Different Effects of Various Vasodilators on Autoregulation of Renal Blood Flow in Anesthetized Dogs

Total Page:16

File Type:pdf, Size:1020Kb

Different Effects of Various Vasodilators on Autoregulation of Renal Blood Flow in Anesthetized Dogs Different Effects of Various Vasodilators on Autoregulation of Renal Blood Flow in Anesthetized Dogs Nobuyuki OGAWA and Hiroshi ONO Department of Pharmacology and Toxicology, Hatano Research Institute, Food and Drug Safety Center, 729-5 Ochiai, Hadano, Kanagawa 257, Japan Accepted March 24, 1986 Abstract-In order to examine whether the autoregulation of renal blood flow is equally influenced by all kinds of vasodilators, kidney perfusion experiments were performed in anesthetized dogs. The perfused kidney usually showed excellent autoregulation of blood flow over the perfusion pressure between 120 and 200 mmHg. Renal blood flow was increased by the renal arterial infusion of diltiazem (100 /cg/min), papaverine (10 mg/min) or nicorandil (300 ig/min) (at the basal perfusion pressure of 100 mmHg) and was maintained at an increased level while the infusion was continued. On the other hand, renal blood flow was increased only transiently by the infusion of nitroglycerin (50 ,ug/min), and the blood flow gradually decreased to the basal level in spite of the continuous infusion. Infusions of diltiazem and papaverine abolished the autoregulation of renal blood flow besides the vasodilator effect, but infusions of nitroglycerin and nicorandil have no effect on the autoregulation. Furthermore, sodium nitroprusside (30 /~g/min) and sodium nitrite (5 mg/min), which are assumed to produce vasodilation through cyclic GMP, also have no effect on the autoregulation of renal blood flow. In conclusion, all the vasodilators do not influence the renal blood flow autoregulation , and vasodilation caused by cyclic GMP is unconnected with the myogenic mechanism regulating the renal blood flow. The autoregulation of renal blood flow is renal blood flow. In other words, some the maintenance of a stable blood flow level substances produce vasodilation without in spite of fluctuation in the renal perfusion affecting the myogenic response of the renal pressure. The presently accepted mechanism vascu lature. of the autoregulation is the myogenic The present study is to examine whether response of the vascular smooth muscle or not there exists a common mechanism adjusting the vascular tone to the change of among vasodilators which do not impair the perfusion pressure. This myogenic theory is autoregulation of renal blood flow. supported by the evidence that the auto regulation is effectively abolished by Materials and Methods vasodilators, such as papaverine, amino Twenty-seven mongrel dogs of either sex, phylline, verapamil and nifedipine (1-3). weighing 11-17 kg, fed on a pellet dog food Kiil et al. (4) reported that infusion of (CD-5, Clea Japan Co.) were anesthetized acetylcholine into the renal artery produced with a-chloralose (40 mg/kg) and urethane potent vasodilation on canine kidney, but (400 mg/kg) intravenously, preceded by failed to impair the autoregulation. We have sedation with morphine hydrochloride (2 mg/ obtained similar results with acetylcholine kg, s.c.). Pressure-controlled perfusion experi (N. Ogawa and H. Ono, unpublished results) ments were performed with the left kidney. and also with prostaglandin E2 and bradykinin Details of the procedure have been described (5). Thus, there are vasodilators devoid of previously (5). The left renal artery was potency to abolish the autoregulation of cannulated and perfused with blood con ducted from the carotid artery. An initial dose values of the control and during a drug of 500 U/kg of sodium heparin was given as treatment was done according to the paired anticoagulant. When necessary, smaller doses t-test, and those between groups was done of a-chloralose and urethane were supple according to Student's t-test (P<0.05). mented, and sodium heparin was supple mented constantly by 100 U/kg/hr. Perfusion Results pressure was controlled by the use of a Systemic blood pressure and renal blood Starling's pneumatic resistance. Perfusion flow: Table 1 shows the mean values for mean pressure and systemic blood pressure in the systemic blood pressure and renal blood flow femoral artery was measured with electric at the perfusion pressure of 100 mmHg, manometers (transducers: Statham P23Db before and during infusion of drugs. Renal and carrier amplifiers: San-ei 1206B). Renal blood flow was increased by the intra blood flow was measured by an electro arterial infusion of diltiazem (100 ttg/min), magnetic flowmeter (Narco RT-500). A test papaverine (10 mg/min), nicorandil (300 drug solution was infused into a rubber tube /-,g/min), sodium nitroprusside (30 fig/min) connected close to the shank of the renal and sodium nitrite (5 mg/min). The increase arterial cannula by the aid of an infusion of blood flow reached a maximum within pump (Harvard Apparatus 901). 3 min after the onset of the infusion and was Renal blood flow was allowed to stabilize sustained at an increased level during the for 30 min at the basal perfusion pressure of infusion. Mean systemic blood pressure was 100 mmHg; then perfusion pressure was significantly decreased by the infusion of changed stepwise between 60 and 200 each one of these drugs. The infusion of mmHg. After the control observation of the nitroglycerin (50 ,ag/min), however, produced blood flow responses to the stepwise changes only a transient vasodilation, and the initial of perfusion pressure between 60 and 200 vasodilation was nullified in spite of con mmHg, the infusion of a drug was started at tinuous infusion, though a decrease in the the basal perfusion pressure of 100 mmHg, systemic blood pressure was obvious and and pressure-flow relation was examined sustained. Then, the effect of nitroglycerin on again. the renal autoregulation was examined at the Following drugs were studied: diltiazem infusion rate of 50 iig/min. The infusion of hydrochloride (Tanabe), papaverine hydro 100 ,ug/min of diltiazem did not cause a chloride (Nakarai), nitroglycerin (NGA significant increase of blood flow below the 800128, 0.5 mg/ml aqueous solution, perfusion pressure of 80 mmHg. The infusion Nippon Kayaku), nicorandil (Chugai), of papaverine and nitro-compounds except sodium nitroprusside (Wako) and sodium nitroglycerin caused vasodilation at all nitrite (Wako). All drugs were dissolved in ranges of perfusion pressure. or diluted with saline. The dose of the drug is Autoregulation of renal blood flow: expressed as the weight of the base. Control observation usually confirmed The efficiency index of autoregulation excellent autoregulation of the renal blood (ARI) was calculated as follows (6): flow between 120 and 200 mmHg of the perfusion pressure and partial autoregulation between 100 and 120 mmHg. The blood flow changed pressure-dependently below where the renal blood flow changes to 100 mmHg. RBF2 from the initial value of RBF1 when Figure 1 illustrates the effects of diltiazem renal arterial (perfusion) pressure is altered (30 and 100 /tg/min) and papaverine (10 to PRA2 from the initial value of PRA,. mg/min) on autoregulation of renal blood Efficiency of the autoregulation was con flow. Autoregulation of renal blood flow was sidered as follows: ARI<0.3: excellently clearly abolished by diltiazem and papaverine. effective, ARI=0.3-0.7: partially effective, Simultaneous infusion of CaCI2 (30 mg/min) and ARI>0.7: virtually absent. restored the autoregulation impaired by 30 Statistical analysis of differences between zcg/min of diltiazem, but it was not effective Table 1. Mean systemic blood pressure and renal blood flow before and during the infusion of a drug at basal perfusion pressure of 100 mmHg Fig. 1. Effects of (A) diltiazem (0Q: control, ~ -A: 30 ug/min, A----A: 100 ,ug/min, 17------V: simultaneous infusion of 30 mg/min of CaC12 and 30 pg/min of diltiazem, n=5) and (B) papaverine (0O: control, A---0: 10 mg/ min, n=5) on the pressure-flow curves in perfused dog kidney. Symbols and vertical bars represent means and S.E., respectively. *shows a significant difference from the corresponding value of the control (P<0.05). on restoring the autoregulation impaired by the vasodilators are shown in Table 2. The papaverine (not shown in the figure). Figures control ARI is in all experiments were less 2 and 3 illustrate the effects of nitroglycerin, than 0.5 between 100 and 120 mmHg and nicorandil, sodium nitroprusside and sodium less than 0.3 between 120 and 200 mmHg, nitrite on the autoregulation of renal blood indicating an effective autoregulation. ARI's flow. The infusion of nicorandil (300 /cg/ during infusion of nitroglycerin, nicorandil, min), sodium nitroprusside (30 /cg/min) or sodium nitroprusside and sodium nitrite sodium nitrite (5 mg/min) caused an increase were also less than 0.3 between 120 and in renal blood flow at all ranges of perfusion 200 mmHg, showing that the autoregulation pressure, but did not impair the auto was not influenced. On the other hand, the regulation, shifting the pressure-flow curve ARI's during infusion of diltiazem were upward. Nitroglycerin (50 /Lg/min) also increased at any perfusion pressure range. could not abolish the autoregulation in This effect was dose-related and ARI became addition to the lack of sustained vasodilation nearly 1.0 with the infusion of 100 /Lg/min as stated above, though the change in the of diltiazem, showing a complete abolition systemic blood pressure obviously showed of the autoregulation. ARI's during simul the effectiveness of the drug. Pressure-flow taneous infusion of CaCl2 (30 mg/min) curves before and during infusion of nitro with diltiazem (30 /ig/min) recovered to the glycerin overlapped each other. control value for 140-200 mmHg of perfusion ARI's before and during the infusion of pressure. ARI's were also increased by 10 Fig. 2. Effects of (A) nitroglycerin (Q Q: Fig. 3. Effects of (A) sodium nitroprusside control, z---0: 50 ,ug/min, n=4) and (B) (0-0: control, 0-- \: 30 yg/min, n=5) and nicorandil (0-0.
Recommended publications
  • Baroreflex and Cerebral Autoregulation Are Inversely
    2460 NASR N et al. Circulation Journal ORIGINAL ARTICLE Official Journal of the Japanese Circulation Society http://www.j-circ.or.jp Hypertension and Circulatory Control Baroreflex and Cerebral Autoregulation Are Inversely Correlated Nathalie Nasr, MD, PhD; Marek Czosnyka, PhD; Anne Pavy-Le Traon, MD, PhD; Marc-Antoine Custaud, MD, PhD; Xiuyun Liu, BSc; Georgios V. Varsos, BSc; Vincent Larrue, MD Background: The relative stability of cerebral blood flow is maintained by the baroreflex and cerebral autoregulation (CA). We assessed the relationship between baroreflex sensitivity (BRS) and CA in patients with atherosclerotic carotid stenosis or occlusion. Methods and Results: Patients referred for assessment of atherosclerotic unilateral >50% carotid stenosis or oc- clusion were included. Ten healthy volunteers served as a reference group. BRS was measured using the sequence method. CA was quantified by the correlation coefficient (Mx) between slow oscillations in mean arterial blood pres- sure and mean cerebral blood flow velocities from transcranial Doppler. Forty-five patients (M/F: 36/9), with a me- dian age of 68 years (IQR:17) were included. Thirty-four patients had carotid stenosis, and 11 patients had carotid occlusion (asymptomatic: 31 patients; symptomatic: 14 patients). The median degree of carotid steno-occlusive disease was 90% (IQR:18). Both CA (P=0.02) and BRS (P<0.001) were impaired in patients as compared with healthy volunteers. CA and BRS were inversely and strongly correlated with each other in patients (rho=0.58, P<0.001) and in healthy volunteers (rho=0.939; P<0.001). Increasing BRS remained strongly associated with im- paired CA on multivariate analysis (P=0.004).
    [Show full text]
  • Cerebral Pressure Autoregulation in Traumatic Brain Injury
    Neurosurg Focus 25 (4):E7, 2008 Cerebral pressure autoregulation in traumatic brain injury LEONARDO RANGE L -CASTIL L A , M.D.,1 JAI M E GAS C O , M.D. 1 HARING J. W. NAUTA , M.D., PH.D.,1 DAVID O. OKONK W O , M.D., PH.D.,2 AND CLUDIAA S. ROBERTSON , M.D.3 1Division of Neurosurgery, University of Texas Medical Branch, Galveston; 3Department of Neurosurgery, Baylor College of Medicine, Houston, Texas; and 2Department of Neurosurgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania An understanding of normal cerebral autoregulation and its response to pathological derangements is helpful in the diagnosis, monitoring, management, and prognosis of severe traumatic brain injury (TBI). Pressure autoregula- tion is the most common approach in testing the effects of mean arterial blood pressure on cerebral blood flow. A gold standard for measuring cerebral pressure autoregulation is not available, and the literature shows considerable disparity in methods. This fact is not surprising given that cerebral autoregulation is more a concept than a physically measurable entity. Alterations in cerebral autoregulation can vary from patient to patient and over time and are critical during the first 4–5 days after injury. An assessment of cerebral autoregulation as part of bedside neuromonitoring in the neurointensive care unit can allow the individualized treatment of secondary injury in a patient with severe TBI. The assessment of cerebral autoregulation is best achieved with dynamic autoregulation methods. Hyperven- tilation, hyperoxia, nitric oxide and its derivates, and erythropoietin are some of the therapies that can be helpful in managing cerebral autoregulation. In this review the authors summarize the most important points related to cerebral pressure autoregulation in TBI as applied in clinical practice, based on the literature as well as their own experience.
    [Show full text]
  • Arterial Baroreflex Regulation of Cerebral Blood Flow in Humans
    J Phys Fitness Sports Med, 1(4): 631-636 (2012) JPFSM: Review Article Arterial baroreflex regulation of cerebral blood flow in humans Shigehiko Ogoh1*, Ai Hirasawa1 and James P. Fisher2 1 Department of Biomedical Engineering, Toyo University, 2100 Kujirai, Kawagoe-shi, Saitama 350-8585, Japan 2 School of Sport and Exercise Sciences, University of Birmingham, Edgbaston, Birmingham, West Midlands B15 2TT UK Received: October 12, 2012 / Accepted: November 19, 2012 Abstract The arterial baroreflex plays an essential role in the short-term regulation of arterial blood pressure, and thus helps ensure that the vital organs are adequately perfused. For stand- ing humans, appropriate arterial baroreflex control of cardiac output and vasomotor tone are particularly important for cerebral blood flow regulation. However, the numerous mechanisms implicated in the regulation of the cerebral vasculature (e.g. cerebral autoregulation, carbon dioxide reactivity) mean that the precise nature of the direct and indirect effects of the arterial baroreflex on cerebral blood flow regulation are highly complex and remain incompletely un- derstood. This review paper provides an update on recent insights into the influence of the arte- rial baroreflex on cerebral circulation. Keywords : arterial blood pressure, cardiac output, cerebral autoregulation, cerebral CO2 reactiv- ity, autonomic nervous system control cerebral vascular resistance3). Introduction The concept that CA is a powerful mechanism of blood Adequate oxygen delivery is essential for the mainte- flow regulation in the brain has become well established. nance of cerebral function, and a loss of consciousness However, in the early studies of Lassen (1959), the CA rapidly results from inadequate cerebral perfusion and curve relating CBF to MAP was derived from eleven oxygen delivery.
    [Show full text]
  • Cardiovascular Physiology
    Dr Matthew Ho BSc(Med) MBBS(Hons) FANZCA Cardiovascular Physiology Electrical Properties of the Heart Physiol-02A2/95B4 Draw a labelled diagram of a cardiac action potential highlighting the sequence of changes in ionic conductance. Explain the terms 'threshold', 'excitability', and 'irritability' with the aid of a diagram. 1. Cardiac muscle contraction is electrically activated by an action potential, which is a wave of electrical discharge that travels along the cell membrane. Under normal circumstances, it is created by the SA node, and propagated to the cardiac myocytes through gap junctions (intercalated discs). 2. Cardiac action potential: a. Phase 4 – resting membrane potential: i. Usually -90mV ii. Dependent mostly on potassium permeability, and gradient formed from Na-K ATPase pump b. Phase 0 - -90mV-+20mV i. Generated by the opening of fast Na channels Na into cell potential inside rises > 65mV (threshold potential) positive feedback further Na channel opening action potential ii. Threshold potential also triggers opening Ca channels (L type) at -10mV iii. Reduced K permeability c. Phase 1 – starts + 20mV i. The positive AP causes rapid closure of fast Na channels transient drop in potential d. Phase 2 – plateau i. Maximum permeability of Ca through L type channels ii. Rising K permeability iii. Maintenance of depolarisation e. Phase 3 – repolarisation i. Na, Ca and K conductance returns to normal ii. Ca. Na channels close, K channels open 3. Threshold: the membrane potential at which an AP occurs a. Usually-65mV in the cardiac cell b. AP generated via positive feedback Na channel opening 4. Excitability: the ease with which a myocardial cell can respond to a stimulus by depolarising.
    [Show full text]
  • Review Course Lectures
    Review Course Lectures International Anesthesia Research Society IARS 2011 REVIEW COURSE LECTURES The material included in the publication has not undergone peer review or review by the Editorial Board of Anesthesia and Analgesia for this publication. Any of the material in this publication may have been transmitted by the author to IARS in various forms of electronic medium. IARS has used its best efforts to receive and format electronic submissions for this publication but has not reviewed each abstract for the purpose of textual error correction and is not liable in any way for any formatting, textual, or grammatical error or inaccuracy. 2 ©2011 International Anesthesia Research Society. Unauthorized Use Prohibited IARS 2011 REVIEW COURSE LECTURES Table of Contents Perioperative Implications of Emerging Concepts In Management of the Malignant Hyperthermia Vascular Aging, Health And Disease Patient In Ambulatory Surgery Charles W. Hogue, MD ..............................1 Denise J. Wedel, MD ...............................38 Professor of Anesthesiology and Professor of Anesthesiology, Mayo Clinic Critical Care Medicine Rochester, Minnesota Chief, Division of Adult Anesthesia The Johns Hopkins University School of Medicine, Central Venous Access Guideline The Johns Hopkins Hospital Development and Recommendations Baltimore, Maryland Stephen M. Rupp, MD ..............................41 Anesthesiologist Perioperative Management of Pain and PONV in Medical Director, Perioperative Services Ambulatory Surgery Virginia Mason Medical Center, Seattle, Washington Spencer S. Liu, MD .................................5 Clinical Professor of Anesthesiology Pediatric Anesthesia and Analgesia Outside the OR: Director of Acute Pain Service What You Need To Know Hospital for Special Surgery Pierre Fiset, MD, FRCPC............................47 New York, New York Department Head, Anesthesiology Montreal Children’s Hospital Colloid or Crystalloid: Any Differences In Outcomes? Montreal, Quebec, Canada Tong J.
    [Show full text]
  • Medical Physiology of the Cardiovascular System October 10
    Medical Physiology of the Cardiovascular System HAPS Institute Graduate Credit Course offered in conjunction with Alverno College October 7 to December 7, 2020 Instructor: Patrick Eggena, M.D. Novateur Medmedia, LLC 39 Terry Hill Road Carmel, NY 10512 [email protected] Class size: 3-7 Graduate Credits: 3 Prerequisite: Human Physiology Description of the course: This course in Medical Physiology of the Cardiovascular System is primarily for HAPS professors who teach pre-medical, medical, or nurse practitioner students. It is a self- study course where participants attend 13 hours of live video-lectures by Dr. Eggena in cardiovascular physiology and read pertinent information related to the lectures. After the lecture series students follow Dr. Eggena on his 16-hour night tour at a hospital where they apply the physiology learned in class to patient care in the emergency room and at the patient’s bedside. Participants taking the course for graduate credits are given a 2-hour proctored examination with 60 true/false and 4 graphic essay questions. The following iBooks are required for this course: 1. Lectures in Cardiovascular Physiology by Patrick Eggena, M.D. Apple iBooks ($10) 2. Physiology Correlates of a Physician’s Diary by Patrick Eggena, M.D. Apple iBooks ($9). 3. Medical Physiology of the Heart-Lung-Kidney by Patrick Eggena, M.D. Apple iBooks ($15). Syllabus A. From: ‘Lectures in Cardiovascular Physiology’ by Patrick Eggena M.D. Apple iBooks. Instructions 1. (1) Watch: Cardiac Electrophysiology: In this 1-hour video-lecture Dr. Eggena gives an overview of the cardiovascular system and considers cardiac action potentials.
    [Show full text]
  • Cerebrovascular Autoregulation Among Very Low Birth Weight Infants
    Journal of Perinatology (2011) 31, 689–691 r 2011 Nature America, Inc. All rights reserved. 0743-8346/11 www.nature.com/jp EDITORIAL Cerebrovascular autoregulation among very low birth weight infants Journal of Perinatology (2011) 31, 689–691; doi:10.1038/jp.2011.54 information on the relationship between cerebral oxygenated hemoglobin (a surrogate for cerebral blood flow) and mean Despite advances in neonatal care, intraventricular hemorrhage arterial BP measured continuously over the first 3 days of life. (IVH) and periventricular leukomalacia (PVL) remain significant The authors contribute the following to our understanding of morbidities in very low birth weight infants. Disturbed cerebral autoregulation among very low birth weight infants: (1) the ability hemodynamics may be a major contributor to the pathogenesis of to autoregulate cerebral blood flow differs from infant to infant, these lesions.1,2 A growing body of literature describes cerebral with some infants able to autoregulate well at all BPs experienced autoregulation among at-risk very low birth weight infants, and others unable to autoregulate despite ‘normal’ BPs; (2) a including an eloquent study by Gilmore et al.,3 which describes given infant may demonstrate intact autoregulation at some BPs, the autoregulatory ability of preterm infants over the first but not others; (3) autoregulation is more likely to be impaired at 3 days of lifeFat the time they are most vulnerable to perinatal lower systemic arterial BP and more likely to be intact at higher brain injury. BPs; (4) average mean arterial BP over the entire 3-day study Autoregulation is the ability to maintain a constant cerebral period is proportional to time spent with intact autoregulation; and blood flow over a physiological range of blood pressures (BPs), (5) although estimated gestational age is proportional to BP, related to the constriction and dilation of the main capacitance estimated gestational age bears no relationship to the time spent vessels of the cerebral circulation.
    [Show full text]
  • Mathematical Model of the Interaction Between Baroreflex and Cerebral Autoregulation
    4th International Conference on Computational and Mathematical Biomedical Engineering - CMBE2015 29 June-1 July 2015, France P. Nithiarasu and E. Budyn (Eds.) MATHEMATICAL MODEL OF THE INTERACTION BETWEEN BAROREFLEX AND CEREBRAL AUTOREGULATION Adam Mahdi1, Mette S. Olufsen2, and Stephen J. Payne1 1Institute of Biomedical Engineering, Department of Engineering Science, University of Oxford, Oxford, UK fadam.mahdi,[email protected] 2Department of Mathematics, NC State University, Raleigh 26795, USA, msolufse@affil2 SUMMARY Baroreflex (BR) and cerebral autoregulation (CA) are two important mechanisms regulating blood pressure and flow. However, the functional relationship between BR and CA in humans is unknown. Since BR impairment is an adverse prognostic indicator for both cardiac and cerebrovascular diseases it would be of clinical interest to better understand the relationship between BR and CA. Motivated by this observation we develop a simple mathematical framework aiming to simulate the effects of BR on the cerebral blood flow dynamics. Key words: cerebral autoregulation, baroreflex, blood pressure, modeling 1 INTRODUCTION Baroreflex (BR) is the main short-term blood pressure (BP) regulation mechanism of the cardiovas- cular system (CVS). It aims to provide adequate perfusion of all tissues by maintaining blood flow and pressure at homeostasis by regulating heart rate (HR), vascular resistance, compliance and other variables of the CVS. Cerebral autoregulation (CA) is a physiological mechanism which aims to maintain blood flow in the brain at an appropriate level during changes in BP. It is achieved by regu- lating cerebral arteriolar vessels to match the cerebral blood flow (CBF) with the metabolic demands of the brain. Although it has been known that both BR and CA are central in maintaining appropriate CBF the functional relationship between the two mechanisms in humans is unknown.
    [Show full text]
  • Autoregulation of Cerebral Blood Flow in the Preterm Fetal Lamb
    003 1-3998/85/0902-0 159$02.00/0 PEDIATRIC RESEARCH Vol. 19, No. 2, 1985 Copyright O 1985 International Pediatric Research Foundation, Inc. Printed in U.S.A. Autoregulation of Cerebral Blood Flow in the Preterm Fetal Lamb LU-ANN PAPILE, ABRAHAM M. RUDOLPH, AND MICHAEL A. HEYMANN Cardiovascular Research Institute and Departments of Pediatrics, Physiology, and Obstetrics, Gynecology and Reproductive Sciences University of California, Sun Francisco, California ABSTRACT. The purpose of the present study was to The ewes were fasted for 24 h prior to operation, and low spinal determine if autoregulation of cerebral blood flow (CBF) analgesia was induced with 2 ml of 1% tetracaine hydrochloride. is present in the preterm fetal lamb and, if present, to Sedation was achieved with ketamine in amounts of 100-150 measure the range of mean arterial blood pressure over mg given intravenously as needed. which autoregulation exists. Thirty-seven measurements Surgical procedures. With the use of aseptic techniques, poly- of CBF were made in seven preterm fetal lambs (118-122 vinyl catheters were inserted in the maternal pedal artery and days gestation) over a mean carotid arterial blood pressure vein and advanced to the descending aorta and abdominal (CBP) range of 18-90 mm Hg. CBF was measured by the inferior vena cava, respectively. The uterus was exposed through radionuclide-labeled microsphere technique. CBP was al- a midline abdominal incision and the fetal parts were identified. tered by graduated inflation of balloons placed around the An incision through the uterine wall was made over a fetal hind brachiocephalic trunk and the aortic isthmus.
    [Show full text]
  • INDE 221 Spring 2010 Syllabus Part 2
    Human Health & Disease Mondays, Tuesdays, Thursdays and Fridays 9:00 - 11:50 AM Lectures: Room M-112, Labs: Fleischmann IINNDDEE 222211 SSpprriinngg 22001100 Syllabus SSyyllllaabbuuss PPaarrtt 22 (2010) Year's Last Syllabus (2010) Year's Last Human Health & Disease Inde 221 Spring 2010 Table of Contents CARDIOVASCULAR BLOCK SYLLABUS SCHEDULE 7 SYLLABUS PREFACE 11 CARDIAC MUSCLE AND FHC 15 EXCITATION-CONTRACTION COUPLING Syllabus27 NERNST POTENTIAL AND OSMOSIS 43 EXCITABILITY AND CONDUCTION 51 CIRCULATORY VESSEL HISTOLOGY LAB 63 CARDIAC ACTION POTENTIAL 71 CONTROL OF HEART RHYTHM (2010) 85 AUTONOMIC DRUGS OVERVIEW I 97 ELECTROCARDIOGRAM (ECG) 99 LESIONS OF BLOOD VESSELS 109 THROMBOEMBOLIC DISEASE 117 CARDIAC REFLEXESYear's 123 AUTONOMIC DRUGS OVERVIEW II 141 ECG SMALL GROUPS 143 LastAUTONOMIC DRUGS: CHOLINERGICS 147 CARDIAC MUSCLE MECHANICS 149 AUTONOMIC DRUGS: ANTICHOLINERGICS 175 ARRHYTHMIAS 177 AUTONOMIC DRUGS: SYMPATHOMIMETICS I 203 VENTRICULAR PHYSIOLOGY 205 AUTONOMIC DRUGS: SYMPATHOMIMETICS II 235 STARLING CURVE AND VENOUS RETURN 237 CARDIAC OUTPUT AND CATHETERIZATION 245 AUTONOMIC DRUGS: ADRENOCEPTOR BLOCKERS 267 PHYSICS OF CIRCULATION Syllabus269 CASE DISCUSSIONS: AUTONOMIC DRUGS 289 SMOOTH MUSCLE 291 ISCHEMIC AND VALVULAR HEART DISEASE 303 RENAL CIRCULATION (2010) 323 HYPERTENSION 333 CARDIOMYOPATHY, MYOCARDITIS AND ATRIAL MYXOMA 351 ENDOTHELIUM AND CORONARY CIRCULATION 369 ANGINA PECTORIS 389 DRUGS USEDYear's IN HYPERTENSION 397 SHOCK 399 ADULT CARDIAC LAB 413 CARDIAC ANESTHESIA & BYPASS 421 LastEXERCISE PHYSIOLOGY 431 ISCHEMIC
    [Show full text]
  • A Multicellular Vascular Model of the Renal Myogenic Response
    Article A Multicellular Vascular Model of the Renal Myogenic Response Maria-Veronica Ciocanel 1,* , Tracy L. Stepien 2 , Ioannis Sgouralis 3 and Anita T. Layton 4,5 1 Mathematical Biosciences Institute, The Ohio State University, Columbus, OH 43210, USA 2 Department of Mathematics, University of Arizona, Tucson, AZ 85719, USA; [email protected] 3 National Institute for Mathematical and Biological Synthesis, University of Tennessee, Knoxville, TN 37996, USA; [email protected] 4 Departments of Mathematics, Biomedical Engineering, and Medicine, Duke University, Durham, NC 27708, USA; [email protected] 5 Department of Applied Mathematics, University of Waterloo, Waterloo, ON N2L 3G1, Canada * Correspondence: [email protected]; Tel.: +1-614-688-3334 Received: 5 June 2018; Accepted: 5 July 2018; Published: 17 July 2018 Abstract: The myogenic response is a key autoregulatory mechanism in the mammalian kidney. Triggered by blood pressure perturbations, it is well established that the myogenic response is initiated in the renal afferent arteriole and mediated by alterations in muscle tone and vascular diameter that counterbalance hemodynamic perturbations. The entire process involves several subcellular, cellular, and vascular mechanisms whose interactions remain poorly understood. Here, we model and investigate the myogenic response of a multicellular segment of an afferent arteriole. Extending existing work, we focus on providing an accurate—but still computationally tractable—representation of the coupling among the involved levels. For individual muscle cells, we include detailed Ca2+ signaling, transmembrane transport of ions, kinetics of myosin light chain phosphorylation, and contraction mechanics. Intercellular interactions are mediated by gap junctions between muscle or endothelial cells. Additional interactions are mediated by hemodynamics.
    [Show full text]
  • The Angiotensin II Type I Receptor Contributes to Impaired Cerebral Blood Flow Autoregulation Caused by Placental Ischemia in Pregnant Rats Junie P
    Warrington et al. Biology of Sex Differences (2019) 10:58 https://doi.org/10.1186/s13293-019-0275-1 RESEARCH Open Access The angiotensin II type I receptor contributes to impaired cerebral blood flow autoregulation caused by placental ischemia in pregnant rats Junie P. Warrington1, Fan Fan1, Jeremy Duncan1, Mark W. Cunningham1, Babette B. LaMarca1, Ralf Dechend2, Gerd Wallukat2, Richard J. Roman1, Heather A. Drummond1, Joey P. Granger1 and Michael J. Ryan1* Abstract Background: Placental ischemia and hypertension, characteristic features of preeclampsia, are associated with impaired cerebral blood flow (CBF) autoregulation and cerebral edema. However, the factors that contribute to these cerebral abnormalities are not clear. Several lines of evidence suggest that angiotensin II can impact cerebrovascular function; however, the role of the renin angiotensin system in cerebrovascular function during placental ischemia has not been examined. We tested whether the angiotensin type 1 (AT1) receptor contributes to impaired CBF autoregulation in pregnant rats with placental ischemia caused by surgically reducing uterine perfusion pressure. Methods: Placental ischemic or sham operated rats were treated with vehicle or losartan from gestational day (GD) 14 to 19 in the drinking water. On GD 19, we assessed CBF autoregulation in anesthetized rats using laser Doppler flowmetry. Results: Placental ischemic rats had impaired CBF autoregulation that was attenuated by treatment with losartan. In addition, we examined whether an agonistic autoantibody to the AT1 receptor (AT1-AA), reported to be present in preeclamptic women, contributes to impaired CBF autoregulation. Purified rat AT1-AA or vehicle was infused into pregnant rats from GD 12 to 19 via mini-osmotic pumps after which CBF autoregulation was assessed.
    [Show full text]