scholarly journals Prostaglandin and antigestagen in pyometra bitches: vascular and stereological effect

2021 ◽  
Vol 2 (2) ◽  
pp. 95-105
Author(s):  
Roberto Rodrigues da Rosa Filho ◽  
Maíra Morales Brito ◽  
Thaís Gomes Faustino ◽  
Leticia Lima de Almeida ◽  
Verônica Correia Manoel ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Blood Vessel ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Uterine Blood Flow ◽  
Color Flow ◽  
Blood Vessel Formation ◽  
Uterine Infection ◽  
Vessel Formation

Effects of conservative treatment on uterine blood flow and morphometric findings are still unknown in bitches. Thus, this study aimed to compare uterine changes of pyometra bitches subjected to distinct modes of treatment. Pyometra bitches were assigned to: OHE (ovariohysterectomy immediately after diagnosis), Aglepristone (days 1, 2 and 8) and Associative (aglepristone treatment coupled with cloprostenol for 7 days) groups. After 9 days, bitches were ovariohysterectomized. Before surgery, uterine area was measured ultrasonographically and the uterine artery Doppler velocimetry analyzed blood flow velocity and indexes. Uterine horns were classified according to resistance index (RI) as more compromised and less compromised. Endometrial vasculature was quantitatively evaluated by color flow Doppler. Blood samples were collected to determine nitric oxide (NO) concentrations. Histological uterine structures were quantified by stereology and VEGF-A (vascular endothelial growth factor) and eNOS were (endothelial nitric oxide synthase) immunohistochemically analyzed. Aglepristone and Associative groups had lower uterine area and vascularization, and higher blood flow velocity and indexes compared to OHE group. Less compromised horn of Associative group had higher blood flow velocity compared to OHE group. Aglepristone group presented lower inflammatory infiltrate and larger uterine stroma. Associative group had lower volume density and absolute surface of endometrial cysts and lower VEGF-A expression for glandular epithelium and stromal cells. Blood NO and e-NOS immunostaining were not different among groups. In conclusion, association between aglepristone and prostaglandin is more effective in decreasing uterine vascularization and modulating uterine blood flow. Moreover, associative therapy promotes marked morphological changes. Lay summary This research compared two medical protocols of treatment for uterine infection (pyometra) in bitches, using a hormone blocker (anti-progesterone aglepristone) solely or in association with a uterine contraction inducer (prostaglandin; associative therapy). After treatment, bitches were gonadectomized and a microscopic analysis of uterine blood vessel formation and uterine tissue elements were performed as well as uterine blood flow evaluation through Doppler ultrasonography. According to vascular resistance, uterine horns were additionally classified as more compromised and less compromised. Both treatment protocols led to reduction of uterine dimensions and vascularization, and higher blood flow compared to untreated bitches. Less compromised uterine horn of the associative treatment had higher blood flow compared to untreated bitches. The hormone blocker treatment had lower inflammatory cells and larger uterine histological structure, while associative treatment had less uterine pathological cysts and lower blood vessel formation. The associative therapy is effective in decreasing uterine vascularization and modulating uterine blood flow as well as reestablishing endometrium structure in bitches with uterine infection.

Uterine blood flow velocity waveforms during early postpartum course following Caesarean section

1997 ◽  
Vol 74 (2) ◽  
pp. 121-124 ◽  
Author(s):  
Yuichiro Nakai ◽  
Motoharu Imanaka ◽  
Junko Nishio ◽  
Takeshi Maeda ◽  
Ayako Ozaki ◽  
...  
Keyword(s):  
Blood Flow ◽  
Caesarean Section ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Uterine Blood Flow ◽  
Early Postpartum

Three Dimensional Simulation of Blood Flow in the Small Arteries of a Truncated Vascular System With Three Levels of Bifurcation

2014 ◽  
Author(s):  
Kamil Kahveci ◽  
Bryan R. Becker
Keyword(s):  
Boundary Condition ◽  
Blood Flow ◽  
Blood Vessel ◽  
Velocity Profile ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Vascular System ◽  
Three Dimensional ◽  
Simulation Software ◽  
Small Arteries

Three dimensional blood flow in a truncated vascular system is investigated numerically using a commercially available finite element analysis and simulation software. The vascular system considered in this study has three levels of symmetric bifurcation. Geometric parameters for daughter vessels, such as their diameters and their angles of bifurcation, are specified according to Murray’s law based on the principle of minimum work. The ratio of blood vessel length to diameter is based upon experimental data found in the literature. An experimentally obtained velocity profile, available in the literature, is used as the inlet boundary condition. An outflow boundary model, consisting of a contraction tube to represent the pressure drop of the small arteries, arterioles, and capillaries that would follow the truncated vascular system, is used to specify the boundary condition at the eight outlets. The results show that although the blood flow velocity experiences a sudden decrease after the bifurcation points due to the higher total cross-sectional area of the daughter vessels as compared to the parent vessel, this decrease in velocity is partially recovered due to the tapering of the blood vessels as they approach the next bifurcation point. The results also show that the secondary flow which is typical after the bifurcation of large arteries does not develop after the bifurcation of small arteries due to the presence of laminar blood flow with very low Reynolds number in the small arteries. The numerical model yields pressure distributions and pressure drops along the vascular system that agree quite well with the physiological data found in the literature. Finally, the results show that, immediately following a bifurcation, the blood flow velocity profile is not symmetrical about the longitudinal axes of blood vessel. However, symmetry is recovered as the blood flow proceeds down the vessel.

scholarly journals Nitric oxide is not obligatory for radial artery flow-mediated dilation following release of 5 or 10 min distal occlusion

2010 ◽  
Vol 298 (1) ◽  
pp. H119-H126 ◽  
Author(s):  
Kyra Pyke ◽  
Daniel J. Green ◽  
Cara Weisbrod ◽  
Matthew Best ◽  
Lawrence Dembo ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Shear Rate ◽  
Flow Velocity ◽  
Radial Artery ◽  
Blood Flow Velocity ◽  
Reactive Hyperemia ◽  
Area Under The Curve ◽  
Flow Mediated Dilation ◽  
Significant Difference

This study investigated the nitric oxide (NO) dependence of radial artery (RA) flow-mediated dilation (FMD) in response to three different reactive hyperemia (RH) shear stimulus profiles. Ten healthy males underwent the following three RH trials: 1) 5 min occlusion (5 trial), 2) 10 min occlusion (10 trial), and 3) 10 min occlusion with cuff reinflation at 30 s (10–30 trial). Trials were performed during saline infusion and repeated during NG-monomethyl-l-arginine (l-NMMA) infusion in the brachial artery. RA blood flow velocity was measured with Doppler ultrasound, and B-mode RA images were analyzed using automated edge detection software. Shear rate estimation of shear stress was calculated as the blood flow velocity/vessel diameter. l-NMMA decreased baseline vascular conductance by 35%. l-NMMA infusion did not affect the peak shear rate stimulus ( P = 0.681) or the area under the curve (AUC) of shear rate to peak FMD ( P = 0.088). The AUC was significantly larger in the 10 trial vs. the 10–30 or 5 trial ( P < 0.001). Although percent FMD (%change in diameter) in the 10 trial was larger than that in the 5 trial ( P = 0.035), there was no significant difference in %FMD between the saline and l-NMMA conditions in any trial: 5 trial, 5.62 ± 1.48 vs. 5.63 ± 1.27%; 10 trial, 9.07 ± 1.16 vs. 11.22 ± 2.21%; 10–30 trial, 6.52 ± 1.43 vs. 7.98 ± 1.51% for saline and l-NMMA, respectively ( P = 0.158). We conclude the following: 1) RH following 10 min of occlusion results in an enhanced stimulus and %FMD compared with 5 min of occlusion. 2) When the occlusion cuff is reinflated 30 s postrelease of a 10 min occlusion, it does not result in an enhanced %FMD compared with that which results from RH following 5 min of occlusion. 3) The lack of effect of l-NMMA on FMD suggests that NO may not be obligatory for radial artery FMD in response to either 5 or 10 min of occlusion in healthy volunteers.

Imaging of basilar artery and measurement of blood flow velocity by real-time color flow Doppler ultrasonography.

Nosotchu ◽  
1993 ◽  
Vol 15 (2) ◽  
pp. 87-90
Author(s):  
Kazumi Kimura ◽  
Yoichiro Hashimoto ◽  
Toshihide Kumamoto ◽  
Kiyoshi Shima ◽  
Masayuki Ando
Keyword(s):  
Blood Flow ◽  
Flow Velocity ◽  
Real Time ◽  
Basilar Artery ◽  
Blood Flow Velocity ◽  
Doppler Ultrasonography ◽  
Color Flow

Efficacy of Transcranial Color Flow Imaging in Patients with Abnormal Blood Flow Velocity of the Middle Cerebral Artery

Neurosonology ◽  
1994 ◽  
Vol 7 (2) ◽  
pp. 71-75
Author(s):  
Kentaro FUJISHIRO ◽  
Kuniyasu KODAIRA ◽  
Takashi WADA ◽  
Ken-ichi MAIE ◽  
Eiji TSUKIYAMA ◽  
...  
Keyword(s):  
Blood Flow ◽  
Middle Cerebral Artery ◽  
Flow Velocity ◽  
Cerebral Artery ◽  
Blood Flow Velocity ◽  
Flow Imaging ◽  
Color Flow ◽  
Color Flow Imaging

scholarly journals Evidence That Acetylcholine Mediates Increased Cerebral Blood Flow Velocity in Crucian Carp through a Nitric Oxide—Dependent Mechanism

1995 ◽  
Vol 15 (3) ◽  
pp. 519-524 ◽  
Author(s):  
Patrick Hylland ◽  
Göran E. Nilsson
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Crucian Carp ◽  
Cerebral Blood Flow Velocity ◽  
Early Event ◽  
Brain Blood Flow ◽  
The Brain

Nitric oxide (NO)–dependent regulation of brain blood flow has not been proven to exist in fish or other ectothermic vertebrates. Using epi-illumination microscopy on the brain surface (optic lobes) of crucian carp ( Carassius carassius), we show that superfusing the brain with acetylcholine (ACh) induces an increase in cerebral blood flow velocity that can be completely blocked by the NO synthase inhibitors NG-nitro-l-arginine methylester (L-NAME) and NG-nitro-l-arginine. Also, sodium nitroprusside, which decomposes to liberate NO, causes an increase in cerebral blood flow velocity. By contrast, L-NAME does not block the increase in blood flow velocity caused by anoxia. The results suggest that NO is an endogenous vasodilator in crucian carp brain that mediates the effects of ACh. Because teleost fish deviated from other vertebrates 400 million years ago, these results suggest that NO-dependent brain blood flow regulation was an early event in vertebrate evolution.

scholarly journals Role of Nitric Oxide in the Elevation of Cerebral Blood Flow Induced by Acetylcholine and Anoxia in the Turtle

1996 ◽  
Vol 16 (2) ◽  
pp. 290-295 ◽  
Author(s):  
Patrick Hylland ◽  
Göran E. Nilsson ◽  
Peter L. Lutz
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Flow Velocity ◽  
Blood Flow Velocity ◽  
Freshwater Turtle ◽  
Brain Blood Flow ◽  
Brain Surface ◽  
Synthase Inhibitor ◽  
The Brain

Nitric oxide (NO)-dependent regulation of brain blood flow has hitherto not been studied in reptiles. By observing the brain surface (telencephalon) of the freshwater turtle (Trachemys scripta) with epiillumination microscopy, we show that topical application of acetylcholine (ACh) induces an increase in CBF velocity that can be completely blocked by the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME). The effect of L-NAME was reversed by L-arginine. Also, sodium nitroprusside (SNP), which decomposes to liberate NO, caused an increase in CBF velocity. By contrast, L-NAME could not block the increase in blood flow velocity caused by anoxia. Interestingly, superfusing the brain with ACh or SNP during anoxia had no effect on the blood flow velocity. The results suggest that NO is an endogenous vasodilator in the turtle brain, mediating the effects of ACh during normoxia. By contrast, anoxia does not rely on NO as a vasodilator.

Sign in / Sign up

Export Citation Format

Share Document