scholarly journals Observations of Translation and Jetting of Ultrasound-Activated Microbubbles in Mesenteric Microvessels

2011 ◽  
Vol 37 (12) ◽  
pp. 2139-2148 ◽  
Author(s):  
Hong Chen ◽  
Andrew A. Brayman ◽  
Wayne Kreider ◽  
Michael R. Bailey ◽  
Thomas J. Matula
Keyword(s):  
Mesenteric Microvessels

Capillary permeability: atrial peptide action is independent of "protein effect"

1990 ◽  
Vol 259 (5) ◽  
pp. H1351-H1356 ◽  
Author(s):  
V. H. Huxley ◽  
D. J. Meyer
Keyword(s):  
Hydraulic Conductivity ◽  
Bovine Serum Albumin ◽  
Atrial Natriuretic Peptide ◽  
Rana Pipiens ◽  
Capillary Permeability ◽  
Barrier Properties ◽  
Effective Area ◽  
Small Rise ◽  
Mesenteric Microvessels ◽  
Exchange Vessel

Perfusion of exchange microvessels with the vasoactive hormone, atrial natriuretic peptide (AP), acutely and reversibly elevates hydraulic conductivity (Lp) by mechanisms that are, as yet, unknown. This, the first of two studies to characterize AP responses when perfusate composition was altered, specifically focuses on the action of AP when perfusate albumin was lowered to change the transcapillary barrier properties for water by passive mechanisms (protein effect). Perfusion of frog (Rana pipiens) mesenteric microvessels with 1 nM AP in 10 mg/ml bovine serum albumin (BSA) elevated Lp by a median 2.1-fold (range 1.2-2.7, n = 13) from control levels (10 mg/ml BSA). Reduction of perfusate albumin from 10 to 1 mg/ml elicited a small rise in Lp (1.8-fold, n = 10); Lp rose a further 2.1-fold (n = 6) when 1 nM AP was added to 1 mg/ml BSA. Likewise, protein-free perfusion elevated Lp from a median 2.2 to 5.1 X 10(-7) cm.s-1.cmH2O-1 (n = 11); 1 nM AP in protein-free perfusate elevated Lp a further 2.1-fold (n = 8). Thus, regardless of protein content, the response to the peptide was a consistent, twofold increase in exchange vessel Lp (n = 27). These data are consistent with the suggestion that the AP-activated rise in Lp (twofold) occurs via an increase in the effective area of the transcapillary pathway for water without influencing the selectivity properties of the paracellular, albumin-sensitive portion of the barrier.

Abstract 052: Placental Growth Factor (PlGF) Reduces Blood Pressure and Improves Endothelin Type B Receptor (ETBR)-Mediated Microvascular Dilation in Hypertensive Pregnant Rats

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Marc Q Mazzuca ◽  
Zongli Ren ◽  
Chen Lin ◽  
Jose S Possomato-Vieira ◽  
Minglin Zhu ◽  
...  
Keyword(s):  
Perfusion Pressure ◽  
Mesenteric Arteries ◽  
Hypertensive Disorder ◽  
Type B ◽  
Pregnant Rats ◽  
Western Blots ◽  
New Approach ◽  
Nitrite Production ◽  
Uterine Perfusion ◽  
Mesenteric Microvessels

Preeclampsia is a pregnancy-related hypertensive disorder (HTN-Preg) with an imbalance between anti-angiogenic soluble fms-like tyrosine kinase-1 (sFlt-1) and angiogenic PlGF, but the vascular targets involved are unclear. We have shown downregulation of endothelial ET B R in Preg rats with reduced uterine perfusion pressure (RUPP), and studies have shown increased plasma sFlt-1 in RUPP rats. We tested if raising PIGF/sFlt-1 ratio by infusing PIGF (10 μg/kg/day) in RUPP rats would improve BP and microvascular ET B R signaling, and vice versa, if lowering PIGF/sFlt-1 ratio by infusing sFlt-1 (10 μg/kg/day) in Preg rats increases BP and reduces ET B R signaling. On day 19, BP was recorded and mesenteric microvessels were isolated for measurement of diameter and [Ca 2+ ] i (fura-2 340/380 ratio). BP was in PlGF-RUPP 105±2 < RUPP 126±1 and in sFlt-Preg 125±4 > Norm-Preg 97±5 mmHg. ET-1 vasoconstriction was in PlGF-RUPP 62.6±3.0 < RUPP 83.4±5.3 and in sFlt-Preg 76.1±4.7 > Norm-Preg 52.1±3.2%. ET-1 caused parallel increases in microvascular [Ca 2+ ] i that was in PlGF-RUPP 0.87±0.02 < RUPP 0.92±0.01 and in sFlt-Preg 0.93±0.02 > Norm-Preg 0.85±0.01. Endothelium removal or microvessel treatment with ET B R antagonist BQ-788 enhanced ET-1 vasoconstriction and [Ca 2+ ] i in Norm-Preg and PlGF-RUPP, but not RUPP or sFlt-Preg. The ET B R agonists sarafotoxin 6c (S6c) and IRL-1620 caused relaxation that was in PlGF-RUPP 42.9±10.8, 38.0±11.2% > RUPP 4.7±3.4, 7.5±2.3% and in sFlt-Preg 3.1±1.0, 5.4±1.6% < Norm-Preg 29.9±7.8, 28.0±9.1%. L-NAME partially reduced ACh- and ET B R-induced relaxation in Norm-Preg, PlGF-RUPP, but not RUPP or sFlt-Preg, suggesting that PlGF improves the decreased NO-dependent and ET B R-mediated vasorelaxation in HTN-Preg. Basal, ACh-, S6c-, and IRL-1620-induced nitrate/nitrite production was enhanced in mesenteric arteries of PIGF-RUPP and Norm-Preg vs. RUPP rats. Western blots and immunohistochemistry revealed greater levels of endothelial ET B R in PlGF-RUPP and Norm-Preg vs. RUPP and sFlt-Preg. Thus improving PlGF/sFlt-1 balance reduces BP and ET-1 vasoconstriction, and enhances ET B R-mediated NO-dependent vasodilation in RUPP rats, and could be a new approach in the management of HTN-Preg.

scholarly journals Interleukin-1-induced leukocyte extravasation across rat mesenteric microvessels is mediated by platelet-activating factor

Blood ◽  
1995 ◽  
Vol 85 (9) ◽  
pp. 2553-2558 ◽  
Author(s):  
S Nourshargh ◽  
SW Larkin ◽  
A Das ◽  
TJ Williams
Keyword(s):  
Vessel Wall ◽  
Interleukin 1 ◽  
Platelet Activating Factor ◽  
Micron Diameter ◽  
Paf Receptor ◽  
Leukocyte Extravasation ◽  
Mesenteric Microvessels ◽  
Adherent Leukocytes

Although our understanding of the molecular interactions that mediate the adhesion of leukocytes to venular endothelial cells has greatly expanded, very little is known about the mechanisms that mediate the passage of leukocytes across the vessel wall in vivo. The aim of the present study was to investigate the role of endogenously formed platelet-activating factor (PAF) in the process of leukocyte extravasation induced by interleukin-1 (IL-1). To determine at which stage of emigration PAF was involved, we studied the behavior of leukocytes within rat mesenteric microvessels by intravital microscopy. Rats were injected intraperitoneally with saline, recombinant rat IL-1 beta (IL-1 beta), or the peptide N-formyl-methionyl-leucyl-phenylalanine (FMLP) 4 hours before the exteriorization of the mesenteric tissue. In animals treated with IL-1 beta there was a significant increase in the number of rolling and adherent leukocytes within venules (20- to 40-micron diameter) and in the number of extravasated leukocytes in the tissue. Pretreatment of rats with the PAF receptor antagonist UK-74,505 had no effect on the leukocyte responses of rolling and adhesion, but significantly inhibited the migration of the leukocytes across the vessel wall induced by IL-1 beta (76% inhibition). A structurally unrelated PAF antagonist, WEB-2170, produced the same effect (64% inhibition). However, in contrast, UK-74,505 had no effect on the leukocyte extravasation induced by FMLP, indicating selectivity for the response elicited by certain mediators. These results provide the first line of direct evidence for the involvement of endogenously formed PAF in the process of leukocyte extravasation induced by IL-1 in vivo.

Reduction of obesity, as induced by leptin, reverses endothelial dysfunction in obese (Lepob ) mice

2000 ◽  
Vol 89 (6) ◽  
pp. 2382-2390 ◽  
Author(s):  
Bradford Winters ◽  
Zhiping Mo ◽  
Esther Brooks-Asplund ◽  
Soonyul Kim ◽  
Artin Shoukas ◽  
...  
Keyword(s):  
Direct Effect ◽  
Vascular Endothelial Cells ◽  
Cardiovascular Effects ◽  
No Production ◽  
Vascular Endothelial ◽  
Major Health ◽  
Vascular Abnormalities ◽  
Leptin Receptors ◽  
Nitrate And Nitrite ◽  
Mesenteric Microvessels

Obesity is a major health care problem and is associated with significant cardiovascular morbidity. Leptin, a neuroendocrine hormone released by adipose tissue, is important in modulating obesity by signaling satiety and increasing metabolism. Moreover, leptin receptors are expressed on vascular endothelial cells (ECs) and mediate angiogenesis. We hypothesized that leptin may also play an important role in vasoregulation. We investigated vasoregulatory mechanisms in the leptin-deficient obese ( ob/ob) mouse model and determined the influence of leptin replacement on endothelial-dependent vasorelaxant responses. The direct effect of leptin on EC nitric oxide (NO) production was also tested by using 4,5-diaminofluorescein-2 diacetate staining and measurement of nitrate and nitrite concentrations. Vasoconstrictor responses to phenylephrine, norepinephrine, and U-46619 were markedly enhanced in aortic rings from ob/ob mice and were modulated by NO synthase inhibition. Vasorelaxant responses to ACh were markedly attenuated in mesenteric microvessels from ob/ob mice. Leptin replacement resulted in significant weight loss and reversal of the impaired endothelial-dependent vasorelaxant responses observed in ob/ob mice. Preincubation of ECs with leptin enhanced the release of NO production. Thus leptin-deficient ob/ob mice demonstrate marked abnormalities in vasoregulation, including impaired endothelial-dependent vasodilation, which is reversed by leptin replacement. These findings may be partially explained by the direct effect of leptin on endothelial NO production. These vascular abnormalities are similar to those observed in obese, diabetic, leptin-resistant humans. The ob/ob mouse may, therefore, be an excellent new model for the study of the cardiovascular effects of obesity.

Effect of blood gases and pH on thromboembolic reactions in rabbit mesenteric microvessels

1989 ◽  
Vol 414 (3) ◽  
pp. 324-330 ◽  
Author(s):  
Mirjam G. A. oude Egbrink ◽  
Geert Jan Tangelder ◽  
Dick W. Slaaf ◽  
Robert S. Reneman
Keyword(s):  
Blood Gases ◽  
Mesenteric Microvessels

An Electrodiffusion Model for the Blood-Brain Barrier Permeability to Charged Molecules

2011 ◽  
Vol 133 (2) ◽  
Author(s):  
Guanglei Li ◽  
Bingmei M. Fu
Keyword(s):  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Steric Interaction ◽  
Charge Densities ◽  
Blood Brain ◽  
Endothelial Surface ◽  
Brain Barrier Permeability ◽  
Mesenteric Microvessels ◽  
Positively Charged ◽  
Constant Charge

The endothelial surface glycocalyx layer (SGL) and the basement membrane (BM) are two important components of the blood-brain barrier (BBB). They provide large resistance to solute transport across the BBB in addition to the tight junctions in the cleft between adjacent endothelial cells. Due to their glycosaminoglycan compositions, they carry negative charge under physiological conditions. To investigate the charge effect of the SGL and BM on the BBB permeability to charged solutes, we developed an electrodiffusion model for the transport of charged molecules across the BBB. In this model, constant charge densities were assumed in the SGL and in the BM. Both electrostatic and steric interaction and exclusion to charged molecules were considered within the SGL and the BM and at their interfaces with noncharged regions of the BBB. On the basis of permeability data for the positively charged ribonuclease (+4,radius=2.01 nm) and negatively charged α-lactalbumin (−10,radius=2.08 nm) measured in intact rat mesenteric and pial microvessels, our model predicted that the charge density in both SGL and BM would be ∼30 mEq/L, which is comparable to that in the SGL of mesenteric microvessels. Interestingly, our model also revealed that due to the largest concentration drop in the BM, there is a region with a higher concentration of negatively charged α-lactalbumin in the uncharged inter-endothelial cleft, although the concentration of α-lactalbumin is always lower than that of positively charged ribonuclease and that of a neutral solute in the charged SGL and BM.

Albumin modulation of capillary permeability: role of endothelial cell [Ca2+]i

1993 ◽  
Vol 265 (1) ◽  
pp. H74-H82 ◽  
Author(s):  
P. He ◽  
F. E. Curry
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Calcium Concentration ◽  
Capillary Permeability ◽  
Common Mechanism ◽  
Cytoplasmic Calcium ◽  
Adsorption Model ◽  
Endothelial Cell Surface ◽  
Mesenteric Microvessels

Albumin is required in vascular perfusates to maintain the normal permeability of microvessel walls. The most common mechanism proposed for action of albumin involves binding to the endothelial cell surface to increase the resistance to water and solute flows through hydraulic pathways across the capillary wall. The results of the present experiments do not conform to this simple adsorption model. Ringer perfusion increased the hydraulic conductivity (Lp) of the wall of single perfused frog mesenteric microvessels by 4.0 +/- 0.5-fold. The increase in Lp was associated with an increase of cytoplasmic calcium concentration ([Ca2+]i) from 59 +/- 5 nM when albumin was in the perfusate to a transient peak of 181 +/- 13 nM, 1–2 min after Ringer perfusion. [Ca2+]i then fell back to close to 100 nM. Processes that reduced Ca2+ influx into endothelial cells (removal of extracellular Ca2+, membrane depolarization) reduced Ca2+ influx and attenuated the increase in [Ca2+]i. The same processes abolished the increase in Lp after Ringer perfusion and restored Lp to close to control values during Ringer perfusion. Thus Ca2+ entry into endothelial cells is required to initiate and maintain the increased permeability during Ringer perfusion.

Erythrocyte flow velocities in mesenteric microvessels of the cat

1970 ◽  
Vol 2 (2) ◽  
pp. 151-162 ◽  
Author(s):  
Peter Gaehtgens ◽  
Herbert J. Meiselman ◽  
Harold Wayland
Keyword(s):  
Mesenteric Microvessels ◽  
Flow Velocities
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