopy to observe and manipulate single capillary pericytes in vivo, we find their optogenetic stimulation decreases lumen diameter and blood flow, but with slower kinetics than mural cells of upstream pial and pre-capillary arterioles. This slow, optogenetically-induced vasoconstriction was inhibited by the clinically-used vasodilator fasudil, a Rho kinase inhibitor that blocks contractile machinery. Capillary pericytes were also slower to constrict back to baseline following hypercapnia-induced dilation, and relax towards baseline following optogenetically-induced vasoconstriction. In a complementary approach, optical ablation of single capillary pericytes led to sustained local dilation and a doubling of blood cell flux in capillaries lacking pericyte contact. Altogether these data indicate that capillary pericytes contribute to basal blood flow resistance and slow modulation of blood flow throughout the capillary bed.


Author(s):  
Yan Zeng ◽  
Bo Yan ◽  
Sun Qiqi ◽  
Sicong He ◽  
Jun Jiang ◽  
...  

2006 ◽  
Vol 101 (1) ◽  
pp. 307-315 ◽  
Author(s):  
Johan Fredrik Brekke ◽  
William F. Jackson ◽  
Steven S. Segal

Intracellular calcium concentration ([Ca2+]i) governs the contractile status of arteriolar smooth muscle cells (SMC). Although studied in vitro, little is known of SMC [Ca2+]i dynamics during the local control of blood flow. We tested the hypothesis that the rise and fall of SMC [Ca2+]i underlies arteriolar constriction and dilation in vivo. Aparenchymal segments of second-order arterioles (diameter 35 ± 2 μm) were prepared in the superfused cheek pouch of anesthetized hamsters ( n = 18) and perifused with the ratiometric dye fura PE-3 (AM) to load SMC (1 μM, 20 min). Resting SMC [Ca2+]i was 406 ± 37 nM. Elevating superfusate O2 from 0 to 21% produced constriction (11 ± 2 μm) that was unaffected by dye loading; [Ca2+]i increased by 108 ± 53 nM ( n = 6, P < 0.05). Cycling of [Ca2+]i during vasomotion (amplitude, 150 ± 53 nM; n = 4) preceded corresponding diameter changes (7 ± 1 μm) by ∼2 s. Microiontophoresis (1 μm pipette tip; 1 μA, 1 s) of phenylephrine (PE) transiently increased [Ca2+]i by 479 ± 64 nM ( n = 8, P < 0.05) with constriction (26 ± 3 μm). Flushing blood from the lumen with saline increased fluorescence at 510 nm by ∼45% during excitation at both 340 and 380 nm with no difference in resting [Ca2+]i, diameter or respective responses to PE ( n = 7). Acetylcholine microiontophoresis (1 μA, 1 s) transiently reduced resting SMC [Ca2+]i by 131 ± 21 nM ( n = 6, P < 0.05) with vasodilation (17 ± 1 μm). Superfusion of sodium nitroprusside (10 μM) transiently reduced SMC [Ca2+]i by 124 ± 18 nM ( n = 6, P < 0.05), whereas dilation (23 ± 5 μm) was sustained. Resolution of arteriolar SMC [Ca2+]i in vivo discriminates key signaling events that govern the local control of tissue blood flow.


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