Role of leukocytes in uterine hypoperfusion and fetal growth retardation induced by ischemia-reperfusion

2001 ◽  
Vol 280 (3) ◽  
pp. H1215-H1221 ◽  
Author(s):  
Kei Miyakoshi ◽  
Hitoshi Ishimoto ◽  
Osamu Nishimura ◽  
Shinji Tanigaki ◽  
Mamoru Tanaka ◽  
...  
Keyword(s):  
Blood Flow ◽  
Fetal Growth ◽  
Growth Retardation ◽  
Ischemia Reperfusion ◽  
Fetal Growth Retardation ◽  
Sprague Dawley ◽  
Pregnant Rats ◽  
Doppler Flowmetry ◽  
Leukocyte Accumulation ◽  
Sprague Dawley Rats

We investigated leukocyte involvement in uterine hypoperfusion and intrauterine fetal growth retardation (IUGR) induced by ischemia-reperfusion (I/R) in Sprague-Dawley rats. On day 17 of gestation, leukocyte accumulation in the uterus and placenta subjected to 30 min of ischemia, followed by reperfusion, was assessed by measuring myeloperoxidase (MPO) activity. Uterine MPO activity was significantly higher after 1 h of reperfusion than it was before ischemia ( P < 0.05), without any increase in placental MPO activity. Immunohistochemical staining showed leukocyte accumulation in the uterus subjected to I/R. The effects of treatment with monoclonal antibodies against CD11a (WT1) and CD18 (WT3) at a dose of 0.8 mg/kg on uterine blood flow and IUGR were investigated. Laser-Doppler flowmetry demonstrated that uterine hypoperfusion at 2 h after ischemia (blood flow, −51.7 ± 1.2%; P < 0.01) was inhibited by WT1 and WT3 treatment. I/R-induced IUGR at full term ( P < 0.05 vs. nonischemic horn) was prevented by WT1 and WT3 treatment on day 17. These results indicate that leukocyte accumulation may play an important role in the pathogenesis of uterine hypoperfusion and IUGR induced by I/R in pregnant rats.

Role of oxygen-derived free radicals in free growth retardation induced by ischemia-reperfusion in rats

1997 ◽  
Vol 272 (2) ◽  
pp. H701-H705 ◽  
Author(s):  
H. Ishimoto ◽  
M. Natori ◽  
M. Tanaka ◽  
T. Miyazaki ◽  
T. Kobayashi ◽  
...  
Keyword(s):  
Blood Flow ◽  
Free Radicals ◽  
Growth Retardation ◽  
Ischemia Reperfusion ◽  
Lipid Peroxides ◽  
Treated Group ◽  
Sprague Dawley ◽  
Doppler Flowmetry ◽  
Oxygen Derived Free Radicals ◽  
The Right

We investigated the involvement of oxygen-derived free radicals in the pathogenesis of the intrauterine growth retardation (IUGR) induced in Sprague-Dawley rats by ischemia-reperfusion. On day 17 of gestation, rats received saline, superoxide dismutase (SOD, 50,000 U/kg), catalase (CAT, 50,000 U/kg), or SOD + CAT subcutaneously 1 h before induction of 30 min of ischemia of the right uterine horn. On day 21 the placental level of lipid peroxides was significantly increased (P < 0.001 vs. sham-operated group) and IUGR was induced (P < 0.001 vs. left horn) in the saline-treated group n = 6). Pretreatment with SOD + CAT (n = 6) significantly inhibited the increase in placental lipid peroxides and prevented IUGR. The effect of ischemia-reperfusion on uterine blood flow, with or without pretreatment with radical scavengers, was investigated in separate experiments by laser-Doppler flowmetry. The induction of hypoperfusion 3 h after ischemia (blood flow -40 +/- 5%, n = 6, P < 0.05) was blocked by pretreatment with SOD + CAT (n = 6). Results indicate that oxygen-derived free radicals may be important in the development of postischemic uteroplacental hypoperfusion and of ischemia-reperfusion-induced IUGR in the rat.

L-NNA decreases cortical hyperemia and brain cGMP levels following CO2 inhalation in Sprague-Dawley rats

1994 ◽  
Vol 267 (2) ◽  
pp. H837-H843 ◽  
Author(s):  
K. Irikura ◽  
K. I. Maynard ◽  
W. S. Lee ◽  
M. A. Moskowitz
Keyword(s):  
Blood Flow ◽  
Vessel Diameter ◽  
Sprague Dawley ◽  
Doppler Flowmetry ◽  
Cranial Window ◽  
Sprague Dawley Rats ◽  
Acetylcholine Inhalation ◽  
Flow Changes ◽  
Pial Vessel

The role of nitric oxide (NO) in the response to 5% CO2 inhalation was investigated by measuring 1) regional cerebral blood flow (rCBF) by laser-Doppler flowmetry and pial vessel diameter through a closed cranial window after topical NG-nitro-L-arginine (L-NNA, 1 mM), and 2) the time-dependent changes in brain guanosine 3',5'-cyclic monophosphate (cGMP) levels after L-NNA (10 mg/kg ip). When L-NNA (but not NG-nitro-D-arginine) was applied topically for 30 or 60 min, the response to hypercapnia was significantly attenuated. A correlation was found between inhibition of brain NO synthase (NOS) activity and the rCBF response (r = 0.77; P < 0.01). However, L-NNA applied 15 min before hypercapnia did not attenuate the increase in rCBF but did attenuate the dilation to topical acetylcholine. Inhalation of CO2 (5%) elevated brain cGMP levels by 20–25%, and L-NNA reduced this response. These data from the rat suggest that 1) a product of NOS activity is associated with hypercapnic hyperemia and the attendant increase in brain cGMP levels, and 2) hypercapnic blood flow changes may not be dependent on endothelial NOS activity within pial vessels.

Temporal profile of vascular changes induced by systemic nitroglycerin in the meningeal and cortical districts

Cephalalgia ◽  
2010 ◽  
Vol 31 (2) ◽  
pp. 190-198 ◽  
Author(s):  
Rosaria Greco ◽  
Cristina Meazza ◽  
Antonina Stefania Mangione ◽  
Marta Allena ◽  
Monica Bolla ◽  
...  
Keyword(s):  
Blood Flow ◽  
Regional Blood Flow ◽  
Sprague Dawley ◽  
No Donor ◽  
Doppler Flowmetry ◽  
Additional Information ◽  
Sprague Dawley Rats ◽  
Before And After ◽  
Pre Treatment ◽  
Induced Changes

Background: Clinical studies indicated that nitric oxide (NO) donors cause regional changes in cerebral blood flow (CBF), similar to those reported in spontaneous migraine. Systemic nitroglycerin (NTG), a NO donor, is a well-accepted experimental model of migraine. In this study we have examined the effects of NTG on the meningeal and cortical blood flow in rats. Methods: Regional blood flow was monitored in male Sprague-Dawley rats using laser Doppler flowmetry before and after NTG/saline injection over 150 minutes. The effect of pre-treatment with Nω-nitro-L-arginine ester (L-NAME) or 7-nitroindazole (7-NI) on NTG-induced changes on blood flow was also investigated. Results: In the dura NTG caused a biphasic response represented by an initial decrease in blood flow followed by a significant increase. At variance, in the cortex NTG caused only an increase in blood flow. Pre-treatment with either L-NAME or 7-NI prevented NTG-induced increase in blood flow in both districts, while only L-NAME also prevented NTG-induced decrease in dural blood flow. Conclusion: The present findings provide additional information on the timing of effects of NTG on blood flow at both the meningeal and cortical levels. These effects seem to be related to vasoregulatory mechanisms and/or metabolic activity in response to the synthesis of endogenous NO.

Role of the Na+-K+-2Cl− Cotransporter in the Development of Capsaicin-Induced Neurogenic Inflammation

2006 ◽  
Vol 95 (6) ◽  
pp. 3553-3561 ◽  
Author(s):  
Sandra Valencia-de Ita ◽  
Nada B. Lawand ◽  
Qing Lin ◽  
Gilberto Castañeda-Hernandez ◽  
William D. Willis
Keyword(s):  
Blood Flow ◽  
Mechanical Allodynia ◽  
Neurogenic Inflammation ◽  
Intradermal Injection ◽  
Plasma Extravasation ◽  
Sprague Dawley ◽  
Doppler Flowmetry ◽  
Plantar Surface ◽  
Sprague Dawley Rats ◽  
Electrophysiological Studies

Recent behavioral and electrophysiological studies have attributed an important role to dorsal root reflexes (DRRs) in the initiation and development of neurogenic inflammation produced by intradermal capsaicin (CAP). The DRRs can occur in peptidergic fibers, resulting in peripheral release of neuromediators that produce vasodilation, plasma extravasation and subsequently hyperalgesia and allodynia. In this study, we have evaluated the effect of spinal administration of bumetanide (a blocker of the Na+K+2Cl− cotransporter, NKCC) on DRR activity, changes in cutaneous blood flow (vasodilation), hindpaw edema, mechanical allodynia, and hyperalgesia induced by intradermal injection of 1% CAP in Sprague-Dawley rats. Vasodilation was monitored using laser Doppler flowmetry, neurogenic edema was evaluated by measurements of hindpaw volume, and secondary mechanical allodynia and hyperalesia were tested using von Frey filaments (10 and 200 mN) applied to the plantar surface of the paw. Changes in the blood flow were blocked significantly by intrathecal bumetanide at 10 and 100 μM in both pre- and posttreatment studies. Spinal bumetanide at 10 and 100 μM blocked neurogenic edema when it was administered before CAP injection, but only bumetanide at 100 μM administered after CAP injection reduced the paw edema significantly. Furthermore, the administration of bumetanide onto the spinal cord reduced the increment in DRR activity produced by CAP. Finally, both secondary mechanical allodynia and hyperalesia were reduced by bumetanide at 1, 10, and 100 μM. Taken together these results suggest that NKCC is involved in the increases in DRR activity, neurogenic inflammation and hyperalgesia and allodynia induced by intradermal CAP.

Working During Pregnancy: Effects on the Fetus

PEDIATRICS ◽  
1982 ◽  
Vol 69 (6) ◽  
pp. 724-727
Author(s):  
Richard L. Naeye ◽  
Ellen C. Peters
Keyword(s):  
Blood Flow ◽  
Fetal Growth ◽  
Growth Retardation ◽  
Late Gestation ◽  
Fetal Growth Retardation ◽  
Maternal Factors ◽  
Third Trimester ◽  
The Third ◽  
Uteroplacental Blood Flow ◽  
Pregnancy Weight

In order to determine whether pregnancy outcome was altered when women were employed outside their homes, 7,722 pregnancies were analyzed. Gestations were not shortened but newborns of women who worked in the third trimester weighed 150 to 400 gm less than newborns of mothers who remained at home. The growth retardation was greatest when women were underweight pregravid and had a low pregnancy weight gain, when they were hypertensive, or when the work required standing. The growth retardation remained after the data were stratified by race, socioeconomic status, and other maternal factors that commonly influence fetal growth. The frequency of large placental infarcts progressively increased when women continued stand-up work into late gestation. Such infarcts reached a peak of 250/1,000 births after the 37th week of gestation in stand-up workers. Low uteroplacental blood flow is a likely explanation for both the fetal growth retardation and the large placental infarcts.

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