全部 标题 作者
关键词 摘要

OALib Journal期刊
ISSN: 2333-9721
费用:99美元

查看量下载量

相关文章

更多...

A Hemodynamic Study to Evaluate the Buffer Response in Cirrhotic Patients Undergoing Liver Transplantation

DOI: 10.1155/2014/757910

Full-Text   Cite this paper   Add to My Lib

Abstract:

The physiological regulation of the liver blood flow is a result of a reciprocal portal vein and hepatic artery flow relationship. This mechanism is defined as the hepatic arterial buffer response (HABR). This study was addressed to investigate whether HABR is maintained in denervated grafts in liver transplant recipients. Portal blood flow (PBF) and hepatic arterial resistance index (PI) were measured 6 months after transplantation using Doppler. In each patient we consecutively measured the vasodilator (Ensure Plus PO versus placebo) and vasoconstrictor (isosorbide dinitrate 5?mg SL versus placebo) stimuli. The meal ingestion caused a significant increase of both parameters, PBF (from to ?mL/min, ) and PI (from to , ). By contrast, isosorbide dinitrate reduced PBF (from to ?mL/min, ) and PI (from to , ). We show that PBF and PI are reciprocally modified with the administration of vasoconstrictor and vasodilator stimuli. These results suggest the persistence of the HABR in a denervated human model, suggesting that this mechanism is independent of the regulation from the autonomic nervous system. 1. Introduction Portal hypertension is associated with systemic hyperdynamic state characterized by a high cardiac output and a low peripheral vascular resistance [1]. The splanchnic circulation is also hyperkinetic, with an increase in portal blood flow, which is an important factor in the development and maintenance of the syndrome [2]. Recent studies have shown that restoration of normal hepatic function after liver transplantation should reverse hemodynamic disturbances [3–5]. During the last years, several experimental and clinical evidences have demonstrated reciprocity between changes in blood flow in the hepatic artery and the portal vein. It has been suggested that hepatic artery plays a passive role; that is, fluctuations in portal blood flow are buffered by inverse changes in arterial flow [6–8]. Until now, this physiological relationship has not been evaluated in stable liver transplant recipients. Therefore, the aims of the present study were (a) to evaluate hepatic arterial and portal blood flows after liver transplantation and (b) to measure the response of the hepatic artery to portal flow variations. 2. Material and Methods 2.1. Patients Systemic and hepatic hemodynamic parameters were evaluated in eight patients with cirrhosis after six months of liver transplantation (ages 21 to 52 years). The cause of chronic liver disease was hepatitis C in 7 patients and cryptogenic in 1. Liver recipients were stable and none of them had clinical or

References

[1]  J. Bosch, R. Mastai, and D. Kravetz, “Hemodynamic evaluation of the patient with portal hypertension,” Seminars in Liver Disease, vol. 6, no. 4, pp. 309–317, 1986.
[2]  J. Vorobioff, J. E. Bredfeldt, and R. J. Groszmann, “Increased blood flow through the portal system in cirrhotic rats,” Gastroenterology, vol. 87, no. 5, pp. 1120–1126, 1984.
[3]  D. Alvarez, S. Gerona, Z. Waisburg, M. Ciardullo, E. de Santibanes, and R. Mastai, “Splanchnic hyperemia after liver transplantation in patients with end- stage liver disease,” Liver Transplantation and Surgery, vol. 4, no. 4, pp. 300–303, 1998.
[4]  J. M. Henderson, G. J. MacKay, M. Hooks et al., “High cardiac output of advanced liver disease persists after orthotopic liver transplantation,” Hepatology, vol. 15, no. 2, pp. 258–262, 1992.
[5]  M. Navasa, F. Feu, J. C. Garcia-Pagan et al., “Hemodynamic and humoral changes after liver transplantation in patients with cirrhosis,” Hepatology, vol. 17, no. 3, pp. 355–360, 1993.
[6]  W. W. Lautt, “Mechanism and role of intrinsic regulation of hepatic arterial blood flow: hepatic arterial buffer response,” American Journal of Physiology—Gastrointestinal and Liver Physiology, vol. 249, no. 5, part 1, pp. G549–G556, 1985.
[7]  W. W. Lautt, “The 1995 Ciba-Ceigy award lecture. Intrinsic regulation of hepatic blood flow,” Canadian Journal of Physiology and Pharmacology, vol. 74, no. 3, pp. 223–233, 1996.
[8]  B. Rocheleau, C. éthier, R. Houle, P. M. Huet, and M. Bilodeau, “Hepatic artery buffer response following left portal vein ligation: its role in liver tissue homeostasis,” American Journal of Physiology—Gastrointestinal and Liver Physiology, vol. 277, no. 5, pp. G1000–G1007, 1999.
[9]  D. Alvarez, D. Golombek, P. Lopez et al., “Diurnal fluctuations of portal and systemic hemodynamic parameters in patients with cirrhosis,” Hepatology, vol. 20, no. 5, pp. 1198–1203, 1994.
[10]  C. Sabba, G. G. Weltin, D. V. Cicchetti et al., “Observer variability in echo-Doppler measurements of portal flow in cirrhotic patients and normal volunteers,” Gastroenterology, vol. 96, no. 6, pp. 1603–1611, 1990.
[11]  C. Sabba, G. Ferraioli, P. Buonamico et al., “A randomized study of propranolol on postprandial portal hyperemia in cirrhotic patients,” Gastroenterology, vol. 102, no. 3, pp. 1009–1016, 1992.
[12]  D. Sacerdoti, C. Merkel, M. Bolognesi, P. Amodio, P. Angeli, and A. Gatta, “Hepatic arterial resistance in cirrhosis with and without portal vein thrombosis: relationships with portal hemodynamics,” Gastroenterology, vol. 108, no. 4, pp. 1152–1158, 1995.
[13]  W. W. Lautt, D. J. Legare, and M. S. d'Almeida, “Adenosine as putative regulator of hepatic arterial flow (the buffer response),” American Journal of Physiology—Heart and Circulatory Physiology, vol. 248, pp. H331–H338, 1985.
[14]  M. Bolognesi, D. Sacerdoti, G. Bombonato et al., “Change in portal flow after liver transplantation: effect on hepatic arterial resistance indices and role of spleen size,” Hepatology, vol. 35, no. 3, pp. 601–608, 2002.
[15]  T. Ayuse, N. Brienza, C. P. O'Donnell, and J. L. Robotham, “Pressure-flow analysis of portal vein and hepatic artery interactions in porcine liver,” American Journal of Physiology—Heart and Circulatory Physiology, vol. 267, no. 4, pp. H1233–H1242, 1994.
[16]  R. T. Mathie and L. H. Blumgart, “The hepatic haemodynamic response to acute portal venous blood flow reductions in the dog,” Pflugers Archiv European Journal of Physiology, vol. 399, no. 3, pp. 223–227, 1983.
[17]  W. W. Lautt, D. J. Legare, and M. S. d'Almeida, “Adenosine as putative regulator of hepatic arterial flow (the buffer response),” American Journal of Physiology—Heart and Circulatory Physiology, vol. 17, no. 3, pp. H331–H338, 1985.
[18]  R. T. Mathie and B. Alexander, “The role of adenosine in the hyperaemic response of the hepatic artery to portal vein occlusion (the “buffer response”),” British Journal of Pharmacology, vol. 100, no. 3, pp. 626–630, 1990.
[19]  W. W. Lautt, “Regulatory processes interacting to maintain hepatic blood flow constancy: vascular compliance, hepatic arterial buffer response, hepatorenal reflex, liver regeneration, escape from vasoconstriction,” Hepatology Research, vol. 37, no. 11, pp. 891–903, 2007.
[20]  M. I. Friedman, “Hepatic nerve function,” in The Liver: Biology and Pathobiology, I. M. Arias, W. B. Jakoby, H. Popper, D. Schacther, and D. A. Shafritz, Eds., pp. 949–959, Raven Press, New York, NY, USA, 2nd edition, 1988.
[21]  P. D. I. Richardson and P. G. Withrington, “The effects of intraportal injections of noradrenaline, adrenaline, vasopressin and angiotensin on the hepatic portal vascular bed of the dog: marked tachyphylaxis to angiotensin,” British Journal of Pharmacology, vol. 59, no. 2, pp. 293–301, 1977.
[22]  M. Kato, Y. Nimura, M. Miyachi et al., “Intravenous catecholamines alter hepatic blood flow in conscious dogs with experimental hepatic denervation,” Journal of Surgical Research, vol. 66, no. 2, pp. 179–184, 1996.
[23]  M. Kjaer, J. Jurlander, S. Keiding, H. Galbo, P. Kirkegaard, and E. Hage, “No reinnervation of hepatic sympathetic nerves after liver transplantation in human subjects,” Journal of Hepatology, vol. 20, no. 1, pp. 97–100, 1994.
[24]  D. M. Payen, M. D. Fratacci, P. Dupuy et al., “Portal and hepatic arterial blood flow measurements of human transplanted liver by implanted Doppler probes: interest for early complications and nutrition,” Surgery, vol. 107, no. 4, pp. 417–427, 1990.
[25]  J. M. Henderson, G. T. Gilmore, G. J. Mackay, J. R. Galloway, T. F. Dodson, and M. H. Kutner, “Hemodynamics during liver transplantation: the interactions between cardiac output and portal venous and hepatic arterial flows,” Hepatology, vol. 16, no. 3, pp. 715–718, 1992.
[26]  S. Gelman, “General anesthesia and hepatic circulation,” Canadian Journal of Physiology and Pharmacology, vol. 65, no. 8, pp. 1762–1779, 1987.
[27]  W. W. Lautt, D. J. Legare, and T. R. Daniels, “The comparative effect of administration of substances via the hepatic artery or portal vein on hepatic arterial resistance, liver blood volume and hepatic extraction in cats,” Hepatology, vol. 4, no. 5, pp. 927–932, 1984.
[28]  W. G. Schenk, J. C. McDonald, K. Mcdonald, and T. Drapanas, “Direct measurement of hepatic blood flow in surgical patients: with related observations on hepatic flow dynamics in experimental animals,” Annals of surgery, vol. 156, pp. 463–471, 1962.
[29]  G. B. G. Klintmalm, L. M. Olson, A. W. Paulsen, C. W. Whitten, and B. S. Husberg, “Hepatic arterial thrombosis after liver transplantation: intraoperative electromagnetic blood flow evaluation,” Transplantation Proceedings, vol. 20, no. 1, pp. 616–618, 1988.

Full-Text

Contact Us

service@oalib.com

QQ:3279437679

WhatsApp +8615387084133