Vasopressin in Septic Shock: Effects on Pancreatic, Renal, and Hepatic Blood Flow

Overview

Journal Crit Care

Specialty Critical Care

Date 2007 Dec 15

PMID 18078508

Citations 13

Authors

Vladimir Krejci

Luzius B Hiltebrand

Stephan M Jakob

Jukka Takala

Gisli H Sigurdsson

Affiliations

Soon will be listed here.

Abstract

Introduction: Vasopressin has been shown to increase blood pressure in catecholamine-resistant septic shock. The aim of this study was to measure the effects of low-dose vasopressin on regional (hepato-splanchnic and renal) and microcirculatory (liver, pancreas, and kidney) blood flow in septic shock.

Methods: Thirty-two pigs were anesthetized, mechanically ventilated, and randomly assigned to one of four groups (n = 8 in each). Group S (sepsis) and group SV (sepsis/vasopressin) were exposed to fecal peritonitis. Group C and group V were non-septic controls. After 240 minutes, both septic groups were resuscitated with intravenous fluids. After 300 minutes, groups V and SV received intravenous vasopressin 0.06 IU/kg per hour. Regional blood flow was measured in the hepatic and renal arteries, the portal vein, and the celiac trunk by means of ultrasonic transit time flowmetry. Microcirculatory blood flow was measured in the liver, kidney, and pancreas by means of laser Doppler flowmetry.

Results: In septic shock, vasopressin markedly decreased blood flow in the portal vein, by 58% after 1 hour and by 45% after 3 hours (p < 0.01), whereas flow remained virtually unchanged in the hepatic artery and increased in the celiac trunk. Microcirculatory blood flow decreased in the pancreas by 45% (p < 0.01) and in the kidney by 16% (p < 0.01) but remained unchanged in the liver.

Conclusion: Vasopressin caused marked redistribution of splanchnic regional and microcirculatory blood flow, including a significant decrease in portal, pancreatic, and renal blood flows, whereas hepatic artery flow remained virtually unchanged. This study also showed that increased urine output does not necessarily reflect increased renal blood flow.

Citing Articles

Purine nucleoside phosphorylase inhibition is an effective approach for the treatment of chemical hemorrhagic cystitis.

Wolf-Johnston A, Ikeda Y, Zabbarova I, Kanai A, Bastacky S, Moldwin R JCI Insight. 2024; 9(5).

PMID: 38271096 PMC: 10972598. DOI: 10.1172/jci.insight.176103.

Efficacy and Safety of Vasopressin and Terlipressin in Preterm Neonates: A Systematic Review.

Al-Saadi A, Sushko K, Bui V, van den Anker J, Razak A, Samiee-Zafarghandy S Int J Environ Res Public Health. 2022; 19(21).

PMID: 36360641 PMC: 9658127. DOI: 10.3390/ijerph192113760.

Myocardial effects of angiotensin II compared to norepinephrine in an animal model of septic shock.

Garcia B, Su F, Dewachter L, Favory R, Khaldi A, Moiroux-Sahraoui A Crit Care. 2022; 26(1):281.

PMID: 36117167 PMC: 9482744. DOI: 10.1186/s13054-022-04161-3.

The effects of vasopressors with and without dobutamine on haemodynamics, metabolism and gut injury during endotoxic shock in rabbits. A controlled study.

de Oliveira N, Gandolfi J, Contrim L, Pereira R, Fernandes L, Silva Jr J Anaesthesiol Intensive Ther. 2022; 54(2):141-149.

PMID: 35792110 PMC: 10156477. DOI: 10.5114/ait.2022.117264.

Purine nucleoside phosphorylase inhibition ameliorates age-associated lower urinary tract dysfunctions.

Birder L, Wolf-Johnston A, Wein A, Cheng F, Grove-Sullivan M, Kanai A JCI Insight. 2020; 5(20).

PMID: 32910805 PMC: 7605521. DOI: 10.1172/jci.insight.140109.

References

Shelly M, Greatorex R, Calne R, Park G . The physiological effects of vasopressin when used to control intra-abdominal bleeding. Intensive Care Med. 1988; 14(5):526-31. DOI: 10.1007/BF00263525. View

Knotzer H, Pajk W, Maier S, Ladurner R, Kleinsasser A, Wenzel V . Arginine vasopressin reduces intestinal oxygen supply and mucosal tissue oxygen tension. Am J Physiol Heart Circ Physiol. 2005; 289(1):H168-73. DOI: 10.1152/ajpheart.01235.2004. View

HOLMES C, Walley K, Chittock D, Lehman T, Russell J . The effects of vasopressin on hemodynamics and renal function in severe septic shock: a case series. Intensive Care Med. 2001; 27(8):1416-21. DOI: 10.1007/s001340101014. View

Kuznetsova L, Tomasek N, Sigurdsson G, Banic A, Erni D, Wheatley A . Dissociation between volume blood flow and laser-Doppler signal from rat muscle during changes in vascular tone. Am J Physiol. 1998; 274(4):H1248-54. DOI: 10.1152/ajpheart.1998.274.4.H1248. View

Kam P, Tay T . The pharmacology of ornipressin (POR-8): a local vasoconstrictor used in surgery. Eur J Anaesthesiol. 1998; 15(2):133-9. DOI: 10.1111/j.0265-0215.1998.00247.x. View

Hof R . Modification of vasopressin- and angiotensin II- induced changes by calcium antagonists in the peripheral circulation of anaesthetized rabbits. Br J Pharmacol. 1985; 85(1):75-87. PMC: 1916755. DOI: 10.1111/j.1476-5381.1985.tb08833.x. View

Klinzing S, Simon M, Reinhart K, Bredle D, Meier-Hellmann A . High-dose vasopressin is not superior to norepinephrine in septic shock. Crit Care Med. 2003; 31(11):2646-50. DOI: 10.1097/01.CCM.0000094260.05266.F4. View

Schmeisch A, de Oliveira D, Ide L, Suzuki-Kemmelmeier F, Bracht A . Zonation of the metabolic action of vasopressin in the bivascularly perfused rat liver. Regul Pept. 2005; 129(1-3):233-43. DOI: 10.1016/j.regpep.2005.03.005. View

Eichinger M, Resta J, Walker B . Myogenic contribution to agonist-induced renal vasoconstriction during normoxia and hypoxia. Am J Physiol. 1997; 272(4 Pt 2):H1945-51. DOI: 10.1152/ajpheart.1997.272.4.H1945. View

10.

Landry D, Levin H, Gallant E, Ashton Jr R, Seo S, DAlessandro D . Vasopressin deficiency contributes to the vasodilation of septic shock. Circulation. 1997; 95(5):1122-5. DOI: 10.1161/01.cir.95.5.1122. View

11.

Haglund U . The splanchnic organs as the source of toxic mediators in shock. Prog Clin Biol Res. 1988; 264:135-45. View

12.

Jakob S . Clinical review: splanchnic ischaemia. Crit Care. 2002; 6(4):306-12. PMC: 137310. DOI: 10.1186/cc1515. View

13.

Dunser M, Mayr A, Ulmer H, Ritsch N, Knotzer H, Pajk W . The effects of vasopressin on systemic hemodynamics in catecholamine-resistant septic and postcardiotomy shock: a retrospective analysis. Anesth Analg. 2001; 93(1):7-13. DOI: 10.1097/00000539-200107000-00003. View

14.

ERWALD R, WIECHEL K, Strandell T . Effect of vasopressin on regional splanchnic blood flows in conscious man. Acta Chir Scand. 1976; 142(1):36-42. View

15.

Hiltebrand L, Krejci V, Banic A, Erni D, Wheatley A, Sigurdsson G . Dynamic study of the distribution of microcirculatory blood flow in multiple splanchnic organs in septic shock. Crit Care Med. 2000; 28(9):3233-41. DOI: 10.1097/00003246-200009000-00019. View

16.

Sakr Y, Dubois M, De Backer D, Creteur J, Vincent J . Persistent microcirculatory alterations are associated with organ failure and death in patients with septic shock. Crit Care Med. 2004; 32(9):1825-31. DOI: 10.1097/01.ccm.0000138558.16257.3f. View

17.

Wheatley A, Hickman R . The influence of flow and hematocrit on the laser Doppler flux signal from the surface of the perfused pig liver. Microcirculation. 1995; 2(1):19-25. DOI: 10.3109/10739689509146756. View

18.

Kerr J, Jain K, Swan K, Rocko J . Effects of vasopressin on cardiac output and its distribution in the subhuman primate. J Vasc Surg. 1985; 2(3):443-9. View

19.

Hiltebrand L, Krejci V, Jakob S, Takala J, Sigurdsson G . Effects of vasopressin on microcirculatory blood flow in the gastrointestinal tract in anesthetized pigs in septic shock. Anesthesiology. 2007; 106(6):1156-67. DOI: 10.1097/01.anes.0000267599.02140.86. View

20.

Malay M, Ashton Jr R, Landry D, Townsend R . Low-dose vasopressin in the treatment of vasodilatory septic shock. J Trauma. 1999; 47(4):699-703; discussion 703-5. DOI: 10.1097/00005373-199910000-00014. View