Hemodynamic pathogenesis of ischemic hepatic injury following cardiogenic shock/resuscitation

Robert W. Bailey, Matthew L. Brengman, Katherine C. Fuh, Stanley R. Hamilton, H. Franklin Herlong, Gregory B. Bulkley

Research output: Contribution to journalArticle

Abstract

Post-ischemic hepatic injury is observed commonly following cardiogenic or hypovolemic shock. We evaluated the putative roles of the α-adrenergic sympathetic nervous system and the reninangiotensin axis in the pathogenesis of hepatic injury following cardiogenic shock. Previous studies have characterized the hepatic hemodynamic response to shock, while the relationship of these hemodynamic changes to ischemic hepatic injury has not been defined. Sustained (4 h) periods of pericardial tamponade (after mild hemorrhage) followed by 2 h of resuscitation generated a reproducible model of cardiogenic shock and consequent post-ischemic hepatic injury in anesthetized pigs. In a separate group of pigs, the a-adrenergic component of the sympathetic nervous system was ablated with phenoxybenzamine or, in other groups, the renin-angiotensin axis was ablated by either prior nephrectomy or, separately, by confirmed angiotensin converting enzyme inhibition with teprotide. The hepatic injury response in each case was reevaluated. Compared to sham-shocked pigs, those subjected to tamponade alone manifested selective splanchnic vasospasm and consequent biochemical and histological evidence of classic post-ischemic liver injury (centrilobular necrosis involving about a third of each hepatic lobule). These manifestations of splanchnic vasospasm and the consequent ischemic injury were not ameliorated by confirmed α-adrenergic blockade, but significantly attenuated by either method of prior ablation of the renin-angiotensin axis. This model of sustained cardiogenic shock and resuscitation generates the manifestations of ischemic hepatic injury associated with selective splanchnic vasospasm, findings consistent with previous, short-term, hemodynamic studies. The major mediator of this response, and the consequent hepatic injury, is the selective hypersensitivity of the mesenteric vasculature to the renin-angiotensin axis.

Original languageEnglish (US)
Pages (from-to)451-459
Number of pages9
JournalShock
Volume14
Issue number4
StatePublished - Oct 2000

Fingerprint

Cardiogenic Shock
Resuscitation
Hemodynamics
Liver
Wounds and Injuries
Viscera
Angiotensins
Renin
Adrenergic Agents
Swine
Sympathetic Nervous System
Shock
Teprotide
Phenoxybenzamine
Cardiac Tamponade
Peptidyl-Dipeptidase A
Nephrectomy
Hypersensitivity
Necrosis
Hemorrhage

Keywords

  • Hepatic circulation
  • Ischemia/reperfusion
  • Ischemic hepatitis
  • Mesenteric circulation
  • Renin-angiotensin axis
  • Shock liver
  • Splanchnic circulation
  • Tamponade

ASJC Scopus subject areas

  • Physiology
  • Critical Care and Intensive Care Medicine

Cite this

Bailey, R. W., Brengman, M. L., Fuh, K. C., Hamilton, S. R., Herlong, H. F., & Bulkley, G. B. (2000). Hemodynamic pathogenesis of ischemic hepatic injury following cardiogenic shock/resuscitation. Shock, 14(4), 451-459.

Hemodynamic pathogenesis of ischemic hepatic injury following cardiogenic shock/resuscitation. / Bailey, Robert W.; Brengman, Matthew L.; Fuh, Katherine C.; Hamilton, Stanley R.; Herlong, H. Franklin; Bulkley, Gregory B.

In: Shock, Vol. 14, No. 4, 10.2000, p. 451-459.

Research output: Contribution to journalArticle

Bailey, RW, Brengman, ML, Fuh, KC, Hamilton, SR, Herlong, HF & Bulkley, GB 2000, 'Hemodynamic pathogenesis of ischemic hepatic injury following cardiogenic shock/resuscitation', Shock, vol. 14, no. 4, pp. 451-459.
Bailey RW, Brengman ML, Fuh KC, Hamilton SR, Herlong HF, Bulkley GB. Hemodynamic pathogenesis of ischemic hepatic injury following cardiogenic shock/resuscitation. Shock. 2000 Oct;14(4):451-459.
Bailey, Robert W. ; Brengman, Matthew L. ; Fuh, Katherine C. ; Hamilton, Stanley R. ; Herlong, H. Franklin ; Bulkley, Gregory B. / Hemodynamic pathogenesis of ischemic hepatic injury following cardiogenic shock/resuscitation. In: Shock. 2000 ; Vol. 14, No. 4. pp. 451-459.
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AB - Post-ischemic hepatic injury is observed commonly following cardiogenic or hypovolemic shock. We evaluated the putative roles of the α-adrenergic sympathetic nervous system and the reninangiotensin axis in the pathogenesis of hepatic injury following cardiogenic shock. Previous studies have characterized the hepatic hemodynamic response to shock, while the relationship of these hemodynamic changes to ischemic hepatic injury has not been defined. Sustained (4 h) periods of pericardial tamponade (after mild hemorrhage) followed by 2 h of resuscitation generated a reproducible model of cardiogenic shock and consequent post-ischemic hepatic injury in anesthetized pigs. In a separate group of pigs, the a-adrenergic component of the sympathetic nervous system was ablated with phenoxybenzamine or, in other groups, the renin-angiotensin axis was ablated by either prior nephrectomy or, separately, by confirmed angiotensin converting enzyme inhibition with teprotide. The hepatic injury response in each case was reevaluated. Compared to sham-shocked pigs, those subjected to tamponade alone manifested selective splanchnic vasospasm and consequent biochemical and histological evidence of classic post-ischemic liver injury (centrilobular necrosis involving about a third of each hepatic lobule). These manifestations of splanchnic vasospasm and the consequent ischemic injury were not ameliorated by confirmed α-adrenergic blockade, but significantly attenuated by either method of prior ablation of the renin-angiotensin axis. This model of sustained cardiogenic shock and resuscitation generates the manifestations of ischemic hepatic injury associated with selective splanchnic vasospasm, findings consistent with previous, short-term, hemodynamic studies. The major mediator of this response, and the consequent hepatic injury, is the selective hypersensitivity of the mesenteric vasculature to the renin-angiotensin axis.

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