Submitted Successfully!
To reward your contribution, here is a gift for you: A free trial for our video production service.
Thank you for your contribution! You can also upload a video entry or images related to this topic.
Version Summary Created by Modification Content Size Created at Operation
1
Sangyoun Hwang
 -- 2116 2023-12-06 11:07:22 |
2 format change
Peter Tang
 + 10 word(s) 2126 2023-12-07 02:45:26 |

Video Upload Options

We provide professional Video Production Services to translate complex research into visually appealing presentations. Would you like to try it?
No, upload directly Yes

Confirm

Are you sure to Delete?
Yes No
Cite
If you have any further questions, please contact Encyclopedia Editorial Office.
Liu, H.; Nguyen, H.H.; Hwang, S.Y.; Lee, S.S. Oxidative Stress in Cirrhosis and Portal Hypertension. Encyclopedia. Available online: https://encyclopedia.pub/entry/52428 (accessed on 21 December 2024).
Liu H, Nguyen HH, Hwang SY, Lee SS. Oxidative Stress in Cirrhosis and Portal Hypertension. Encyclopedia. Available at: https://encyclopedia.pub/entry/52428. Accessed December 21, 2024.
Liu, Hongqun, Henry H. Nguyen, Sang Youn Hwang, Samuel S. Lee. "Oxidative Stress in Cirrhosis and Portal Hypertension" Encyclopedia, https://encyclopedia.pub/entry/52428 (accessed December 21, 2024).
Liu, H., Nguyen, H.H., Hwang, S.Y., & Lee, S.S. (2023, December 06). Oxidative Stress in Cirrhosis and Portal Hypertension. In Encyclopedia. https://encyclopedia.pub/entry/52428
Liu, Hongqun, et al. "Oxidative Stress in Cirrhosis and Portal Hypertension." Encyclopedia. Web. 06 December, 2023.
Oxidative Stress in Cirrhosis and Portal Hypertension
Edit
This entry is adapted from the peer-reviewed paper 10.3390/ijms242316805

Oxidative stress is an imbalance between the production of reactive oxygen species (ROS) and the antioxidant system reducing its capability to detoxify ROS or repair the resulting damage, i.e., ROS overwhelms antioxidants. Oxidative stress is a key pathogenic factor in chronic liver injury of various etiologies, such as alcoholic liver disease.

oxidative stress cardiovascular cirrhosis liver portal hypertension

1. Introduction

Oxidative stress is an imbalance between the production of reactive oxygen species (ROS) and the antioxidant system reducing its capability to detoxify ROS or repair the resulting damage, i.e., ROS overwhelms antioxidants. Oxidative stress is a key pathogenic factor in chronic liver injury of various etiologies, such as alcoholic liver disease [1], nonalcoholic fatty liver diseases (NAFLD) [2], chronic viral hepatitis, and cholestatic diseases. This damage will ultimately lead to cirrhosis (defined as hepatic architectural damage characterized by nodular regeneration and diffuse fibrosis) [3]. Furthermore, oxidative stress also plays an important pathogenic role in portal hypertension (defined as a portal venous pressure of greater than 12 mm Hg) [4], cirrhotic cardiomyopathy (CCM) [5], hepatorenal syndrome (HRS) [6], cirrhosis-related pulmonary complications [7], and hepatic encephalopathy [8].

2. Pathogenic Mechanisms of Oxidative Stress

Oxidative stress plays a crucial role in the progression of chronic liver diseases to cirrhosis and the development of associated complications. The liver plays a central role in the detoxification of endogenous and exogenous toxins, and harbors a high antioxidant function [3]. In cirrhosis, liver function is significantly impaired and therefore antioxidant function is also jeopardized. This is coupled with excess oxidative stress resulting from portal hypertension driven by gastrointestinal congestion and bacterial translocation [9]. The overactivated ROS can damage the intestine structurally and functionally, as increased lipid peroxidation and protein oxidation have been found in the intestinal mucosa of cirrhotic rats [10] and decompensated cirrhotic patients [11]. Using a carbon tetrachloride (CCl4) model of cirrhosis, Ramachandran and coworkers [10] evaluated oxidative stress status in the gastrointestinal tract. In comparison with controls, xanthine oxidase (XO) activity (an index of oxidative stress) was significantly increased, and xanthine dehydrogenase activity (a parameter of antioxidant status) was significantly decreased in the intestine of cirrhotic rats. This alteration of oxidative stress was associated with a significant reduction in villus fraction, increased enterocyte necrosis, loss of tight junctions, and abnormal intestinal brush border. The damaged intestinal mucosa is thought to enhance intestinal permeability and bacterial translocation that in combination with collateral circulation and an impaired liver results in endotoxemia. Endotoxemia can then further increase oxidative stress, intestinal barrier dysfunction, and organ injury, leading to a ‘vicious cycle’: gut barrier dysfunction → endotoxemia → organ injury. Endotoxemia in cirrhotic subjects plays critical role in cirrhotic complications such as CCM [11], and AKI/HRS [12].

3. Overview of Cardiovascular Abnormalities of Cirrhosis and Portal Hypertension

The cardiovascular system in cirrhotic patients is abnormal, and is characterized by portal hypertension, systemic hyperdynamic circulation (increased cardiac output and decreased peripheral vascular resistance), and arterial pressure [13]. The decrease in peripheral vascular resistance is thought to be due to an imbalance between vasoconstrictive and vasodilatory factors. The former is mainly driven by the sympathetic system [14], renin–angiotensin system (RAS) [15], endothelin-1 [16], and thromboxane [17]; the latter by glucagon [18], prostaglandins [19], bile acids, nitric oxide (NO) [20], carbon monoxide (CO) [21], and hydrogen sulfate (H2S) [22]. Although the vasoconstrictors such as the sympathetic system [23][24] and RAS [25][26] are increased in subjects with cirrhosis, the response of cirrhotic subjects to vasoconstrictors as a whole is impaired [27]. Vasodilators play a dominant role in cirrhotic patients and therefore the cardiovascular system in patients with cirrhosis is characterized by peripheral vascular dilation, decreased systemic vascular resistance (SVR), and mean arterial pressure (MAP). The cardiac output is increased at rest with cirrhotic patients having been described to have hyperdynamic circulation [22]. Under stress, the cardiac functional reserve is insufficient in cirrhosis, with decreased left ventricular responsiveness having been described [28]. Moreover, cardiac diastolic dysfunction has also been reported and can lead to significantly smaller increases in stroke volume when challenged [28]. This collection of cardiac functional abnormalities in patients with cirrhosis is called cirrhotic cardiomyopathy. The diagnosis of cirrhotic cardiomyopathy is based on advanced imaging examination at rest [29].
The pathophysiology of cardiovascular changes in cirrhosis is multifaceted, with inflammation (evidenced by increases of proinflammatory cytokines) [30] and oxidative stress as significant contributors to these changes [5]. There is evidence that oxidative stress also plays an essential role in non-cirrhotic cardiovascular diseases [31]. However, the role of oxidative stress in the pathophysiology of cardiovascular changes in cirrhosis remains incompletely clarified.

4. Oxidative Stress in Pathogenesis of Hyperdynamic Circulation

Cirrhosis and portal hypertension cause hyperdynamic circulation. There are two theories explaining hyperdynamic circulation in subjects with cirrhosis and portal hypertension: the humoral theory and central neural dysregulation [9].

5. Oxidative Stress in the Humoral Theory

The humoral hypothesis suggests that in cirrhosis, mesenteric congestion causes endotoxemia. Endotoxin stimulates the generation of vasodilators such as glucagon [18], prostaglandins [19], NO [32], CO [33], and H2S [34]. All these vasodilators additively/synergically dilate peripheral vasculature which results in hyperdynamic circulation.
Oxidative stress also plays an important role in hyperdynamic circulation. In bile duct ligation (BDL)-induced cirrhosis in rats, Lee et al. [35] found that mesenteric markers of oxidative stress, such as thiobarbituric acid reactive substances (TBARS, an index of lipoperoxidation), and malondialdehyde (MDA), are significantly increased. Congruent with these data, researchers' group has also shown that mesenteric myeloperoxidase (MPO) is significantly increased in portal hypertensive rats [9]. Furthermore, the levels of oxidative stress in the mesentery are closely related to circulating proinflammatory cytokines, such as TNF-α, IL-1β, and IL-6. Lee’s study suggests that oxidative stress may have an additive/synergic effect on systemic inflammation on hyperdynamic circulation in cirrhotic animal models [35]. Now it is clear that cellular enzymes called nicotinamide adenine dinucleotide phosphate (NADPH) oxidases produce a considerable amount of ROS in humans [36] and a rat model of partial portal vein ligation (PPVL) [37]. Deng and coworkers [37] demonstrated that H2O2 is significantly increased in mesenteric tissues and in parallel, phosphorylated eNOS (p-eNOS) is elevated. NADPH oxidase inhibitor, GKT137831, significantly reduces mesenteric H2O2 and p-eNOS, linking oxidative stress and the vasodilator, NO [37]. Interestingly, GKT137831 also reduces cardiac index, portal vein pressure, portal vein blood flow, and portal–systemic shunting in PPVL rats. GKT137831 reverses the decreased mesenteric artery contractile response to norepinephrine in PPVL rats. The final effect of NADPH oxidase inhibition is ameliorating hyperdynamic circulation [37].
In 1998, the Moore lab [38] demonstrated that PPVL rats develop hyperdynamic circulation; this was reversed when these rats were treated with N-acetylcysteine (NAC). Licks et al. [39] later found that in PPVL rats, in parallel with hyperdynamic circulation, the levels of gastric TBARS, nitrates, and nitrites are increased. In their four groups of rats (Sham, Sham + NAC, PPVL, and PPVL + NAC), the levels of oxidative stress markers paralleled that of nitrates and nitrites. The antioxidant parameters, such as superoxide dismutase (SOD) and glutathione peroxidase (GPx), were significantly decreased in PPVL rats. Histology showed that the vessels in the gastric mucosa in the PPVL group were dilated. NAC treatment significantly reversed these changes and resulted in a circulation that resembled what was observed in sham operated control rats. With these results, they concluded that oxidative stress contributes to portal hypertension and hyperdynamic circulation via the regulation of nitrates and nitrites, and antioxidant reverses these changes in the rat PPVL model.
Interestingly, Iwakiri et al. [40] used a double knockout (iNOS, eNOS) mice in a PPVL model and observed that these mice still develop hyperdynamic circulation. This suggests that other variables in addition to the humoral theory may be at play in this complex condition.

6. Oxidative Stress in Central Neural Dysregulation

Hyperdynamic circulation due to the dysregulation of the central neural system [41] has also been described in subjects with cirrhosis and portal hypertension. This theory proposes that there is a reflex arc which regulates the cardiovascular system. The reflex arc includes the receptors in mesentery, afferent nerves, cardiovascular nuclei, and efferent nerves. The signals originating from receptors in mesentery are relayed via afferent nerves to the central neural system which then dispatches signals to the cardiovascular system via efferent nerves. The integrity of the reflex arc is essential for the regulation of the cardiovascular system [9][41][42]. Portal hypertension causes congestion in the mesentery which activates chemoreceptors and/or baroreceptors in the splanchnic area. Researchers' research found that 10 days after PPVL, the MAP and SVR are significantly decreased and cardiac output significantly increased, indicating a hyperdynamic circulation [42]. The researchers examined different interventions to test the role of this reflex arc in hyperdynamic circulation. The researchers first tested the role of capsaicin-sensitive nerves in hyperdynamic circulation. Capsaicin was used to denervate the afferent nerves in rat pups. These rats were subjected to PPVL or BDL-induced cirrhosis when they reached adulthood [43]. The researchers showed that capsaicin-treated PPVL or cirrhotic rats had similar cardiac output and systemic vascular resistance compared to the sham-operated group. In comparison, the PPVL or cirrhotic rats treated with vehicle (DMSO + ethanol) demonstrated hyperdynamic circulation. These data confirmed that capsaicin-treated rats have no capacity to develop hyperdynamic circulation when subjected to PPVL or cirrhosis. Capsaicin had no hemodynamic effect on sham-operated rats. These results showed that capsaicin treatment blocks the development of vasodilation in cirrhotic and portal hypertensive rats. Thus, primary afferent innervation is important in the pathogenesis of hyperdynamic circulation in portal hypertension and cirrhosis.
The researchers then tested the central neural system in the regulation of hyperdynamic circulation in PPVL rats [42]. c-fos is an immediate-early gene and has important roles in cellular signal transduction. The c-fos protein product Fos is significantly increased in central cardiovascular nuclei such as the nucleus tractus solitarius (NTS) and paraventricular nucleus (PVN). Fos is an activation marker in the central neural system. The researchers found that Fos expression is the prerequisite of hyperdynamic circulation in PPVL rats. Fos is detectable at day 1 after PPVL with immunohistochemistry and persistently increased when examined daily in the PPVL rats. However, the hyperdynamic circulation developed on day 3 and remained thereafter. When Fos expression in the NTS was blocked by local microinjection of c-fos antisense oligonucleotides, the increased cardiac output decreased SVR and MAP were reversed in PPVL rats. c-fos antisense oligonucleotides had no effect on circulation in sham-control rats. This experiment indicated that cardiovascular nuclei are crucial to the regulation of hyperdynamic circulation in PPVL rats [42].
The researchers then tried to clarify the afferent nervous pathway. An inflatable cuff around the portal vein was used to acutely increase the portal pressure, then the vagal nerve electrical activity in the cervical area was recorded [41]. The acute increase in portal pressure immediately increased the vagal nerve electrical activity. In another experiment, the cervical vagus nerve was ablated by capsaicin. Three weeks after vagal ablation, the rats were subjected to PPVL. The results showed that vagal nerve ablation significantly decreased Fos expression in the PVN of PPVL rats. Furthermore, vagal nerve blocked the development of hyperdynamic circulation in PPVL rats. This implied that an intact vagal nerve is a sine qua non in the pathogenesis of hyperdynamic circulation in PPVL rats [41].
The initial signal that triggers the hyperdynamic circulation in PPVL rats is thought to be mesenteric congestion. The congestion impacts two types of receptors, baroreceptors and chemoreceptors, as congestion not only increases the mesenteric venous pressure, but also causes ischemia. Chen et al. [44] induced cirrhosis in rats by CCl4, and reported that H2O2 content in the mesenteric arterial wall was significantly increased in comparison to control animals. Several studies demonstrated that an antioxidant such as NAC significantly reverses hyperdynamic circulation in portal hypertensive animal models.
One of these studies from the Moore Lab demonstrated that NAC alleviates oxidative stress and prevents hyperdynamic circulation in the PPVL rats. They showed that the portal pressure remains significantly higher in the PPVL + NAC animals compared with sham + NAC rats [38]. However, that study did not further investigate the mechanism of NAC on the attenuation of hyperdynamic circulation.
The researchers therefore performed a research to investigate the role of oxidative stress in the pathogenesis of hyperdynamic circulation, specifically aiming to evaluate whether oxidative stress is the initiating signal in the gut. The researchers also used the PPVL model in rats because prehepatic portal hypertension creates mesenteric congestion and ischemia without significant liver parenchymal injury. Researchers' research also reconfirmed the effect of NAC on hyperdynamic circulation in PPVL rats [10]. Furthermore, the researchers found that jejunal MPO, an index of intestinal oxidative stress, is significantly increased in the PPVL model in rats; NAC treatment significantly decreased the activity of jejunal MPO. Interestingly, NAC also significantly decreased cardiac output, increased MAP and SVR, and reversed the hyperdynamic circulation in PPVL rats. To confirm that it is the oxidative stress that inaugurates hyperdynamic circulation, H2O2 was applied directly to the mesenteric area. The researchers confirmed that H2O2 stimulates Fos expression in PVN, and decreased MAP, a direct index of hyperdynamic circulation. All these data indicate that it is the oxidative stress that triggers the hyperdynamic circulation in portal hypertension [9].

References

  1. Salete-Granado, D.; Carbonell, C.; Puertas-Miranda, D.; Vega-Rodriguez, V.J.; Garcia-Macia, M.; Herrero, A.B.; Marcos, M. Autophagy, Oxidative Stress, and Alcoholic Liver Disease: A Systematic Review and Potential Clinical Applications. Antioxidants 2023, 12, 1425.
  2. Barrea, L.; Verde, L.; Savastano, S.; Colao, A.; Muscogiuri, G. Adherence to Mediterranean Diet: Any Association with NAFLD? Antioxidants 2023, 12, 1318.
  3. Tanikawa, K.; Torimura, T. Studies on oxidative stress in liver diseases: Important future trends in liver research. Med. Mol. Morphol. 2006, 39, 22–27.
  4. Boyer-Diaz, Z.; Morata, P.; Aristu-Zabalza, P.; Gibert-Ramos, A.; Bosch, J.; Gracia-Sancho, J. Oxidative Stress in Chronic Liver Disease and Portal Hypertension: Potential of DHA as Nutraceutical. Nutrients 2020, 12, 2627.
  5. Mousavi, K.; Niknahad, H.; Ghalamfarsa, A.; Mohammadi, H.; Azarpira, N.; Ommati, M.M.; Heidari, R. Taurine mitigates cirrhosis-associated heart injury through mitochondrial-dependent and antioxidative mechanisms. Clin. Exp. Hepatol. 2020, 6, 207–219.
  6. Nickovic, V.P.; Miric, D.; Kisic, B.; Kocic, H.; Stojanovic, M.; Buttice, S.; Kocic, G. Oxidative stress, NOx/l-arginine ratio and glutathione/glutathione S-transferase ratio as predictors of ‘sterile inflammation’ in patients with alcoholic cirrhosis and hepatorenal syndrome type II. Ren. Fail. 2018, 40, 340–349.
  7. Ommati, M.M.; Mobasheri, A.; Ma, Y.; Xu, D.; Tang, Z.; Manthari, R.K.; Abdoli, N.; Azarpira, N.; Lu, Y.; Sadeghian, I.; et al. Taurine mitigates the development of pulmonary inflammation, oxidative stress, and histopathological alterations in a rat model of bile duct ligation. Naunyn Schmiedebergs Arch. Pharmacol. 2022, 395, 1557–1572.
  8. Bai, Y.; Li, K.; Li, X.; Chen, X.; Zheng, J.; Wu, F.; Chen, J.; Li, Z.; Zhang, S.; Wu, K.; et al. Effects of oxidative stress on hepatic encephalopathy pathogenesis in mice. Nat. Commun. 2023, 14, 4456.
  9. Liu, H.; Alhassan, N.; Yoon, K.T.; Almutlaq, L.; Lee, S.S. Oxidative stress triggers hyperdynamic circulation via central neural activation in portal hypertensive rats. Hepatol. Int. 2023, 17, 689–697.
  10. Ramachandran, A.; Prabhu, R.; Thomas, S.; Reddy, J.B.; Pulimood, A.; Balasubramanian, K.A. Intestinal mucosal alterations in experimental cirrhosis in the rat: Role of oxygen free radicals. Hepatology 2002, 35, 622–629.
  11. Assimakopoulos, S.F.; Tsamandas, A.C.; Tsiaoussis, G.I.; Karatza, E.; Zisimopoulos, D.; Maroulis, I.; Kontogeorgou, E.; Georgiou, C.D.; Scopa, C.D.; Thomopoulos, K.C. Intestinal mucosal proliferation, apoptosis and oxidative stress in patients with liver cirrhosis. Ann. Hepatol. 2013, 12, 301–307.
  12. Gilchrist, I.C. Dorsal Radial Access: Is the Back Door to the Arterial System Ready to Be the Workhorse Entry? Cardiovasc. Revasc. Med. 2019, 20, 735–736.
  13. Danielsen, K.V.; Wiese, S.; Busk, T.; Nabilou, P.; Kronborg, T.M.; Petersen, C.L.; Hove, J.D.; Moller, S.; Bendtsen, F. Cardiovascular Mapping in Cirrhosis From the Compensated Stage to Hepatorenal Syndrome: A Magnetic Resonance Study. Am. J. Gastroenterol. 2022, 117, 1269–1278.
  14. Dietrich, P.; Moleda, L.; Kees, F.; Muller, M.; Straub, R.H.; Hellerbrand, C.; Wiest, R. Dysbalance in sympathetic neurotransmitter release and action in cirrhotic rats: Impact of exogenous neuropeptide Y. J. Hepatol. 2013, 58, 254–261.
  15. Fialla, A.D.; Thiesson, H.C.; Bie, P.; Schaffalitzky de Muckadell, O.B.; Krag, A. Internal dysregulation of the renin system in patients with stable liver cirrhosis. Scand. J. Clin. Lab. Investig. 2017, 77, 298–309.
  16. Hsu, S.J.; Lin, T.Y.; Wang, S.S.; Chuang, C.L.; Lee, F.Y.; Huang, H.C.; Hsin, I.F.; Lee, J.Y.; Lin, H.C.; Lee, S.D. Endothelin receptor blockers reduce shunting and angiogenesis in cirrhotic rats. Eur. J. Clin. Investig. 2016, 46, 572–580.
  17. Sola, E.; Gines, P. Challenges and Management of Liver Cirrhosis: Pathophysiology of Renal Dysfunction in Cirrhosis. Dig. Dis. 2015, 33, 534–538.
  18. Ohara, N.; Jaspan, J.; Chang, S.W. Hyperglucagonemia and hyperdynamic circulation in rats with biliary cirrhosis. J. Lab. Clin. Med. 1993, 121, 142–147.
  19. Oberti, F.; Sogni, P.; Cailmail, S.; Moreau, R.; Pipy, B.; Lebrec, D. Role of prostacyclin in hemodynamic alterations in conscious rats with extrahepatic or intrahepatic portal hypertension. Hepatology 1993, 18, 621–627.
  20. Papagiouvanni, I.; Sarafidis, P.; Theodorakopoulou, M.P.; Sinakos, E.; Goulis, I. Endothelial and microvascular function in liver cirrhosis: An old concept that needs re-evaluation? Ann. Gastroenterol. 2022, 35, 471–482.
  21. Liu, H.; Song, D.; Lee, S.S. Role of heme oxygenase-carbon monoxide pathway in pathogenesis of cirrhotic cardiomyopathy in the rat. Am. J. Physiol. Gastrointest. Liver Physiol. 2001, 280, G68–G74.
  22. Moller, S.; Bendtsen, F. The pathophysiology of arterial vasodilatation and hyperdynamic circulation in cirrhosis. Liver Int. 2018, 38, 570–580.
  23. Henriksen, J.H.; Ring-Larsen, H.; Christensen, N.J. Sympathetic nervous activity in cirrhosis. A survey of plasma catecholamine studies. J. Hepatol. 1985, 1, 55–65.
  24. Vidal Gonzalez, D.; Perez Lopez, K.P.; Vera Nungaray, S.A.; Moreno Madrigal, L.G. Treatment of refractory ascites: Current strategies and new landscape of non-selective beta-blockers. Gastroenterol. Hepatol. 2022, 45, 715–723.
  25. Gunarathne, L.S.; Rajapaksha, H.; Shackel, N.; Angus, P.W.; Herath, C.B. Cirrhotic portal hypertension: From pathophysiology to novel therapeutics. World J. Gastroenterol. 2020, 26, 6111–6140.
  26. Hartl, L.; Rumpf, B.; Domenig, O.; Simbrunner, B.; Paternostro, R.; Jachs, M.; Poglitsch, M.; Marculescu, R.; Trauner, M.; Reindl-Schwaighofer, R.; et al. The systemic and hepatic alternative renin-angiotensin system is activated in liver cirrhosis, linked to endothelial dysfunction and inflammation. Sci. Rep. 2023, 13, 953.
  27. Jimenez, W.; Rodes, J. Impaired responsiveness to endogenous vasoconstrictors and endothelium-derived vasoactive factors in cirrhosis. Gastroenterology 1994, 107, 1201–1203.
  28. Wong, F.; Girgrah, N.; Graba, J.; Allidina, Y.; Liu, P.; Blendis, L. The cardiac response to exercise in cirrhosis. Gut 2001, 49, 268–275.
  29. Izzy, M.; VanWagner, L.B.; Lin, G.; Altieri, M.; Findlay, J.Y.; Oh, J.K.; Watt, K.D.; Lee, S.S.; Cirrhotic Cardiomyopathy Consortium. Redefining Cirrhotic Cardiomyopathy for the Modern Era. Hepatology 2020, 71, 334–345.
  30. Yang, Y.Y.; Liu, H.; Nam, S.W.; Kunos, G.; Lee, S.S. Mechanisms of TNFalpha-induced cardiac dysfunction in cholestatic bile duct-ligated mice: Interaction between TNFalpha and endocannabinoids. J. Hepatol. 2010, 53, 298–306.
  31. Teuber, J.P.; Essandoh, K.; Hummel, S.L.; Madamanchi, N.R.; Brody, M.J. NADPH Oxidases in Diastolic Dysfunction and Heart Failure with Preserved Ejection Fraction. Antioxidants 2022, 11, 1822.
  32. Groszmann, R.J. Hyperdynamic state in chronic liver diseases. J. Hepatol. 1993, 17 (Suppl. 2), S38–S40.
  33. Bolognesi, M.; Di Pascoli, M.; Verardo, A.; Gatta, A. Splanchnic vasodilation and hyperdynamic circulatory syndrome in cirrhosis. World J. Gastroenterol. 2014, 20, 2555–2563.
  34. Ebrahimkhani, M.R.; Mani, A.R.; Moore, K. Hydrogen sulphide and the hyperdynamic circulation in cirrhosis: A hypothesis. Gut 2005, 54, 1668–1671.
  35. Lee, P.C.; Yang, Y.Y.; Huang, C.S.; Hsieh, S.L.; Lee, K.C.; Hsieh, Y.C.; Lee, T.Y.; Lin, H.C. Concomitant inhibition of oxidative stress and angiogenesis by chronic hydrogen-rich saline and N-acetylcysteine treatments improves systemic, splanchnic and hepatic hemodynamics of cirrhotic rats. Hepatol. Res. 2015, 45, 578–588.
  36. Bardaweel, S.K.; Gul, M.; Alzweiri, M.; Ishaqat, A.; ALSalamat, H.A.; Bashatwah, R.M. Reactive Oxygen Species: The Dual Role in Physiological and Pathological Conditions of the Human Body. Eurasian J. Med. 2018, 50, 193–201.
  37. Deng, W.; Duan, M.; Qian, B.; Zhu, Y.; Lin, J.; Zheng, L.; Zhang, C.; Qi, X.; Luo, M. NADPH oxidase 1/4 inhibition attenuates the portal hypertensive syndrome via modulation of mesenteric angiogenesis and arterial hyporeactivity in rats. Clin. Res. Hepatol. Gastroenterol. 2019, 43, 255–265.
  38. Fernando, B.; Marley, R.; Holt, S.; Anand, R.; Harry, D.; Sanderson, P.; Smith, R.; Hamilton, G.; Moore, K. N-acetylcysteine prevents development of the hyperdynamic circulation in the portal hypertensive rat. Hepatology 1998, 28, 689–694.
  39. Licks, F.; Marques, C.; Zetler, C.; Martins, M.I.; Marroni, C.A.; Marroni, N.P. Antioxidant effect of N-acetylcysteine on prehepatic portal hypertensive gastropathy in rats. Ann. Hepatol. 2014, 13, 370–377.
  40. Iwakiri, Y.; Cadelina, G.; Sessa, W.C.; Groszmann, R.J. Mice with targeted deletion of eNOS develop hyperdynamic circulation associated with portal hypertension. Am. J. Physiol. Gastrointest. Liver Physiol. 2002, 283, G1074–G1081.
  41. Liu, H.; Schuelert, N.; McDougall, J.J.; Lee, S.S. Central neural activation of hyperdynamic circulation in portal hypertensive rats depends on vagal afferent nerves. Gut 2008, 57, 966–973.
  42. Song, D.; Liu, H.; Sharkey, K.A.; Lee, S.S. Hyperdynamic circulation in portal-hypertensive rats is dependent on central c-fos gene expression. Hepatology 2002, 35, 159–166.
  43. Lee, S.S.; Sharkey, K.A. Capsaicin treatment blocks development of hyperkinetic circulation in portal hypertensive and cirrhotic rats. Am. J. Physiol. 1993, 264 Pt 1, G868–G873.
  44. Chen, W.; Liu, D.J.; Huo, Y.M.; Wu, Z.Y.; Sun, Y.W. Reactive oxygen species are involved in regulating hypocontractility of mesenteric artery to norepinephrine in cirrhotic rats with portal hypertension. Int. J. Biol. Sci. 2014, 10, 386–395.
More
© Text is available under the terms and conditions of the Creative Commons Attribution (CC BY) license; additional terms may apply. By using this site, you agree to the Terms and Conditions and Privacy Policy.
Upload a video for this entry
Information
Subjects: Physiology
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Hongqun Liu
,
Henry H. Nguyen
,
Sang Youn Hwang
,
Samuel S. Lee
View Times: 439
Revisions: 2 times (View History)
Update Date: 07 Dec 2023
Table of Contents
    1000/1000
    Hot Most Recent
    Video Production Service
    Feedback