http://www.ncbi.nlm.nih.gov/pubmed/20711229Cell Mol Immunol. 2011 Jan;8(1):1-11. Epub 2010 Aug 16.
Natural killer cell-triggered vascular transformation: maternal care before birth?
Zhang J, Chen Z, Smith GN, Croy BA.
Department of Anatomy and Cell Biology, Queen's University, Kingston, ON, Canada.
Natural killer (NK) cells are found in lymphoid and non-lymphoid organs. In addition to important roles in immune surveillance, some NK cells contribute to angiogenesis and circulatory regulation. The uterus of early pregnancy is a non-lymphoid organ enriched in NK cells that are specifically recruited to placental attachment sites. In species with invasive hemochorial placentation, these uterine natural killer (uNK) cells, via secretion of cytokines, chemokines, mucins, enzymes and angiogenic growth factors, contribute to the physiological change of mesometrial endometrium into the unique stromal environment called decidua basalis. In humans, uNK cells have the phenotype CD56(bright)CD16(dim) and they appear in great abundance in the late secretory phase of the menstrual cycle and early pregnancy. Gene expression studies indicate that CD56(bright)CD16(dim) uterine and circulating cells are functionally distinct. In humans but not mice or other species with post-implantation decidualization, uNK cells may contribute to blastocyst implantation and are of interest as therapeutic targets in female infertility. Histological and genetic studies in mice first identified triggering of the process of gestation spiral arterial modification as a major uNK cell function, achieved via interferon (IFN)-γ secretion. During spiral arterial modification, branches from the uterine artery that traverse the endometrium/decidua transiently lose their muscular coat and ability to vasoconstrict. The expression of vascular markers changes from arterial to venous as these vessels dilate and become low-resistance, high-volume channels. Full understanding of the vascular interactions of human uNK cells is difficult to obtain because endometrial time-course studies are not possible in pregnant women. Here we briefly review key information concerning uNK cell functions from studies in rodents, summarize highlights concerning human uNK cells and describe our preliminary studies on development of a humanized, pregnant mouse model for in vivo investigations of human uNK cell functions.
PMID: 20711229 [PubMed - indexed for MEDLINE] PMCID: PMC3079746
http://www.nda.ox.ac.uk/wfsa/html/u09/u09_003.htmgestation and the venous ends of capillaries become dilated, causing reduced blood flow. These vascular changes contribute to delayed absorption of subcutaneously or intramuscularly injected substances. Distension of the extradural veins heightens the risk of vascular damage during institution of a regional block. The increased venous volume within the rigid spinal canal reduces the volume or capacity of the extradural and intrathecal spaces for local anaesthetic solutions. This will therefore increase the spread of injected drugs.
http://www.ncbi.nlm.nih.gov/pubmed/20599183Am J Obstet Gynecol. 2010 Nov;203(5):475.e1-6.
Maternal cerebral blood flow during normal pregnancy: a cross-sectional study.
Nevo O, Soustiel JF, Thaler I.
Department of Obstetrics and Gynecology, Sunnybrook Health Sciences Centre, University of Toronto, 60 Grosvenor Street, Toronto, Ontario, Canada. email@example.com
Pregnancy is associated with substantial changes in the maternal circulatory physiology. Our aim was to investigate maternal cerebral blood flow (CBF) during normal pregnancies.
We prospectively measured maternal CBF in 210 low-risk pregnant women at different gestational ages, and in 15 nonpregnant women. CBF was assessed by measuring blood flow volume in the internal carotid artery (ICA) by dual-beam angle-independent digital Doppler ultrasound.
ICA blood flow volume increased during pregnancy from 318 mL/min ± 40.6 mL/min in the first trimester to 382.1 mL/min ± 50.0 mL/min during the third trimester, corresponding to CBF values of 44.4 and 51.8 mL/min(-1)/100 g(-1), respectively (P < .0001). CBF changes were associated with progressive decrease in cerebral vascular resistance and moderate increase in ICA diameter.
Maternal CBF is gradually increasing during normal pregnancy. Vasorelaxing impact of estrogens and other factors on cerebral vessels may explain the changes in CBF during pregnancy.
Copyright © 2010 Mosby, Inc. All rights reserved.
PMID: 20599183 [PubMed - indexed for MEDLINE]
Cerebral vascular adaptation to pregnancy and its role in the neurological complications of eclampsia
Marilyn J. Cipolla,
Julie G. Sweet, and
+ Author Affiliations
Departments of Neurology, Obstetrics, Gynecology and Reproductive Sciences, and Pharmacology, University of Vermont College of Medicine, Burlington, Vermont
Address for reprint requests and other correspondence: M. J. Cipolla, Dept. of Neurology, Univ. of Vermont, 89 Beaumont Ave., Given C454, Burlington, VT 05405 (e-mail: Marilyn.Cipolla@uvm.edu).
Submitted 1 October 2010.
accepted in final form 8 November 2010.
The cerebral circulation has a central role in mediating the neurological complications of eclampsia, yet our understanding of how pregnancy and preeclampsia affect this circulation is severely limited. Here, we show that pregnancy causes outward remodeling of penetrating arterioles and increased capillary density in the brain due to activation of peroxisome proliferator-activated receptor-γ (PPARγ), a transcription factor involved in cerebrovascular remodeling and highly activated in pregnancy. Pregnancy-induced PPARγ activation also significantly affected cerebral hemodynamics, decreasing vascular resistance and increasing cerebral blood flow by ∼40% in response to acute hypertension that caused breakthrough of autoregulation. These structural and hemodynamic changes in the brain during pregnancy were associated with substantially increased blood-brain barrier permeability, an effect that could promote passage of damaging proteins into the brain and cause the neurological complications of eclampsia, including seizure.
I'm now in my 27th week of pregnancy. The walking and spasticity have remained very, very poor and are a severe deterioration from the walking problems I suffered during the first pregnancy. However my bladder remains significantly better than it was during my first pregnancy. The night spasms have started to become quite problematic and I am getting only a few hours sleep as I can no longer calm them down particularly if there is any urine in the bladder. There is definitely a link between the bladder and the night spasms. In fact if my bladder is full my walking takes a turn for the worse. As it is difficult to void with the baby I should imagine and hope that a certain amount of the walking deterioration is due to a constantly near full bladder. My walking improves modestly once the bladder is more properly voided although this is now quite a difficult manouevre with the baby girl in the way. So far I have noticed only the most minor of nose bleeds. During the last pregnancy my nose bled a very great deal, which I'm sure is indicative of widespread venous permeability. I believe my blood pressure to be very low now as I am suffering quite a bit in the mornings from complete exhaustion coupled with a sensation of dizziness/head tingling. I have noticed a few more movement induced phosphenes. The sensory deficit in the left foot has been pretty noticeable too. All in all a bad update. 84 days until the c section.
The pdf file shows the chart update.
I am thinking of visiting Professor Sclafani in New York after this delivery.
I'm now in my 30th week of pregnancy. My right leg motor function has continued to deteriorate with terrible spasticity in the foot and knee area. I can barely walk around the house and need to use the wall for stability. I pray that this improves after delivery, like after the last pregnancy but fear that this relapse has left a permanent scar. However the areas of disability which have improved after venoplasty, the bladder and the myoclonus are still much better than the last pregnancy so I believe that the right leg motor dysfunction is not caused or affected by jugular stenosis. There is something else causing the nerve cells to die and this may be a different vein stenosis or simply the immune system. Given the immediacy of the motor deterioration after conception I expect that the heightened vascular permeability caused by chorionic gonadotropin is partly to blame. This hormone increases a lot in the first and second trimester and then declines precipitously in the third trimester. I will visit Dr Sclafani in New York next year to have the renal and iliac veins and the dural sinuses assessed. I will also have an upright MRI scan assessment to see what else might be disturbing the cerebro spinal fluid.
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