Mapping vascular response to in vivo Hemodynamics: application to increased flow at the basilar terminus

2010 ◽  
Vol 9 (4) ◽  
pp. 421-434 ◽  
Author(s):  
Markus Tremmel ◽  
Jianping Xiang ◽  
Yiemeng Hoi ◽  
John Kolega ◽  
Adnan H. Siddiqui ◽  
...  
Keyword(s):  
Biochemistry ◽  
2003 ◽  
Vol 42 (22) ◽  
pp. 6904-6911 ◽  
Author(s):  
D. W. Sandall ◽  
N. Satkunanathan ◽  
D. A. Keays ◽  
M. A. Polidano ◽  
X. Liping ◽  
...  

2012 ◽  
Vol 39 (6Part29) ◽  
pp. 3983-3983 ◽  
Author(s):  
M Dewhirst ◽  
A Fontanella ◽  
G Palmer ◽  
M Boss ◽  
J Zhang ◽  
...  

1991 ◽  
Vol 70 (2) ◽  
pp. 947-952 ◽  
Author(s):  
H. L. Lippton ◽  
G. A. Cohen ◽  
I. F. McMurtry ◽  
A. L. Hyman

The present study was undertaken to investigate the effects of endothelin (ET) isopeptides on the pulmonary vascular bed of the intact spontaneously breathing cat under conditions of constant pulmonary blood flow and left atrial pressure. When pulmonary vasomotor tone was actively increased by intralobar infusion of U-46619, intralobar bolus injections of ET-1 (1 microgram), ET-2 (1 microgram), and ET-3 (3 micrograms) produced marked reductions in pulmonary and systemic vascular resistances. The pulmonary vasodilator response to each ET isopeptide was not altered by atropine (1 mg/kg iv), indomethacin (2.5 mg/kg iv), and ICI 118551 (1 mg/kg iv) but was significantly diminished by glybenclamide (5 mg/kg iv). This dose of glybenclamide significantly diminished the decrease in lobar arterial and systemic arterial pressures in response to intralobar injection of pinacidil (30 and 100 micrograms) and cromakalim (10 and 30 micrograms), whereas pulmonary vasodilator responses to acetylcholine (0.03 and 0.1 microgram), prostaglandin I2 (0.1 and 0.3 microgram), and isoproterenol (0.03 and 0.1 microgram) were not altered. The systemic vasodilator response to each ET isopeptide was not changed by glybenclamide or by the other blocking agents studied. The present data comprise the first publication demonstrating that ET-1, ET-2, and ET-3 dilate the pulmonary vascular bed in vivo. The present data further suggest that the pulmonary vasodilator response to ET isopeptides depends, in part, on activation of potassium channels and is mediated differently from the systemic vasodilator response to these substances. Contrary to earlier work, the present data indicate the pulmonary vascular response to ET isopeptides does depend on the preexisting level of pulmonary vasomotor tone.(ABSTRACT TRUNCATED AT 250 WORDS)


2010 ◽  
Vol 28 (2) ◽  
pp. 278-284 ◽  
Author(s):  
Mordechai Muszkat ◽  
Daniel Kurnik ◽  
Gbenga G Sofowora ◽  
Joseph Solus ◽  
Hong-Guang Xie ◽  
...  

2006 ◽  
Vol 79 (2) ◽  
pp. P31-P31
Author(s):  
M MUSZKAT ◽  
G SOFOWORA ◽  
D KURNIK ◽  
J SOLUS ◽  
L JIANG ◽  
...  

1981 ◽  
Author(s):  
J W D McDonald ◽  
M Ali ◽  
J D Cooper ◽  
E R Townsend

The infusion of plasma containing Zymosan-activated complement (ZAC) into sheep produces leukopenia with pulmonary leukostasis and transient pulmonary arterial hypertension (PAH). Previous work has related PAH to elevations of plasma thromboxane B2 (TXB2) rather than to mechanical obstruction by sequestered leukocytes (WBC). We have investigated the source of the TXB2 formation in this model. Incubation of platelet-poor WBC preparations with arachi- donate resulted in negligible TXB2 formation. WBC-poor platelet preparations on the other hand formed significant amounts of TXB2 (approximately 6-18 ng/108 platelets). Incubation of whole sheep blood or plasma with ZAC failed to generate significant amounts of TXB2. Thus, WBC agglutination in vitro did not induce platelet TXB2 formation.Pretreatment of sheep with aspirin (ASA)(10 mg/kg IV) completely blocked TXB2 formation and PAH in response to infusion of plasma containing ZAC. The infusion of 10-50% nonnal platelets into sheep 4 hours after ASA pretreatment failed to restore TXB2 formation and pulmonary vascular response to subsequent challenge with ZAC. TXB2 formation during blood clotting ex vivo was restored by the platelet infusions. These experiments make it appear unlikely that platelets are the source of the TXB2. It is possible that the transfused platelets respond to thrombin but are unable to interact with sequestered leukocytes. Sheep lung and pulmonary artery were incubated in vitro with arachidonate. Lung formed 630 ng TXB2 and 39 ng 6-keto-PGF1α/g of wet tissue. Pulmonary artery formed 9 ng TXB2 and 180 ng 6-keto-PGF1α/g of wet tissue. The relative proportions of TXB2 and 6-keto-PGF1α formed by lung parenchyma but not pulmonary artery resemble the proportions observed in previous in vivo experiments with ZAC. It appears that lung tissue is the most likely source of TXB2 formation causing PAH in response to ZAC-mediated pulmonary leukostasis.


2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Kaspar Trocha ◽  
Ming Tao ◽  
Alban Longchamp ◽  
Michael Macarthur ◽  
James Mitchell ◽  
...  

Objective: Vein graft failure secondary to intimal hyperplasia remains a challenge. Hydrogen sulfide (H 2 S) is produced endogenously by cystathionine γ-lyase (CGL) in endothelial cells, and as a gasotransmitter holds numerous beneficial vascular effects. We thus hypothesized that increased endogenous H 2 S would attenuate the vascular response to injury. Here, we leveraged a CGL transgenic overexpressing mouse model to test the potential of increased endogenous H 2 S to attenuate the vascular response to injury in a vein graft model. Approach and Results: A murine carotid-interposition cuff technique vein graft model was employed, including an artificial bacterial chromosome-based CGL transgenic (Tg) strain with an extra copy of the CGL gene locus randomly inserted in the genome. CGL Tg mice were fed a high-fat/high-cholesterol diet, implanted with a vein graft from CGL Tg donors (n=8), and compared to wild-type (WT) controls (n=7; WT/ WT conduits); all on C57BL/6 background. Grafts were imaged in vivo with ultrasound biomicropscopy and harvested after 28 days. CGL Tg mice demonstrated an approximate two-fold increase in serum H 2 S production capacity (lead acetate assay) compared to controls. The CGL Tg mice exhibited a significant decrease in their intimal thickness (p=<0.05, Fig.A) and intimal/medial+adventia ratios (p=<0.05, Fig.B) 28 days after implantation. In vivo biomicroscopy was supportive: CGL tg mice had a larger mean luminal diameter relative to WT controls (p=<0.05, Fig.C). Conclusion: Elevated endogenous H 2 S production reduces the fibroproliferative response to vein graft arterialization. Manipulation of this gasotransmitter’s biology stands as a novel approach to impact the durability of vascular reconstructions.


2013 ◽  
Vol 164 (3) ◽  
pp. e35-e37 ◽  
Author(s):  
Bill D. Gogas ◽  
Takashi Muramatsu ◽  
Hector M. Garcia-Garcia ◽  
Christos V. Bourantas ◽  
Niels R. Holm ◽  
...  

2014 ◽  
Vol 112 (3) ◽  
pp. 504-513 ◽  
Author(s):  
J Cebulla ◽  
E M Huuse ◽  
K Pettersen ◽  
A van der Veen ◽  
E Kim ◽  
...  

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