Bstetric Anesthesia Handbook Fourth Edition O BSTETRIC ANESTHESIA HANDBOOK Fourth Edition Sanjay Datta, MD, FFARCS (Eng)

Total Page:16

File Type:pdf, Size:1020Kb

Bstetric Anesthesia Handbook Fourth Edition O BSTETRIC ANESTHESIA HANDBOOK Fourth Edition Sanjay Datta, MD, FFARCS (Eng) O bstetric Anesthesia Handbook Fourth Edition O BSTETRIC ANESTHESIA HANDBOOK Fourth Edition Sanjay Datta, MD, FFARCS (Eng) Professor of Anesthesia Brigham and Women’s Hospital Harvard Medical School Boston, Massachusetts With 72 Illustrations Sanjay Datta, MD, FFARCS (Eng) Professor of Anesthesia Brigham and Women’s Hospital Harvard Medical School Boston, MA 02115 USA Library of Congress Control Number: 2005926767 ISBN 0-387-26075-7 ISBN 978-0387-26075-4 Printed on acid-free paper. © 2006 Springer Science+Business Media, Inc. Third edition © 2000 by Hanley & Belfus, Inc All rights reserved. This work may not be translated or copied in whole or in part without the written permission of the publisher (Springer Science+Business Media, Inc., 233 Spring Street, New York, NY 10013, USA), except for brief excerpts in connection with reviews or scholarly analysis. Use in connection with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed is forbidden. The use in this publication of trade names, trademarks, service marks, and similar terms, even if they are not identified as such, is not to be taken as an expression of opinion as to whether or not they are subject to proprietary rights. While the advice and information in this book are believed to be true and accurate at the date of going to press, neither the author nor the editor nor the publisher can accept any legal responsibility for any errors or omissions that may be made. The publisher makes no war- ranty, express or implied, with respect to the material contained herein. The recommendations in this book should not be viewed as an exclu- sive treatment option or serve as a standard medical practice. Neither the author nor the publisher can accept any legal responsibility for any errors or omissions that may be made. Printed in the United States of America. (BS/MVY) 987654321 springeronline.com Preface ᭢ Three previous editions of Obstetric Anesthesia Handbook have proven valuable in serving those interested in managing pregnant women, each edition has become popular among anesthesiology residents, fellows, staff, and also among obste- tricians. This book has enjoyed strong international appeal and has been widely translated. Obstetric anesthesia has undergone changes in its field, changes in the technique as well as in its specific pharma- ceutical agents. Updating these fields has been the primary focus for the fourth edition. The text has been written to retain the cohesiveness of a single-author work; all efforts have been made to keep the text concise and to keep it in a true hand- book format. I sincerely hope the fourth edition will be as useful and as popular as previous editions. I thank Mrs. Elizabeth Kiernan, whose help has been immeasurable. Sanjay Datta, MD Contents ᭢ Preface . v 1. Maternal Physiological Changes During Pregnancy, Labor, and the Postpartum Period . 1 2. Local Anesthetic Pharmacology . 14 3. Perinatal Pharmacology . 27 4. Drug Interactions and Obstetric Anesthesia . 38 5. Uteroplacental Blood Flow . 59 6. Physiology of Labor and Delivery . 72 7. Relief of Labor Pain by Systemic Medication . 79 8. Spinal Opiates in Obstetrics . 89 9. Effect of Maternally Administered Anesthetics and Analgesics on Neonates and Neurobehavioral Testing . 100 10. Fetal Monitoring . 117 11. Relief of Labor Pain by Regional Analgesia/Anesthesia . 130 12. Anesthesia for Cesarean Delivery . 172 13. High-Risk Pregnancy . 211 14. Neonatal Resuscitation . 302 viii CONTENTS 15. Postpartum Tubal Ligation . 325 16. Anesthesia for Surgery During Pregnancy . 333 17. In Vitro Fertilization . 347 18. Maternal Mortality and Morbidity . 353 Index . 381 1 Maternal Physiological Changes During Pregnancy, Labor, and the Postpartum Period ᭢ Changes in Blood Volume Clinical Implications Changes in the Cardiovascular System Clinical Implications Changes in the Respiratory System Clinical Implications Changes in the Renal System Clinical Implications Changes in the Gastrointestinal System Clinical Implications Changes in the Central and Peripheral Nervous Systems Clinical Implications Changes in the Musculoskeletal System Changes in the Dermatological System Changes in the Mammary Tissue Changes in the Ocular System Clinical Implications Parturients undergo remarkable changes during pregnancy, labor, and the immediate postpartum period that can directly affect anesthetic techniques; hence a broad knowledge of these changes is essential for proper management of these women. 2MATERNAL PHYSIOLOGICAL CHANGES Changes in Blood Volume Maternal blood volume increases during pregnancy, and this involves an increase in plasma volume as well as in red cell and white cell volumes.1 The plasma volume increases by 40% to 50%, whereas the red cell volume goes up by only 15% to 20%, which causes a situation that is described as “physiological anemia of pregnancy” (normal hemoglobin, 12 g/dL; hematocrit, 35).2 Because of this apparent hemodi- lution, blood viscosity decreases by approximately 20%. The exact mechanism of this increase in plasma volume is unknown. However, several hormones such as renin- angiotensin-aldosterone, atrial natriuretic peptide, estrogen, and progesterone may be involved in this interesting phe- nomenon. Two current hypothesis attribute the increase to (1) an underfill state caused by initial vasodilation, which stimu- lates hormones such as renin, angiotensin, and aldosterone or (2) an overfill state characterized by an early increase in sodium retention (due to an increase in mineralcorticoids) that retains fluid, causing an increase in blood volume. Levels of clotting factors I, VII, VIII, IX, X, and XII, and the fibrinogen count are elevated during pregnancy as well. At present the majority of observers report a statistically significant fall in platelet count as pregnancy progresses.3 A recent study that observed an increase in thrombopoietin with the advance- ment of the gestational age also confirmed this finding.3a Sys- temic fibrinolysis also may increase slightly. Clinical Implications The increased blood volume serves several important functions: (1) it takes care of the increased circulatory need of the enlarging uterus as well as the needs of the fetopla- cental unit, (2) it fills the ever-increasing venous reservoir, (3) it protects the parturient from the bleeding at the time of delivery, and (4) parturients become hypercoaguable as the gestation progresses. It takes about 8 weeks after delivery for the blood volume to return to normal. MATERNAL PHYSIOLOGICAL CHANGES 3 Changes in the Cardiovascular System An increase in cardiac output is one of the most important changes of pregnancy. Cardiac output increases by 30% to 40% during pregnancy, and the maximum increase is attained around 24 weeks’ gestation.4 The increase in heart rate lags behind the increase in cardiac output initially and then ulti- mately rises by 10 to 15 beats per minute by 28 to 32 weeks’ gestation. The increase in cardiac output initially depends mainly on the rise in stroke volume, and later the increase in heart rate also becomes an important factor. With Doppler and M-mode echocardiography technique, increases in end dias- tolic chamber size and total left ventricular wall thickness have been observed in recent years. Cardiac output can vary depend- ing on the uterine size as well as on the maternal position at the time of measurement. The enlarged gravid uterus can cause aortocaval compression while the pregnant woman is in the supine position, and this will lead to reduced venous return and ultimately maternal hypotension. This effect will be exaggerated in parturients with polyhydramnios or multiple gestations. Cardiac output increases further during labor and may show values 50% higher than prelabor values. In the imme- diate postpartum period, cardiac output increases maximally and can rise 80% above prelabor values and approximately 100% above nonpregnant measurements. The increase in stroke volume as well as in heart rate maintains the increased cardiac output. Clinical Implications An increased cardiac output might not be well tolerated by pregnant women with valvular heart disease (e.g., aortic or mitral stenosis) or coronary arterial disease. A severe decom- pensation in myocardial function can develop at 24 weeks’ ges- tation, during labor, and especially immediately after delivery. Cardiac output, heart rate, and stroke volume decrease to pre-labor values 24 to 72 hours postpartum and return to non- pregnant levels within 6 to 8 weeks after delivery.5 Even with this increase in cardiac output the systolic blood pressure does not change during pregnancy; however, the dia- 4MATERNAL PHYSIOLOGICAL CHANGES stolic blood pressure drops by I to 15 mm Hg. There is a decrease in mean arterial pressure because of an associated decrease in systemic vascular resistance. Pregnancy hormones like estradiol-17b and progesterone are probably responsible for these vascular changes.6 Prostacyclin as well as nitric oxide also may play an important role. The down regulation of a and b receptors may also be an important factor. The heart is displaced to the left and upward during pregnancy because of the progressive elevation of the diaphragm by the gravid uterus. The electro- cardiogram of normal parturients may include: (1) benign dysrhythmia, (2) reversal of ST, T, and Q waves, and (3) left axis deviation. Aortocaval compression is one of the most important events during pregnancy, especially when the
Recommended publications
  • Doppler Velocimetry of the Uteroplacental Circulation
    Chapter 16 Doppler Velocimetry of the Uteroplacental Circulation Edwin R. Guzman, Eftichia Kontopoulos, Ivica Zalud Introduction blood flow at term was estimated at 500±700 ml/min with a two- to threefold decrease in uteroplacental Since the last edition of this volume, interest has con- perfusion noted in the presence of preeclampsia. tinued in uterine artery Doppler velocimetry (UADV) Uterine artery Doppler velocimetry was first re- as a screening technique to predict adverse pregnancy ported by Campbell and colleagues in 1983 [10]. They outcomes such as preeclampsia, for pregnancy risk showed that, compared to pregnancies with normal scoring, and as an entry criterion for randomized uterine artery waveforms, pregnancies with abnormal trials on medical therapies for the prevention of pre- uterine artery Doppler waveforms were associated with eclampsia and intrauterine growth restriction. These more proteinuric hypertension, required more antihy- areas have been updated and UADV for predicting pertensive therapy, and resulted in lower birth weights pregnancy outcome in medical conditions other than and younger gestational ages at birth. Thus the capabil- preeclampsia has been added. The areas regarding ity for this potentially safe, noninvasive, prospective non-Doppler assessment of uterine artery flow, phys- means of analyzing uterine artery blood flow during iology and development of uterine artery flow, and pregnancy was realized and set off a wave of interest the development of uterine artery Doppler waveform and research that has continued until today. remain essential and have been retained for historical purposes. Anatomy of Uterine Circulation Non-Doppler Methods The uterine artery originates from the internal iliac to Measure Uterine Artery Blood Flow artery and meets the uterus just above the cervix.
    [Show full text]
  • Proceedings Of
    MODEL BASED ASSESSMENT OF SYSTEMIC AND UTERINE CIRCULATION CONTRIBUTION TO AN ABNORMAL UTERINE ARTERY DOPPLER Shivbaskar Rajesh and Sanjeev G. Shroff Department of Bioengineering, University of Pittsburgh INTRODUCTION properties are not the sole determinants of an abnormal UAD In present day obstetrics, the Uterine Artery Doppler (UAD) waveform; the generalized maternal systemic arterial is a noninvasive sonography method used to measure the uterine dysfunction may play a significant role. The first success artery blood flow in pregnant women with the goal of criterion for this project is to develop a baseline model that characterizing the state of placentation and fetal blood supply. produces physiologically realistic pressure and flow waveforms UAD generates waveforms to monitor the velocity of blood at different systemic arterial locations. For example, the average flowing through the uterine artery. An abnormal UAD pressure that we expect to see in the ascending aorta and femoral waveform, representing the failure of proper gestational artery is around 97 mmHg, while the average flow in the adaptations, is associated with high-risk for pregnancy ascending aorta and femoral artery is 83 and 4 ml/s, respectively. complications or adverse fetal outcome such as preeclampsia or We will strive to have our model-based outputs within 5% of the fetal growth restriction (FGR) [1]. physiological values obtained from the literature. In normal pregnancy, vascular adaptations occur in the maternal body to help accommodate the placenta and fetus. METHODS Blood volume, heart rate, and cardiac output increase, while the The baseline model was built using Matlab/Simulink and vascular resistance decreases. Within the uterine circulation, the PLECS simulation software, and it is based on several validated endovascular extravillous and interstitial trophoblast cells models of the human circulatory system.
    [Show full text]
  • Sapporo Medical University 2004 – 2009
    RESEARCH ACTIVITIES OF SAPPORO MEDICAL UNIVERSITY 2004 – 2009 Hokkaido,Japan March 2010 RESEARCH ACTIVITIES OF SAPPORO MEDICAL UNIVERSITY 2004 – 2009 Edited by Committee for International Affairs and Medical Exchanges Sapporo Medical University Toshikazu Saito Neuropsychiatry, School of Medicine Shin Morioka English, Center for Medical Education Hiroki Takahashi Internal Medicine ( III ), School of Medicine Tsuyoshi Saito Obstetrics and Gynecology, School of Medicine Michiaki Yamakage Anesthesiology, Center for Medical Education Makoto Nemoto Liberal Arts and Sciences (English), School of Health Sciences Kimiharu Inui Applied Physical Therapy , Schhl of Health Sciences Contents ΣޓOUTLINE OF SAPPORO MEDICAL UNIVERSITYȤȤ!ȁ2 ޓޓޓޓޓPediatrics ȤȤȤȤȤȤȤȤȤȤȤȤȤȤȤȁ78 ޓ㧝ޓOUTLINE ȤȤȤȤȤȤȤȤȤȤȤȤȤȤȤȤȤ!ȁ3 ޓޓޓޓޓOphthalmology ȤȤȤȤȤȤȤȤȤȤȤȤȤȁ7: ޓޓޓޓޓDermatology ȤȤȤȤȤȤȤȤȤȤȤȤȤȤȁ82 ޓ㧞ޓORGANIZATION ȤȤȤȤȤȤȤȤȤȤȤȤȤȤ!ȁ6 ޓޓޓޓޓUrology ȤȤȤȤȤȤȤȤȤȤȤȤȤȤȤȤȁ84 ޓޓޓޓOrganization ȤȤȤȤȤȤȤȤȤȤȤȤȤȤȤ!ȁ6 ޓޓޓޓޓOtolaryngology ȤȤȤȤȤȤȤȤȤȤȤȤȤȁ86 ޓޓޓޓNumber of Teaching Staffs & Fellows ȤȤȤȤȤ!ȁ9 ޓޓޓޓޓNeuropsychiatry ȤȤȤȤȤȤȤȤȤȤȤȤȤȁ88 ޓޓޓޓNumber of Students ȤȤȤȤȤȤȤȤȤȤȤȤ!ȁ: ޓޓޓޓޓRadiology ȤȤȤȤȤȤȤȤȤȤȤȤȤȤȤȁ8: ޓޓޓޓޓAnesthesiology ȤȤȤȤȤȤȤȤȤȤȤȤȤȁ92 ΤޓRESEARCH ACTIVITIES ȤȤȤȤȤȤȤȤȤȤȤȤ!!22 ޓޓޓޓޓCommunity and General Medicine ȤȤȤȤȤȁ94 ޓ㧭ޓSCHOOL OF MEDICINE ȤȤȤȤȤȤȤȤȤȤȤ!!23 ޓޓޓޓޓClinical Laboratory Medicine ȤȤȤȤȤȤȤȤȁ96 ޓޓ㧝ޓMedical Sciences ȤȤȤȤȤȤȤȤȤȤȤȤȤȁ23 ޓޓޓޓޓTraumatology and Critical Care Medicine ȤȤȤȁ98 ޓޓޓޓޓObstetrics and Perinatal Medicine ȤȤȤȤȤȤȁ23 ޓޓޓޓޓOral Surgery ȤȤȤȤȤȤȤȤȤȤȤȤȤȤȁ9: ޓޓޓޓޓPlastic
    [Show full text]
  • Normal and Abnormal Transformation of the Spiral Arteries During Pregnancy
    Article in press - uncorrected proof J. Perinat. Med. 34 (2006) 447–458 • Copyright ᮊ by Walter de Gruyter • Berlin • New York. DOI 10.1515/JPM.2006.089 Normal and abnormal transformation of the spiral arteries during pregnancy Jimmy Espinoza1,2, Roberto Romero1,3,*, Yeon Keywords: Atherosis; immunohistochemistry; impe- Mee Kim1,4, Juan Pedro Kusanovic1, Sonia dance to blood flow; integrin; physiologic transformation Hassan1,2, Offer Erez1, Francesca Gotsch1, of the spiral arteries; placental bed. Nandor Gabor Than1, Zoltan Papp5 and Chong Jai Kim1,4 1 Perinatology Research Branch, NICHD, NIH, DHHS, Anatomy and physiology of the uterine Detroit MI 48201, and Bethesda MD 20892, USA circulation 2 Department of Obstetrics and Gynecology, Wayne The blood supply of the uterus is provided by the uterine State University School of Medicine, Detroit MI 48201, and ovarian arteries w102x. After entering the myome- USA trium, the uterine arteries give rise to the ‘‘arcuate arter- 3 Center for Molecular Medicine and Genetics, Wayne ies,’’ which branch into the ‘‘radial arteries’’ w102x. The State University School of Medicine, Detroit MI 48201, radial arteries divide into the ‘‘basal arteries,’’ which sup- USA ply the basal portion of the endometrium (critical for 4 Department of Pathology, Wayne State University endometrial regeneration after menstruation) and the School of Medicine, Detroit MI 48201, USA ‘‘spiral arteries,’’ which continue toward the endometrial 5 First Department of Obstetrics and Gynecology, surface w95x. The term ‘‘spiral arteries’’ reflects the coiled Semmelweis University, Budapest, Hungary appearance of these vessels, whose role is to supply blood to the upper functional layer of the endometrium, thought to be shed during menstruation w95x.
    [Show full text]
  • Transformation of the Spiral Arteries in Human Pregnancy: Key Events in the Remodelling Timeline
    Placenta 32, Supplement B, Trophoblast Research, Vol. 25 (2011) S154eS158 Contents lists available at ScienceDirect Placenta journal homepage: www.elsevier.com/locate/placenta IFPA Gabor Than Award lecture: Transformation of the spiral arteries in human pregnancy: Key events in the remodelling timeline L.K. Harris* Maternal and Fetal Health Research Group, University of Manchester, UK article info abstract Article history: During human pregnancy, the uterine spiral arteries are progressively remodelled to form dilated Accepted 23 November 2010 conduits lacking maternal vasomotor control. This phenomenon ensures that a constant supply of blood is delivered to the materno-fetal interface at an optimal velocity for nutrient exchange. Conversion of Keywords: a tonic maternal arteriole composed of multiple layers of vascular smooth muscle, elastin and numerous Artery other extracellular matrix components, into a highly dilated yet durable vessel, requires tight regulatory Decidua control and the coordinated actions of multiple cell types. Initial disruption of the vascular wall, char- Elastin acterised by foci of endothelial cell loss, and separation and misalignment of vascular smooth muscle EVT fl Extracellular matrix cells (VSMC), is coincident with an in ux of uterine natural killer (uNK) cells and macrophages. uNK cells Invasion are a source of angiogenic growth factors and matrix degrading proteases, thus they possess the capacity Leukocytes to initiate changes in VSMC phenotype and instigate extracellular matrix catabolism. However, complete Macrophages vascular cell loss, mediated in part by apoptosis and dedifferentiation, is only achieved following colo- Myometrium nisation of the arteries by extravillous trophoblast (EVT). EVT produce a variety of chemokines, cytokines Remodelling and matrix degrading proteases, enabling them to influence the fate of other cells within the placental Trophoblast bed and complete the remodelling process.
    [Show full text]
  • And Fetoplacental Arterial Vascular Resistance in Enos-Deficient Mice Due to Impaired Arterial Enlargement1
    BIOLOGY OF REPRODUCTION (2015) 92(2):48, 1–11 Published online before print 17 December 2014. DOI 10.1095/biolreprod.114.123968 Site-Specific Increases in Utero- and Fetoplacental Arterial Vascular Resistance in eNOS-Deficient Mice Due to Impaired Arterial Enlargement1 Monique Y. Rennie,4,5 Anum Rahman,4,5 Kathie J. Whiteley,8 John G. Sled,2,3,4,5 and S. Lee Adamson3,6,7,8 4Mouse Imaging Centre, Hospital for Sick Children, Toronto, Ontario, Canada 5Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada 6Department of Obstetrics and Gynecology, University of Toronto, Toronto, Ontario, Canada 7Department of Physiology, University of Toronto, Toronto, Ontario, Canada 8Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Ontario, Canada ABSTRACT INTRODUCTION The sites of elevated vascular resistance that impede placental Placental vascular defects underlie some of the most perfusion in pathological pregnancies are unknown. In the current common and severe pregnancy complications, but the specific study, we identified these sites in a knockout mouse model location of those vascular defects remains unclear. Preeclamp- (eNOSÀ/À) with reduced uterine (À55%) and umbilical (À29%) sia is thought to stem from blunted uteroplacental vessel artery blood flows caused by endothelial nitric oxide synthase dilation and failure of the spiral arteries to be transformed into deficiency. Uteroplacental and fetoplacental arterial vascular wide flaccid tubes [1–3]. Intrauterine growth restriction Downloaded from www.biolreprod.org. trees of pregnant mice near term were imaged using x-ray (IUGR) is thought to stem from a hypovascular fetoplacental microcomputed tomography (n ¼ 5–10 placentas from 3–5 dams/ tree [4, 5].
    [Show full text]
  • Uteroplacental Vasculature
    J. clin. Path., 29, Suppl. (Roy. Coll. Path.), 10, 9-17 Uteroplacental vasculature W. B. ROBERTSON From St George's Hospital Medical School, Tooting, London Pregnancy requires physiological adaptations in placental bed and the mechanisms involved in its every bodily system, not the least important being establishment and development we will remain in those involving the cardiovascular system. Associated ignorance of the basic defects of many types of with an increased plasma volume and cardiac output abnormal pregnancy. there are probably changes in the walls of the blood vessels themselves that so far have not been defined Development of the Uteroplacental Arteries in (Robertson and Manning, 1974). Suggestive evidence Normal Pregnancy for this is to be found in the remarkable changes seen in the blood vessels of the pregnant uterus (Brosens The blood supply to the non-pregnant uterus is et al, 1967). shown in figure 1, and particular note should be The blood supply to the endometrium of the made of the spiral or coiled arteries (fig 2), hormone- non-pregnant uterus is only a few millilitres per minute whereas something like half a litre of blood per minute must be delivered to the placenta at term (Browne and Veall, 1953). Hypertrophy and hyper- plasia of the major uterine and ovarian arteries ensures this supply but if it is to be delivered to the conceptus then the arteries of the placental bed must be considerably modified since human placentation is haemochorial, that is, maternal blood must be brought into direct contact with the villous tropho- blast of the fetal placenta.
    [Show full text]
  • June 04, 2021 Fast Super-Resolution Ultrasound Microvessel Imaging
    Ultrasound localization microscopy (ULM) June 04, Fast super-resolution ultrasound microvessel imaging using has been proposed to image 2021 spatiotemporal data with deep fully convolutional neural network microvasculature beyond the ultrasound diffraction limit. Pregnancy is a unique physiological state January A Protocol for Evaluating Vital Signs and Maternal-Fetal in which two individuals coexist: the 04, 2021 Parameters Using High-Resolution Ultrasound in Pregnant Mice mother and the fetus. Abdominal aortic aneurysm (AAA) is January Pharmacological inhibition of Notch signaling regresses pre- characterized by transmural infiltration of 01, 2019 established abdominal aortic aneurysm myeloid cells at the vascular injury site. A decline in capillary density and blood January Impairment of an Endothelial NAD + -H 2 S Signaling Network Is a flow with age is a major cause of mortality 01, 2018 Reversible Cause of Vascular Aging and morbidity. Abdominal aortic aneurysms are January Development and growth trends in angiotensin II-induced murine pathological dilations that can suddenly 01, 2018 dissecting abdominal aortic aneurysms rupture, causing more than 15,000 deaths in the U.S. annually. Disruption of vulnerable atherosclerotic August 24, Ultraselective Carbon Nanotubes for Photoacoustic Imaging of plaques often leads to myocardial 2021 Inflamed Atherosclerotic Plaques infarction and stroke, the leading causes of morbidity and mortality in the We presently show that sEH knockout repressed nicotine-induced arterial August 24, Soluble epoxide hydrolase deletion attenuated nicotine-induced stiffness and extracellular matrix 2021 arterial stiffness via limiting the loss of SIRT1 remodeling via SIRT1-induced YAP deacetylat Fish protein consumption exerts Anti-atherogenic effect of 10% supplementation of anchovy August 24, beneficial metabolic effects on human (Engraulis encrasicolus) waste protein hydrolysates in apoe- 2021 health, also correlat-ing with a decreased deficient mice risk for cardiovascular disease.
    [Show full text]
  • Uterine Natural Killer Cells Initiate Spiral Artery Remodeling in Human Pregnancy
    The University of Manchester Research Uterine natural killer cells initiate spiral artery remodeling in human pregnancy DOI: 10.1096/fj.12-210310 Document Version Accepted author manuscript Link to publication record in Manchester Research Explorer Citation for published version (APA): Robson, A., Harris, L. K., Innes, B. A., Lash, G. E., Aljunaidy, M. M., Aplin, J. D., Baker, P. N., Robson, S. C., & Bulmer, J. N. (2012). Uterine natural killer cells initiate spiral artery remodeling in human pregnancy. Faseb Journal, 26(12), 4876-4885. https://doi.org/10.1096/fj.12-210310 Published in: Faseb Journal Citing this paper Please note that where the full-text provided on Manchester Research Explorer is the Author Accepted Manuscript or Proof version this may differ from the final Published version. If citing, it is advised that you check and use the publisher's definitive version. General rights Copyright and moral rights for the publications made accessible in the Research Explorer are retained by the authors and/or other copyright owners and it is a condition of accessing publications that users recognise and abide by the legal requirements associated with these rights. Takedown policy If you believe that this document breaches copyright please refer to the University of Manchester’s Takedown Procedures [http://man.ac.uk/04Y6Bo] or contact [email protected] providing relevant details, so we can investigate your claim. Download date:06. Oct. 2021 Uterine natural killer cells initiate spiral artery remodelling in human pregnancy A Robson1,4; LK Harris2,4; BA Innes1; GE Lash1; MM Aljunaidy2; JD Aplin2; PN Baker2,3; SC Robson1; JN Bulmer1,5 5 1Reproductive and Vascular Biology Group, Institute of Cellular Medicine, Newcastle University, Newcastle upon Tyne, UK; 2Maternal and Fetal Health Research Centre, University of Manchester, UK; 3Department of Obstetrics and Gynecology, University of Alberta, Edmonton, Alberta.
    [Show full text]
  • 2 DMA’S Most Anticipated One Liners 1
    Anatomy 1 Authors: M.Balakrishnana, S.Sakthivel & Roshan Akthar www.dmaedu.com www.dmaedu.com 2 DMA’s Most Anticipated One Liners 1. Father of modern anatomy: Andreus vesalius 2. Cartilage has no blood vessels and nerves 3. Artery : thick walled, has smaller lumen 4. Veins : thin walled, has larger lumen 5. Lateral thyroid develops from 4th pharyngeal pouch 6. Trapezius is supplied by spinal part of accessory nerve 7. Rotator cuff muscles: Supraspinatus, Infraspinatus, Teres minor and Subscapularis 8. Dupytren contracture: 9. Knee joint is the largest and most complex joint of the body inflammation of ulnar side of palmar aponeurosis 10. Typical ribs are ribs 3-9 11. Atypical ribs are ribs 1,2,10,11,12 12. Inspiration is an active process and expiration is a passive process 13. Deep fascia of penis: Buck’s fascia 14. Deep fascia of thigh: Fascia lata 15. Nerve of laterjet is a branch of vagus nerve (present in stomach) 16. Arnold’s nerve is a branch of vagus nerve 17. Esophagus pierces the diaphragm at the level of 10th vertebra 18. Peyer’s patches are seen in Ileum 19. Stylopharyngeus muscle is a muscle of the 3rd pharyngeal arch 20. Risorius is the ‘Grinning muscle’ 21. Notochord Develops Into nucleus pulposus 22. Most frequently fractured bone in the body is clavicle 23. Azygous means unpaired 24. Midgut is supplied by SMA (superior mesenteric artery) 25. Length of small intestine is 6 metres 26. Length of thoracic duct is 45 cms 27. Left testicular vein drains into Left renal vein & Right testicular vein drains into IVC Uterine artery is a branch of Internal Iliac artery (IIA) 28.
    [Show full text]
  • Uteroplacental Vasculature
    J Clin Pathol: first published as 10.1136/jcp.s3-10.1.9 on 1 January 1976. Downloaded from J. clin. Path., 29, Suppl. (Roy. Coll. Path.), 10, 9-17 Uteroplacental vasculature W. B. ROBERTSON From St George's Hospital Medical School, Tooting, London Pregnancy requires physiological adaptations in placental bed and the mechanisms involved in its every bodily system, not the least important being establishment and development we will remain in those involving the cardiovascular system. Associated ignorance of the basic defects of many types of with an increased plasma volume and cardiac output abnormal pregnancy. there are probably changes in the walls of the blood vessels themselves that so far have not been defined Development of the Uteroplacental Arteries in (Robertson and Manning, 1974). Suggestive evidence Normal Pregnancy for this is to be found in the remarkable changes seen in the blood vessels of the pregnant uterus (Brosens The blood supply to the non-pregnant uterus is et al, 1967). shown in figure 1, and particular note should be The blood supply to the endometrium of the made of the spiral or coiled arteries (fig 2), hormone- non-pregnant uterus is only a few millilitres per minute whereas something like half a litre of blood per minute must be delivered to the placenta at term (Browne and Veall, 1953). Hypertrophy and hyper- plasia of the major uterine and ovarian arteries ensures this supply but if it is to be delivered to the conceptus then the arteries of the placental bed must be considerably modified since human placentation is haemochorial, that is, maternal blood must be brought into direct contact with the villous tropho- blast of the fetal placenta.
    [Show full text]
  • Walsh University
    Walsh University Effects of Reduced Uterine Perfusion Pressure on Cerebral Artery Tone in Pregnant Rats Treated with Nanoparticles Containing VEGF Receptor A Thesis by Matthew D. Thomas Mathematics and Sciences Submitted in partial fulfillment of the requirements for a Bachelor of Science Degree with University Honors May 2016 Accepted by the Honors Program Jacqueline Novak, Ph.D., Advisor Date Adam Underwood, Ph.D., Reader Date Ty Hawkins, Ph.D., Honors Director Date Acknowledgments I would like to offer a special thanks to Dr. Jackie Novak and Dr. J.J. Ramirez for graciously sharing their time and knowledge and their persistent patience. Additionally, I would like to thank Dr. Adam Underwood for being the reader of this thesis and his assistance in the lab. I would like to thank Dr. Ty Hawkins, Dr. Koop Berry, and Walsh University’s Honors program for the wonderful opportunity to grow intellectually and personally. Lastly, I would like to thank my family for their continued support throughout this entire process. iv Table of Contents Figures, Tables, and Graphs………………………………….………….....…..………v Abstract and Introduction……………………………….….…………………….……1 Literature Review………..…………….………….…………………………..……...…4 Purpose……………………………………………...…….….…………………….……13 Methodology………………………………..…………….….…………………….……14 Results……………………………………………………….….………………….……26 Discussion……………………………………………..….….…………………….……37 Limitations……………………………………………….….…………………….……40 Conclusion……………………………………………….….……………………..……41 References……………………………….….…………………………….……….……42 Appendix………………………...……………………….….……………………...….A-1
    [Show full text]