DOCSLIB.ORG

Derived Resuscitation Fluids on Euvolemic and Hypovolemic Rats

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Derived Resuscitation Fluids on Euvolemic and Hypovolemic Rats PHYSIOLOGIC CHANGES INDUCED BY INTRAVENOUS INFUSION OF KERATIN- DERIVED RESUSCITATION FLUIDS ON EUVOLEMIC AND HYPOVOLEMIC RATS By FIESKY A. NUÑEZ JR, MD A Dissertation Submitted to the Graduate Faculty of WAKE FOREST UNIVERSITY GRADUATE SCHOOL OF ARTS AND SCIENCES In Partial Fulfillment of the Requirements For the Degree of DOCTOR OF PHILOSOPHY Physiology and Pharmacology May 2012 Winston-Salem, North Carolina ApProved by Thomas L. Smith, PhD, Advisor Mark Van Dyke, PhD, Chair George Christ, PhD Patricia Gallagher, PhD Ann Tallant, PhD DEDICATION To my wife: Alejandra, your infinite patience and understanding allowed me to mature as a Person and as a scientist. Without you I would not have accomplished this feat. I love you To my Parents, for your unconditional support that allowed this road to be filled with joy and success. To my sister: Mary, your wisdom and emotional suPPort gave me the strength and hope I needed in order to achieve many things. You always make me think of a better tomorrow and a better me. ii ACKNOWLEDGEMENTS Special Thanks to: Tom: For your impeccable mentorshiP and disPosition to always put my best interests first. Mark: For your dedication and Patience to teach such an impatient subject. Mike: For your knowledge and hard work in day-to-day lab efforts. Maria: Thank you for your patience in the lab and for sharing your immense knowledge of keratin with me. Keratin Krew and Biomaterials core: Roche, Bailey, Chris, Lauren, Mary, Julie, Jill, Carmen, DeePika. Your collaborations allow individual contributions to flourish into an extraordinary lab. OrthoaPedic Lab: Beth, Eileen, Martha, Jan, Casey. All of you make this workplace Pleasant and successful, I hoPe for years to come it remains this way because it’s my second home. Keranetics Personnel: Thank you for your assistance and support during our collaboration. iii TABLE OF CONTENTS LIST OF ILLUSTRATIONS AND TABLES……………………………………………………………… V LIST OF ABBREVIATIONS……………………………………………………………….………………… VII ABSTRACT……………………………………………………………………………..………………………….. IX CHAPTER I – Introduction…………………………………………………………………………………… 1 CHAPTER II – Vasoactive Properties of Keratin-Derived Compounds……………..…… 28 CHAPTER III – Hemodynamic Recovery After HyPovolemic Shock and Resuscitation with Lactated Ringer’s and Keratoe Resuscitation Fluid; A Novel Colloid………………………………………………………………………….… 58 CHAPTER IV – Conclusions……………………………………………………………………………… 93 APPENDICES…....................................................................................................................................... 104 SCHOLASTIC VITA………………………………………………………………………………………… 112 iv LIST OF ILLUSTRATIONS AND TABLES CHAPTER I - Introduction Figure 1 – Renin-Angiotensin-Aldosterone system………….…………………………………... 6 Figure 2 – Shear stress-mediated release of NO from the endothelium………….…..…8 Table 1 – Safety tests conducted on a Keratose biomaterial…………………..…………… 16 CHAPTER II - Vasoactive Properties of Keratin-Derived Compounds Figure 1 - Size eXclusion chromatograPhy of keratose samples………………………… 52 Figure 2 - Video stills of the same vessel before and after KRF administration……53 Figure 3 - Change in arteriolar diameter with i.v. administration of Fluid…………… 54 Figure 4 - Effect on arteriolar diameter with and without L-nitro-arginine…………. 55 Figure 5 - Average arteriolar diameter increase with KRF of different viscosities……………………………….……………………………………… 56 Figure 6 - Average arteriolar diameter increase with infusion of AlPha and KAP containing fluids………………………………….…… 57 CHAPTER III - Hemodynamic Recovery After HyPovolemic Shock and Resuscitation with Lactated Ringer’s and Keratoe Resuscitation Fluid; A Novel Colloid Figure 1 – Hemodynamic changes after hyPovolemic shock and treatment with low-volume resuscitation fluids ………………… 83 Figure 2 - Circulating blood volume changes after hyPovolemic shock and v treatment with low-volume resuscitation fluids........................................ 84 Figure 3 – Hemodynamic changes after hyPovolemic shock and treatment with full-volume resuscitation fluids……………………...…… 85 Figure 4 - Circulating blood volume changes after hyPovolemic shock and treatment with full-volume resuscitation fluids......................................86 Figure 5 – Tissue Histology………………………………………………………………………......… 87 Supplemental Figure 1 - Ultrasound Transit Flow Probes................................................ 88 Supplemental Figure 2 - Mean Arterial Pressure and Heart Rate Monitoring…….89 Supplemental Table 1 - Hemodynamics and Arterial Blood Gases: Low Volume Resuscitation, Short Term Assessment……………………….… 90 Supplemental Table 2 - Hemodynamics and Arterial Blood Gases: Full Volume Resuscitation, Short Term Assessment………………………..… 91 Supplemental Table 3 - Hemodynamics, Arterial Blood Gases and Electrolytes: Long Term Assessment………………………………………………………………………. 92 CHAPTER IV - CONCLUSIONS Figure 1 - Blood Pressure Recovery After HyPovolemic Shock and Treatment with KIF-KRF and AK-KRF…………………………………..…… 98 APPENDICES Table 1 - Different Fractions of Keratose: vi Classification by components, their respective biologic activity and potential clinical uses……………….. 107 Figure 1 - Concentration of Keratose needed to Prepare a compound with a viscosity of 3.88cP at 10dynes/cm2........................................................ 109 vii LIST OF ABBREVIATIONS Abs Absorbance ACV Actively circulating volume ANOVA Analysis of variance CBV Central blood volume CI Cardiac Index CO Cardiac outPut cP Centipoise DI Deionized Hb Hemoglobin HCT Hematocrit HEPES Hydroxyethyl- piperazine ethanesulfonic acid HR Heart rate i.v. or IV Intravenous IEx Ion exchange KAP Keratin-associated protein KDa Kilo Dalton KIF Keratose Intermediate Filament KRF Keratin resuscitation fluid l-NA l-nitroarginine MAP Mean Arterial Pressure viii mmHg Millimeters of mercury NLMWCO Nominal low molecular weight cutoff NO Nitric oxide PBS Phosphate buffered saline Phe Phenylephrine SEC Size eXclusion chromatograPhy SNP Sodium NitroPrusside ULF Unit length filament. ix ABSTRACT Fiesky A. Nuñez Jr. MD PHYSIOLOGIC CHANGES INDUCED BY INTRAVENOUS INFUSION OF KERATIN- DERIVED RESUSCITATION FLUIDS ON EUVOLEMIC AND HYPOVOLEMIC RATS Research Problem: The field of cardiovascular research has evolved significantly over the last decade, and yet cardiovascular related deaths remain a Primary cause of trauma related death. Shock and resuscitation are toPics of high importance in the field of emergency medicine due to the high mortality that they carry, which has not been ProPerly addressed in the Past decades. The develoPment of better treatment oPtions for this entity is essential. Methods: 1) The vasoactive properties of intravenously infused keratin- derived compounds were assessed, with the use of cremaster muscle microvascular observations in the Sprague-Dawley rat. 2) After assessing feasibility for intravenous infusion in the microvascular model, hemodynamic and metabolic recovery after hemorrhage and resuscitation with commercially available crystalloids and keratin compounds was studied. Ultrasound dilution method was used to determine changes in cardiac indeX, stroke volume and circulating volumes. Femoral cannulation was used to determine changes in arterial blood pressure and heart rate. Arterial blood gases were measured to compare acid-base profile changes. Conclusions: The initial keratin compounds tested in this research elicited an uneXPected vasodilatory effect on the microvasculature of the cremaster muscle, which can be further developed for other uses. Further purification allowed the formulation of keratin compounds without vasodilatory effects, improved osmotic effects, and enhanced viscosity. These compounds are biocompatible colloids for resuscitation PurPoses. These enhancements will allow the use of this compound with lower volumes than the current gold standard and significantly reduce complications. X CHAPTER I INTRODUCTION Fiesky A. Nunez Jr. MD 1 Clinical Significance Traumatic injuries account for 9% of annual global mortality and it is estimated that half of these deaths occur in individuals between 15 and 44 years of age (1). Hemorrhagic shock is the leading cause of death among trauma Patients worldwide. 50% of Patients that suffer bleeding severe enough to cause shock will die despite aggressive and Prompt treatment (2). Although not reliable as an isolated measure of disease severity, a systolic blood Pressure below 100mmHg at emergency dePartment admission increases hosPital mortality threefold and sudden death risk tenfold (3, 4). However, continuous research has proven that the only factor that decreases mortality is early diagnosis and Prompt restoration of volume and cardiac function (5-7). Shock is a state of severe impairment in tissue Perfusion that results in diminished tissue oxygen delivery and utilization as well as impaired removal of metabolic waste byproducts. Untreated, shock triggers a chain of pathologic events that result in localized cellular death followed by multiPle organ dysfunction and death of the individual. The Primary treatment for all tyPes of shock remains ProPer fluid resuscitation and specific efforts to correct the factors that Precipitate shock. Etiology of Shock Shock is defined as the incaPacity of the cardiovascular system to maintain ProPer tissue perfusion (8, 9). Causes of shock are variable and are grouped into four sPecific categories according to the Pathologic mechanisms involved: 2 1. Cardiogenic Shock: IncaPacity of the heart to maintain ProPer cardiac outPut due to
Load more

Recommended publications
  • THE CARDIO-CIRCULATORY EFFECTS in MAN of NEO- SYNEPHRIN (1-Α-Hydroxy-Β-Methylamino-3-Hydroxy- Ethylbenzene Hydrochloride)
    THE CARDIO-CIRCULATORY EFFECTS IN MAN OF NEO- SYNEPHRIN (1-α-hydroxy-β-methylamino-3-hydroxy- ethylbenzene hydrochloride) Ancel Keys, Antonio Violante J Clin Invest. 1942;21(1):1-12. https://doi.org/10.1172/JCI101270. Research Article Find the latest version: https://jci.me/101270/pdf THE CARDIO-CIRCULATORY EFFECTS IN MAN OF NEO-SYNEPHRIN (1-a-hydroxy-,8-methylamino-3-hydroxy-ethylbenzene hydrochloride) 1 BY ANCEL KEYS AND ANTONIO VIOLANTE (From the Laboratory of Physiological Hygiene, Medical School, University of Minnesota, Minneapolis) (Received for publication June 20, 1941) Neo-synephrin 2 differs chemically from epi- at least one day was allowed to elapse between studies nephrine only in the absence of the hydroxy group on any one subject. The general procedure in all studies was the same. para on the benzene ring. The in the position The subject rested quietly for 10 to 30 minutes and then first pharmacological studies with this substance measurements and observations were begun and continued emphasized the conclusion that the pharmacologi- for 10 minutes or more before the drug was adminis- cal action of neo-synephrin resembles that of epi- tered. Observations were continued for 1 to 4 hours nephrine in all respects, but the potency is less and following the administration. In all cases blood pressure the duration of effects is longer (12, 13, 21). and pulse rate were measured at frequent intervals throughout the entire experimental period. The same Inspection of the data in these papers shows, how- observer measured blood pressures throughout any one ever, that the pressor effect is relatively much experiment.
    [Show full text]
  • A New Treatment for Abdominal Surgical Shock
    Where it is possible the mucous membrane of and the skin is closed, except for a point at the the roof of the canal should not be destroyed and lower angle through which the catheter is brought the ends of the urethra will thus be prevented out. When the closure of the wound is complete, from retracting excessively. In the worst cases, ¿he patient is placed in a horizontal position, the where the urethra has been practically destroyed, catheter is adjusted at the proper point and is transverse division may be necessary. In many then fastened in position by a suture in the skin. of the inflammatory strictures, however, it is After-treatment. The important points in the possible to leave this strip on the roof which does after-treatment are— the care of the anterior not in any way interfere with the free mobilization urethra and the retention of the catheter until the of the anterior segment. For convenience of wound is completely healed. The care of the description, the steps of the operation will be anterior urethra has been described above, and given in order. the essential thing is that the urethra should be (1) With the patient in the lithotomy position a kept entirely clean with some solution which will free median incision is made down to the urethra, not produce undue irritation, and by some method dividing the structures of the bulb in the median which will not traumatize the suture. It has line and turning them aside. It is important that seemed to us that injection with a small syringe is this incision should be carried well backward so preferable to irrigation, either with a catheter or that the membranous urethra can be exposed.
    [Show full text]
  • Coronary Thrombosis
    University of Nebraska Medical Center DigitalCommons@UNMC MD Theses Special Collections 5-1-1938 Coronary thrombosis R. W. Karrer University of Nebraska Medical Center This manuscript is historical in nature and may not reflect current medical research and practice. Search PubMed for current research. Follow this and additional works at: https://digitalcommons.unmc.edu/mdtheses Part of the Medical Education Commons Recommended Citation Karrer, R. W., "Coronary thrombosis" (1938). MD Theses. 669. https://digitalcommons.unmc.edu/mdtheses/669 This Thesis is brought to you for free and open access by the Special Collections at DigitalCommons@UNMC. It has been accepted for inclusion in MD Theses by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. CORONARY THROMBOSIS by R. w. Karrer Senior Thesis presented to the College of Medicine, University of Nebraska Omaha, 1938. 480947 INTRODUCTION The terms coronary thrombosis, coronary occlusion, and cardiac or myocardial infarction are often em- ployed as synonyms, although there are useful differences in their meanings. In this thesis the author will deal only with that special type of coronary occlusion in which coronary thrombosis is the final event in the process of occlusion. Also, the thesis will be limited, more or less, to that type of thrombosis which is acute thrombosis of a coronary artery, rather than to the chronic type which is neither as spec­ tacular a disease nor as clean cut in its clinical picture. The definition of coronary thrombosis as given by Dorland {1935} is, "The formation of a clot in a branch of the coronary arteries which supply blood to the heart muscle, resulting in obstruction of the artery and infarction of the area of the heart supplied by the occluded vessel." Cecil (1935) modifies the definition in that he mentions the obstruction is generally acute.
    [Show full text]
  • The Action of Epinephrin Upon the Muscle Tissue of the Vein
    Proceedings of the Iowa Academy of Science Volume 18 Annual Issue Article 27 1911 The Action of Epinephrin upon the Muscle Tissue of the Vein J. T. M'Clintock Copyright ©1911 Iowa Academy of Science, Inc. Follow this and additional works at: https://scholarworks.uni.edu/pias Recommended Citation M'Clintock, J. T. (1911) "The Action of Epinephrin upon the Muscle Tissue of the Vein," Proceedings of the Iowa Academy of Science, 18(1), 125-129. Available at: https://scholarworks.uni.edu/pias/vol18/iss1/27 This Research is brought to you for free and open access by the Iowa Academy of Science at UNI ScholarWorks. It has been accepted for inclusion in Proceedings of the Iowa Academy of Science by an authorized editor of UNI ScholarWorks. For more information, please contact [email protected]. M'Clintock: The Action of Epinephrin upon the Muscle Tissue of the Vein THE ACTION OF EPINEPHBIN UPON THE MUSCLE TISSUE OP THE VEIN. The physiology of the venous circulation has, in comparison to that of the arterial, received very little consideration. It has been looked upon as a circulation carried on in a system of inert, elastic tubes, carrying the blood back to the heart from the periphery and without much, if any, physiological action on the part of the venous wall in the process. We are in the habit of looking to the heart, the arterial tension and the skeletal muscle action as being the forces driving the blood through the venous system. The venous part of the circulation is of equal importance to the arterial, for under the conditions as they exist the one cannot be with out the other and it is hardly to be expected that in so important a process the tissue would be left with only the physical force of elas ticity upon which to depend for meeting the variable conditions to which it must be subjected.
    [Show full text]
  • Controlled Hypotension 443 Some Other Than That at the Neuro-Muscular GRIFFITH, H
    Postgrad Med J: first published as 10.1136/pgmj.31.359.443 on 1 September 1955. Downloaded from September 1955 SCURR: Control of the Blood Pressure and Controlled Hypotension 443 some other than that at the neuro-muscular GRIFFITH, H. R., and JOHNSON, G. E. (1942), Anaesthesiology action, 3, 4I8. junction, which is as yet unknown. BENNETT, A. E. (1940), J.A.M.A., 144, 322. GRAY, R. W., et al. (I941), Psych. Quart., 15, 159. BIBLIOGRAPHY WATERTON. C. (x812), 'Wanderings in S. America,' Everyman BERNARD, CLAUDE (1843), ' Note sur la Curarine et ses effects Series, Dent, London. physiologiques,' Paris. BEECHER, H. K., and TODD, D. P. (I954), Ann. Surg., I, 140. >CONTROL OF THE BLOOD PRESSURE AND CONTROLLED HYPOTENSION By C. F. SCURR, M.V.O., M.B., B.S., D.A., R.C.S., F.F.A. Consultant Anaesthetist, Westminster Hospital; Honorary Anaesthetist, Hospital of Ss. John and Elizabeth Control of the Blood Pressure during the vagus and sympathetic, it can be improved by Anaesthesia humoral agents (adrenaline) and inotropic drugs, Blood pressure is the lateral pressure exerted by and is readily depressed by certain anaesthetic the blood on the vessel walls; our considerations agents which produce dilatation. Protected by copyright. are especially directed to the arterial system. The (b) Cardiac Filling: This depends on the length difference between systolic and diastolic pressure of diastole and the effective venous pressure. is the pulse pressure which depends on the stroke Venous pressure: The venous system accounts volume of the heart and the volume, elasticity and for 70 per cent.
    [Show full text]
  • Vascular Responses to Acute Intracranial Hypertension
    J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.34.5.587 on 1 October 1971. Downloaded from J. Neurol. Neurosurg. Psychiat., 1971, 34, 587-601 Vascular responses to acute intracranial hypertension S. S. HAYREH1 AND J. EDWARDS From the Department of Experimental Ophthalmology, Institute of Ophthalmology, University of London SUMMARY In 27 rhesus monkeys the cerebrospinal fluid pressure (CSFP) was raised by injections into the cisterna magna to about 40 to 50 mm Hg in steps of 5 mm Hg every five minutes. During the initial phase of the rise of the CSFP to about 15 mm Hg normal animals showed a significant fall in the systolic arterial blood pressure. With a further elevation of the CSFP the BP rose till the CSFP reached 30 to 40 mm Hg. If the CSFP were raised higher than that, a large number of the animals showed a significant fall in the BP. In animals which were shocked before the CSFP was raised there was no drop in the systolic BP during the initial phase. This study indicates that vascular decompensation occurs in the majority of animals when the CSFP goes higher than 30 to 40 mm guest. Protected by copyright. Hg; there is a significant rise in the pulse rate, superior sagittal sinus pressure (SSP), and internal jugular vein pressure (JVP). The JVP was related to the SSP, indicating that the JVP most probably reflected the pressure changes in the intracranial venous sinuses. Four animals suddenly collapsed at the highest CSFP. In the remaining 23 animals, on a sudden lowering of the CSFP to zero from the highest level, 13 monkeys died in less than half an hour and four in about an hour, while six animals stood this elevation of the CSFP well, with a good recovery.
    [Show full text]
  • Resuscitation-Fluid Replacement W
    Postgrad Med J: first published as 10.1136/pgmj.43.503.592 on 1 September 1967. Downloaded from Postgrad. med. J. (September 1967) 43, 592-598. Resuscitation-fluid replacement W. G. PROUT R. VAUGHAN JONES M.B., F.R.C.S. M.B., M.R.C.P., M.C.Path. Surgical Registrar, Consultant Pathologist, St Peter's Hospital, Chertsey, and St Thomas' Hospital, London North West Surrey Group Laboratory St Peter's Hospital, Chertsey THIS short account will be confined to the dromes with no common single clinical manifesta- management of circulatory failure in the first few tion. hours after reception of the patient in a Casualty Bloch et al. (1966) define shock as a state of Department. Where shock is due to trauma the progressive circulatory failure in which the cardiac cause will usually be obvious, but many shocked output is insufficient to meet tissue requirements cases brought to Casualty Departments suffer for nutrition, oxygenation or waste disposal. This from other diseases in which circulatory failure definition serves to emphasize the basic patho- may be complex in origin. For this reason we have logical feature, that of defective tissue perfusion. also discussed non-traumatic causes. For the different forms of shock, further terms have been introduced. Shires (1967) has suggested Traumatic shock subdivision into haematogenic, neurogenic, vaso- It is generally agreed that reduction in the genic and cardiogenic forms, but these are termsby copyright. circulating blood volume is the main factor in the without therapeutic implication. McGowan & production of traumatic shock. When external or Walters (1966) point out that clinically two internal haemorrhage takes place, the fluid lost is, patterns of circulatory upset are most often seen of course, blood.
    [Show full text]
  • Cardiogenic Shock
    Res Medica, Spring 1969, Volume VI, Number 3 Page 1 of 8 Cardiogenic Shock Andrew G. Leitch B.Sc. Abstract DEFINITION AND PATHOGENESIS INCIDENCE Cardiogenic shock is shock occurring after myocardial infarction. It has been variously described as occurring in 6%, 8%, 10%, 12% and 20% of patients with myocardial infarction. Shock accompanies the onset of pain in few eases and most cases occur in the first twenty-four hours after infarction although they may occur several days after. CLINICAL CRITERIA The criteria for diagnosis of shock may vary with different authors (hence the anomalous 20% above) but, in general, it is agreed that shock is suggested clinically by the following features: cold, clammy extremities, pallor and cyanosis, rapid, thready pulse, anuria or oliguria, anxiety, restlessness or apathy, and prolonged hypotension. The only objective assessment is of blood pressure and this alone does not define shock. Considerable variation may therefore be expected in diagnosis. In view of the difficulties in defining the criteria for diagnosis of shock, the individual criteria and the interpretations placed upon them warrant further discussion. Copyright Royal Medical Society. All rights reserved. The copyright is retained by the author and the Royal Medical Society, except where explicitly otherwise stated. Scans have been produced by the Digital Imaging Unit at Edinburgh University Library. Res Medica is supported by the University of Edinburgh’s Journal Hosting Service: http://journals.ed.ac.uk ISSN: 2051-7580 (Online) ISSN: 0482-3206 (Print) Res Medica is published by the Royal Medical Society, 5/5 Bristo Square, Edinburgh, EH8 9AL Res Medica, Spring 1969, 6(3): 13-19 doi: 10.2218/resmedica.v6i3.851 Leitch, A.
    [Show full text]
  • The Effect of Total Sympathectomy on the Occurrence of Shock from Hemorrhage
    THE EFFECT OF TOTAL SYMPATHECTOMY ON THE OCCURRENCE OF SHOCK FROM HEMORRHAGE N. E. Freeman, … , H. E. Holling, N. E. Marean J Clin Invest. 1938;17(3):359-368. https://doi.org/10.1172/JCI100960. Research Article Find the latest version: https://jci.me/100960/pdf THE EFFECT OF TOTAL SYMPATHECTOMY ON THE OCCURRENCE OF SHOCK FROM HEMORRHAGE By N. E. FREEMAN, S. A. SHAFFER, A. E. SCHECTER AND H. E. HOLLINGi WITH THE TECHNICAL ASSISTANCE OF N. E. MAREAN (From the Harrison Department of Surgical Research, School of Medicine, University of Pennsylvania, Philadelphia) (Received for publication January 20, 1938) Shock has been differentiated from hemor- shock in the experimental animal. This apparent rhage on the basis of hemoconcentration, nega- paradox was attributed to a reduction in the tive reaction to blood transfusions, and pathologi- volume flow of blood to the peripheral tissues cal changes in the tissues (1). In hemorrhage, produced by constriction of the arterioles. The dilution of the blood occurs while concentration hypothesis was advanced that vasoconstriction takes place in shock. After simple loss of blood, enabled the organism to adjust to the immediate prompt recovery follows transfusion, whereas in crisis. If this reaction were so intense and pro- severe shock, the administration of blood is fre- tracted, however, as to reduce the nutrient flow quently unavailing. It has been held that the to the tissues, shock would be produced. tissues are anemic after hemorrhage while the The reaction of normal dogs to hemorrhage pathological picture of shock is that of " dilatation was, therefore, compared with that of completely and engorgement of capillaries and vessels " (2).
    [Show full text]
  • Study on Alterations of Blood Flow and Blood Viscosity Under Hemorrhagic Shock and Effects of Plasma Expander
    Nagoya J. me d. Sci. 31: 339-355. 1969. STUDY ON ALTERATIONS OF BLOOD FLOW AND BLOOD VISCOSITY UNDER HEMORRHAGIC SHOCK AND EFFECTS OF PLASMA EXPANDER YosHIKAzu MATSUNAGA 1st Department of Surgery, Nagoya Univeys?fy School of Medicine (Director: Prof. Yoshio Hashimoto) ABSTRACT Experiments were performed in 48 dogs subjected to a shock produced by hemorrhage after the modified Wiggers' method. Dogs were infused 90 minutes after hemorrhage with one of six test substances; shed blood, 5% glucose solution, or four kinds of dextran ( mw. 75,000, 47,000, 29,000 and 12,000 ). Infusion of dextran with mw. 29,000 produced the most remarkable increase in femoral arterial blood flow above the prehemorrhagic level. This flow improvement was thought to be more attributable to reduction in blood viscosity than an increase in blood volume. INTRODUCTION The development of shock is a complicated phenomenon not necessarily causally related to any one factor. The shock may be resulted from a multi­ plicity of influences such as hormonal, neural, circulatory and so onn. Hemorrhage, if it is significant in amount, may cause irreversible responses of the circulatory system. Maintenance of blood volume and blood pressure is necessary, but there is no guarantee to restore capillary circulation even with an adequate blood replacement. The circulatory conditions after hemorrhage are accompanied by cellular aggregation or sludging, increased blood viscosity and venular stasis of cells11 - 41 • Cellular aggregation, if uncorrected, may reduce nutritive capillary blood flow and result in hypoxic damages of the parenchy­ matous organs. A failure of capillary circulation is related to a principal cause of a fatal process.
    [Show full text]
  • Irwin and Rippe's Intensive Care Medicine
    BOOKS,SOFTWARE,&OTHER MEDIA findings. This chapter emphasizes a step- therapy and explains the various classes of ment chart would have been extremely help- ␤ by-step approach to thorough physical ex- drugs, such as anti-infectives, 2 adrener- ful. amination and defining normal findings with gics, corticosteroids, and xanthines. In- The highlights in each of these chapters abnormal findings that the practitioner may cluded in this section are drug-delivery were the author’s inclusion of educational encounter. The chapter also includes “age methods (eg, metered-dose inhaler, powder discharge notes, which will help clinicians awareness” alerts to which the clinician inhaler), indications, adverse effects, and and student prepare the patient and family should pay close attention when assessing points to which the clinician should pay close for discharge by making them aware of pos- children or the elderly, and “red flags” to attention when delivering medications. Also sible outcomes. Overall, each of these chap- highlight subjects that could be of great im- included are discussions on inhalation ther- ters was what I would call the “CliffNotes” portance (eg, during chest inspection, watch apy, continuous positive airway pressure, for most common respiratory diseases and for areas of abnormal collapse during inspi- mechanical ventilation, and bronchial hy- problems. These supplement big heavy ration or abnormal expansion during expi- giene. I found all the treatments to be very pathophysiology books very well, and this ration, which could signify paradoxical accurate and according to the American As- book is an easy-to-use reference. movement). The “age awareness” and “red sociation for Respiratory Care clinical prac- The last chapter, on emergencies, mainly flag” alerts appear throughout the book and tice guidelines.
    [Show full text]
  • Historical Paper in Surgery a Brief History of Shock
    Historical Paper in Surgery A brief history of shock Frederick Heaton Millham, MD, Newton, MA From Newton Wellesley Hospital, Newton, MA RECENTLY,2MIDDLE-AGED COUSINS were admitted to context. My intention is to discuss the term as it is the Level I trauma center where I attend as a used in the surgical and trauma literature. In a trauma surgeon. Each had been shot twice. Their setting of hemodynamic instability, this word is wounds were similar; both suffered a single gun- frequently used to indicate a syndrome of hypoten- shot wound to the epigastrium and a second sion, tachycardia, and mental status change owing, wound in the left flank. The first cousin (let us presumably, to ‘‘inadequate tissue perfusion.’’ To- call him Joe), had a normal pulse and blood pres- day we use the word shock to describe patients in sure and was oriented and composed; his skin was extremis who suffer from a variety of distinct pink and dry. The second cousin (let us call him pathophysiologic processes, such as severe cardiac Frank) was hypotensive and tachycardic; he was ap- dysfunction or overwhelming infection that share athetic and disoriented, although paramedics re- insufficient tissue perfusion as a consequence. ported that he had been agitated and combative The story of how this word came to be attached in the field just minutes before. His skin was pale to these dramatic clinical syndromes and how our and he was diaphoretic. There was 1 operating predecessors conceptualized the physiology of room immediately available and 1 that would be shock is a central theme of the past 300 years of ready in 20 minutes.
    [Show full text]