Lung Pericytes in Pulmonary Vascular Physiology and Pathophysiology

Objective 1) Better recognize pathophysiology of postoperative tonsillectomy hemorrhage. 2) Be able to better differentiate the different types of post-tonsillectomy hemorrhage based upon understanding the vascular physiology and adjust management accordingly. Methods Post-tonsillectomy complications in children and adults were reviewed. 7 cases of hemorrhage, including 5 deaths, were carefully reviewed. Patients ranged between 2–40 years of age. This represents the largest series of post-tonsillectomy deaths reported to date. All postoperative deaths were due to bleeding and cardiopulmonary arrest. Post-mortem analysis was undertaken on those patients. CT angiography was reviewed in one surviving patient and the utility of this type of scanning is discussed. Results Post-tonsillectomy bleeding is one of the most worrisome otolaryngology concerns. Patients with bleeding on postoperative days 2–3 reported episodic bleeding stopping spontaneously. In these patients, the episode of unobserved bleeding signaled a vascular spasm with a likehood of recurrence. When the bleeding recurred it was massive and occured in a uncontrolled setting, leading to a poor outcome. Vascular trauma and spasm is likely. Conclusions Postoperative tonsillectomy bleeding is better managed by differentiating those patients with early stage bleeding on postoperative days 2–3. Direct examination of the operative field is imperative. Ancillary testing including CT angiograpy is helpful in the evaluation.

The role of the anti-ageing protein Klotho in vascular physiology and pathophysiology

Ageing Research Reviews ◽

10.1016/j.arr.2016.09.001 ◽

2017 ◽

Vol 35 ◽

pp. 124-146 ◽

Cited By ~ 40

Author(s):

Rik Mencke ◽

Jan-Luuk Hillebrands

Keyword(s):

Vascular Physiology

MicroRNA-10a is crucial for endothelial response to different flow patterns via interaction of retinoid acid receptors and histone deacetylases

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1621425114 ◽

2017 ◽

Vol 114 (8) ◽

pp. 2072-2077 ◽

Cited By ~ 25

Author(s):

Ding-Yu Lee ◽

Ting-Er Lin ◽

Chih-I Lee ◽

Jing Zhou ◽

Yi-Hsuan Huang ◽

...

Keyword(s):

Shear Stress ◽

Histone Deacetylases ◽

Inflammatory Responses ◽

Nuclear Accumulation ◽

Hemodynamic Forces ◽

Endothelial Response ◽

Vascular Physiology ◽

Responsive Element ◽

Retinoid Acid

Histone deacetylases (HDACs) and microRNAs (miRs) have emerged as two important epigenetic factors in the regulation of vascular physiology. This study aimed to elucidate the relationship between HDACs and miRs in the hemodynamic modulation of endothelial cell (EC) dysfunction. We found that miR-10a has the lowest expression among all examined shear-responsive miRs in ECs under oscillatory shear stress (OS), and a relatively high expression under pulsatile shear stress (PS). PS and OS alter EC miR-10a expression to regulate the expression of its direct target GATA6 and downstream vascular cell adhesion molecule (VCAM)-1. PS induces the expression, nuclear accumulation, and association of retinoid acid receptor-α (RARα) and retinoid X receptor-α (RXRα). RARα and RXRα serve as a “director” and an “enhancer,” respectively, to enhance RARα binding to RA-responsive element (RARE) and hence miR-10a expression, thus down-regulating GATA6/VCAM-1 signaling in ECs. In contrast, OS induces associations of “repressors” HDAC-3/5/7 with RARα to inhibit the RARα-directed miR-10a signaling. The flow-mediated miR-10a expression is regulated by Krüppel-like factor 2 through modulation in RARα–RARE binding, with the consequent regulation in GATA6/VCAM-1 in ECs. These results are confirmed in vivo by en face staining on the aortic arch vs. the straight thoracic aorta of rats. Our findings identify a mechanism by which HDACs and RXRα modulate the hormone receptor RARα to switch miR-10a expression and hence the proinflammatory vs. anti-inflammatory responses of vascular endothelium under different hemodynamic forces.

Vascular Physiology

Science ◽

10.1126/science.193.4248.140 ◽

1976 ◽

Vol 193 (4248) ◽

pp. 140-140

Author(s):

P. M. GOOTMAN

Keyword(s):

Vascular Physiology

Thrombin-Activated Protein C: Integrated to Regulate Vascular Physiology

Thrombin ◽

10.1007/978-0-387-09637-7_4 ◽

2008 ◽

pp. 63-80

Author(s):

Matthias Riewald

Keyword(s):

Protein C ◽

Activated Protein C ◽

Vascular Physiology

Metabolism and Redox in Pulmonary Vascular Physiology and Pathophysiology

Antioxidants and Redox Signaling ◽

10.1089/ars.2018.7657 ◽

2019 ◽

Vol 31 (10) ◽

pp. 752-769 ◽

Cited By ~ 2

Author(s):

Norah Alruwaili ◽

Sharath Kandhi ◽

Dong Sun ◽

Michael S. Wolin

Keyword(s):

Vascular Physiology

The Effects of Exercise on Vascular Physiology in Systemic Sclerosis Patients

10.7190/shu-thesis-00213 ◽

2018 ◽

Author(s):

Alexandros Mitropoulos

Keyword(s):

Systemic Sclerosis ◽

Vascular Physiology

Abstract 153: Automated Angiographic Assessment Of Coronary Artery Vasomotion In Kawasaki Disease Patients

Circulation ◽

10.1161/circ.131.suppl_2.153 ◽

2015 ◽

Vol 131 (suppl_2) ◽

Author(s):

Mitchel Benovoy ◽

Farida Cheriet ◽

Roch L Maurice ◽

Nagib Dahdah

Keyword(s):

Health Assessment ◽

Assessment System ◽

Vascular Health ◽

Pressure Gradients ◽

Intracoronary Imaging ◽

Temporal Tracking ◽

Vascular Physiology ◽

The Mean ◽

Spatio Temporal ◽

Stiffness Characteristics

Background: Mechanical properties of coronary arteries (CA) hold clues to vascular health and viability. Traditionally assessed with intracoronary imaging, we present an angiography-based system to assess CA vasomotion using automatic vessel segmentation and spatio-temporal tracking. Elastic moduli computed from dynamic CA calibers are compared between non-KD patients (CTL), KD patients with no CA aneurysms (KDAN-), and those with aneurysms (KDAN+). Methods: Proximal CA angiograms are automatically segmented and tracked over a cardiac cycle. CA centerline is extracted and the mean caliber is computed from diameters along its length. The resulting caliber variation reflects the CA vasomotion (Figure 1a). We then calculated the Vasomotion Standard Deviation (VSD) and CA recoil with the mean constriction velocity (MCV). Finally, Elastic Pressure moduli were computed using trans-myocardium pressure gradients. Results: We analyzed 51 left CA segments from 23 patients (5 CTL, 5 KDAN-, 13 KDAN+). Data are mean ± SD normalized pixels (npx). VSD was significantly reduced ( p <0.01) in KDAN+ (0.25±0.05) and KDAN- (0.27±0.04) vs CTL (0.38±0.07 npx). Coronary recoil was significantly reduced (p<0.05) in KDAN+ vs CTL, with MCV 3.50±0.67 vs 4.59±1.94 npx/sec. Pressure-dependent stiffness characteristics were equally atypical (Figure 1b). Conclusion: The proposed angiography-based stiffness assessment system shows abnormal CA vascular physiology in our cohort of KD patients. These results concur with previous invasive studies. The potential usability of this system for vascular health assessment could be applied to previously recorded CA angiograms for risk stratification.

Capillary-associated microglia regulate vascular structure and function through PANX1-P2RY12 coupling in mice

Nature Communications ◽

10.1038/s41467-021-25590-8 ◽

2021 ◽

Vol 12 (1) ◽

Cited By ~ 1

Author(s):

Kanchan Bisht ◽

Kenneth A. Okojie ◽

Kaushik Sharma ◽

Dennis H. Lentferink ◽

Yu-Yo Sun ◽

...

Keyword(s):

Myeloid Cell ◽

Structure And Function ◽

Pannexin 1 ◽

Vascular Physiology ◽

Blood Flow Increase ◽

Bona Fide ◽

Spatio Temporal ◽

And Function ◽

The Brain

AbstractMicroglia are brain-resident immune cells with a repertoire of functions in the brain. However, the extent of their interactions with the vasculature and potential regulation of vascular physiology has been insufficiently explored. Here, we document interactions between ramified CX3CR1 + myeloid cell somata and brain capillaries. We confirm that these cells are bona fide microglia by molecular, morphological and ultrastructural approaches. Then, we give a detailed spatio-temporal characterization of these capillary-associated microglia (CAMs) comparing them with parenchymal microglia (PCMs) in their morphological activities including during microglial depletion and repopulation. Molecularly, we identify P2RY12 receptors as a regulator of CAM interactions under the control of released purines from pannexin 1 (PANX1) channels. Furthermore, microglial elimination triggered capillary dilation, blood flow increase, and impaired vasodilation that were recapitulated in P2RY12−/− and PANX1−/− mice suggesting purines released through PANX1 channels play important roles in activating microglial P2RY12 receptors to regulate neurovascular structure and function.