Abstract
Our understanding of the underlying pathophysiological processes in the development of severe shock, multiple organ failure, and death following trauma, hemorrhage, and sepsis was quite vague around 1950, and is still not complete. World War II and the wars during the following decades, in Korea and Vietnam, stimulated much research aimed at achieving further knowledge in this area. A major part of this research was experimental, and based on large experimental animals such as dogs, pigs, and cats, and techniques commonly used in studies of normal physiology. During the 1930s and 1940s, the very basic principles of shock, such as the importance of hypovolemia following hemorrhage, became established. Moreover, around 1950, the importance of early fluid resuscitation was also recognized. At that time, however, it was not clear what disturbances took place in the peripheral circulation during shock, and to what extent, if any, these disturbances influenced the outcome. This chapter focuses on publications from 1950 and onwards which were of importance for our understanding of the role of the peripheral circulation during shock. I have included papers that focus on the splanchnic circulation, and those which explore mechanisms by which this particular area could exert an influence on the outcome of the shock state. The mechanisms discussed in these papers are still considered important in the pathophysiology of shock today. Most of the experimental papers discussed here study whole animal physiology and outcome of induced shock. The results and mechanisms discussed in these papers were verified in clinical studies, and it is this clinical correlation that makes the reported papers important and classical. One paper cited (Parrillo et al.1985) is both clinical and experimental. It is included since it verified in patients a mechanism that was originally described in experimental studies, but that had become very controversial because of the lack of a clear clinical correlate.
This is a preview of subscription content, log in via an institution to check access.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
Similar content being viewed by others
Reference
Surgery 1957; 42: 1043–1054
Related references
Wiggers CJ.The Physiology of Shock. New York: Commonwealth Fund, 1950.
Marston A. The bowel in shock. Lancet 1962; 2b: 881.
Lillehei, RC, Longerbeam JK, Bloch JH, Manax WG. The nature of irreversible shock: experimental and clinical observations. Ann Surg 1964; 160: 682–708.
Reference
N Engl J Med 1959; 260: 214–220
Related references
Kuida H. Discussion of ‘the intestinal circulation in shock’. Gastroenterology1967; 52: 458–460.
Deitch E. Multiple organ failure. Pathophysiology and potential future therapy. Ann Surg 1992; 216: 117–134.
Marshal JC, Christou NV, Meakins JL. The gastrointestinal tract. The ‘undrained abscess’ of multiple organ failure. Ann Surg 1993; 218: 111–119.
Reference
Circ Res 1963; 13: 105–118
Related references
Lewis DH, Mellander S. Competitive effects of sympathetic control and tissue metabolites on resistance and capacitance vessels and capillary filtration in skeletal muscle. Acta Physiol Scand 1962; 56: 162–188.
Lillehei RC, Longerbeam JK, Bloch JH, Manax WG. The nature of irreversible shock: experimental and clinical observations. Ann Surg 1964; 160: 682–708.
Haglund U, Lundgren O. The effects of vasoconstrictor nerve stimulation on consecutive vascular sections of cat small intestine during hemorrhagic hypotension. Acta Physiol Scand 1973; 88: 95–108.
Reference
Ann Surg 1969; 169: 227–232
Related references
Hardaway RM. The problem of acute severe trauma and shock. Surg Gynecol Obstet 1971; 133: 799–806.
Schlichtig R, Bowles SA. Distinguishing between aerobic and anaerobic appearance of dissolved CO2 in intestine during low flow. J Appl Physiol 1994; 76: 2443–2451.
Consensus Report. Tissue hypoxia. How to detect, how to correct, how to prevent. Intensive Care Med 1996; 22: 1250–1257.
Reference
Arch Surg 1970; 101: 478–483
Related references
Haglund U, Lundgren O. Non-occlusive acute intestinal vascular failure. Br J Surg 1979; 66: 155–158.
Bounous G. Acute necrosis of the intestinal mucosa. Gastroenterology 1982; 82: 1457–1467.
Park PO, Haglund U, Bulkley GB, Fält K. The sequence of development of intestinal tissue injury after strangulation ischemia and reperfusion. Surgery 1990; 107: 575–580.
Reference
Am J Physiol 1980; 239: H664–H77
Related references
Younes RN, Aun F, Accioly CQ et al. Hypertonic solutions in the treatment of hypo-volemic shock: a prospective, randomized study in patients admitted to the emergency room. Surgery 1992; 111: 380–385.
Wade CE, Kramer GC, Grady JJ et al. Efficacy of hypertonic 7.5% saline and 6% Dex-tran-70 in treating trauma: a meta-analysis of controlled clinical studies. Surgery 1997; 122: 609–616.
Angle N, Hoyt DB, Coimbra R et al. Hypertonic saline resuscitation diminishes lung injury by suppressing neutrophil activation after hemorrhagic shock. Shock 1998; 9: 164–170.
Reference
Gastroenterlogy 1981; 81: 22–29
Related references
Haglund U, Bulkley G, Granger DN. On the pathophysiology of intestinal ischaemic injury. Acta Chir Scand 1987; 153: 321–324.
Hoshino T, Maley WR, Bulkley GB, Williams GM. Ablation of free radical-mediated reperfusion injury for the salvage of kidneys taken from non-heartbeating donors. Transplantation 1988; 45: 284–289.
Granger DN. Role of xanthine oxidase and granulocytes in ischaemia-reperfusion injury. Am J Physiol 1988; 255 (Heart Circ Physiol 24): H1269–H275.
Reference
J Appl Physiol 1984; 56: 1065–1069
Reference
Circ Res 1963; 13: 105–118
Related references
Doglio D, Pusajo J, Egurrola M et al. Gastric mucosal pH as a prognostic index of mortality in critically ill patients. Crit Care Med 1991; 19: 1037–1040.
Hartman M, Montgomery A, Jönsson K et al. Tissue oxygenation in hemorrhagic shock measured as transcutaneous oxygen tension, subcutaneous oxygen tension, and gastrointestinal intramucosal pH in pigs. Crit Care Med 1991; 19: 205–210.
Gutierrez G, Palizas F, Doglio G et al. Gastric intramucosal pH as a therapeutic index of tisssue oxygenation in critically ill patients. Lancet 1992; 339: 195–199.
Reference
J Clin Invest 1985; 76: 1539–1553
Related references
Lefer AM. Role of myocardial depressant factor in the pathogenesis of circulatory shock. Fed Proc 1970; 29: 1836–1847.
Haglund U, Lundgren O. Cardiovascular effects of blood borne material released from the cat small intestine during simulated shock conditions. Acta Physiol Scand 1973; 89: 558–570.
Carli AM, Auclair MC, Vernimmen C, Jourdon P. Reversal by calcium of rat heart cell dysfunction induced by human sera in septic shock. Circ Shock 1979; (Suppl) 6: 147–157.
Reference
Arch Surg 1991; 126: 211–218
Related references
Dahn M, Lange P, Lobdell K et al. Splanchnic and total body oxygen consumption differences in septic and injured patients. Surgery 1987; 101: 69–80.
Van der Meer TJ, Wang H, Fink MP. Endotoxemia causes ileal mucosal acidosis in the absence of mucosal hypoxia in a normodynamic porcine model of septic shock. Crit Care Med 1995; 23: 1217–1226.
Antonsson JB, Haglund UH. Gut intramucosal pH and intraluminal pO2 in a porcine model of peritonitis and hemorrhage. Gut 1995; 37: 791–797.
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2008 Springer-Verlag London Limited
About this chapter
Cite this chapter
Haglund, U.H. (2008). The gut and its role in circulatory shock. In: Fink, M., Hayes, M., Soni, N. (eds) Classic Papers in Critical Care. Springer, London. https://doi.org/10.1007/978-1-84800-145-9_5
Download citation
DOI: https://doi.org/10.1007/978-1-84800-145-9_5
Publisher Name: Springer, London
Print ISBN: 978-1-84882-005-0
Online ISBN: 978-1-84800-145-9
eBook Packages: MedicineMedicine (R0)