Summary Heart failure and liver disease often coexist because of systemic disorders and diseases that affect both organs as well as complex cardio-hepatic interactions. Heart failure can cause acute or chronic liver injury due to ischaemia and passive venous congestion, respectively. Congestive hepatopathy is frequently observed in patients with congenital heart disease and after the Fontan procedure, but also in older patients with chronic heart failure. As congestive hepatopathy can evolve into cirrhosis and hepatocellular carcinoma, screening for liver injury should be performed in patients with chronic cardiac diseases and after Fontan surgery. Fibrosis starts in the centro-lobular zone and will extend progressively to the portal area. Chronic liver injury can be reversible if heart function improves. However, in the case of terminal heart failure, uncontrolled by medical resources or by assistive device support, the combination of heart and liver transplants must be discussed in patients with chronic advanced liver fibrosis. In this review of the literature, we will focus on congestive hepatopathy and its complications, such as liver fibrosis and hepatocellular carcinoma, with the aim of improving the management and surveillance of patients experiencing these complications.

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Human umbilical arteries are known to be modulated by oxygen partial pressure. To further understand the underlying mechanisms, rings were suspended in organ chambers for the measurement of isometric force. The effects of 5-hydroxytryptamine (10^–9 to 10^–5 M) were first investigated before and after hypoxic conditions (5% O₂–5% CO₂ in N₂). Then after pretreatment, we tested indomethacin (10^–5 M), N-nitro-L-arginine (L-NNA, 10^–5 M) and nicorandil (10^–5 M) each separately, then each of the three substances together with hypoxia. In separate experiments the contractions to 5-hydroxytryptamine (10^–9 to 10^–5 M) were effectuated in a glucose-free medium, and mitochondrial respiration was inhibited by cyanide (2 mM). Hypoxic conditions significantly reduced the contractive response to 5-hydroxytryptamine. Contractions were enhanced after indomethacin, but remained unchanged after L-NNA. Pretreatment with nicorandil decreased the contraction. Furthermore, hypoxia and nicorandil dramatically decreased the contraction to 5-hydroxytryptamine. In glucose-free medium under normoxia or in hypoxic conditions, 5-hydroxytryptamine did not induce any contraction. Moreover, cyanide (2 mM) remained without effect on the contraction obtained by 5-hydroxytryptamine. These results suggest that hypoxia and nicorandil attenuate vasoconstrictor responses to 5-hydroxytryptamine in human umbilical arteries. Furthermore, these findings suggest that prostacyclin acts as a functional antagonist to vasoconstriction whereas nitric oxide does not. Finally, glycolysis seems to be involved rather than mitochondrial metabolism.

Ž .Heart failure HF is a common clinical problem confronting physicians and is often the final manifestation of many cardiovascular disorders. Despite recent advances in the pharmacological management of HF, it remains a highly lethal and disabling disorder. A number of animal models have been developed to study both the pathophysiology of HF and new therapeutic approaches to this complex syndrome. Only through an improved understanding of the basic biology of the early stages of the syndrome can HF be prevented or at least anticipated. With this in view, we have developed an easily realisable and inexpensive model in the guinea pig, which presents numerous structural, metabolic and biochemical similarities compared with the human heart. Thirty guinea pigs, aged 5 weeks and weighing 300 g were used. After anaesthesia, left Ž . Ž . nephrectomy was performed. After 1 week the guinea pigs were divided into: a control group n s 15 , which received an Ž . Ž . injection of vehicle as well as tap water for 10 weeks; b DOCA-salts group n s 15 , where the animals were treated with an IM injection of 10 mg DOCA 5 days a week for 10 weeks and with drinking water containing 9 grl y1 NaCl and 2 grl y1 KCl. Our results demonstrate that the administration of DOCA-salts to guinea pigs for 10 weeks caused a significant increase in Ž . Ž . Ž . blood pressure BP q 30% associated with left ventricular hypertrophy LVH , evaluated by LV weight q37% , LV wall Ž . Ž . Ž . q36% , by the ratio LV weightrBody weight q23% and by an increase in LV volume q51% . Concerning HF, the latter was clinically evident through an increase in body weight, heart rate and dyspnoea. Indeed, guinea pigs presented pleural andror pericardial effusion often associated with ascite. This model, which combines pressure and volume overload, results in a slow evolution towards HF. This allows a better understanding of the mechanisms in early LV remodelling which has the potential to develop into HF. Some recent studies have emphasised the value of using guinea pigs. The guinea pig heart muscle presents two major regulatory mechanisms of contractility that are closer to those found in humans, the isomyosin pattern which is predominantly V and the phenomenon of Ca 2q -induced Ca 2q -release from the sarcoplasmic reticulum. The 3 DOCA-salts model in the guinea pig is an easy surgical procedure with high post-operative survival, which causes an increase in arterial BP, LVH associated with HF. This model is a useful tool for studying some of the basic mechanisms of cardiovascular diseases. ᮊ

Ž .Heart failure HF is a common clinical problem confronting physicians and is often the final manifestation of many cardiovascular disorders. Despite recent advances in the pharmacological management of HF, it remains a highly lethal and disabling disorder. A number of animal models have been developed to study both the pathophysiology of HF and new therapeutic approaches to this complex syndrome. Only through an improved understanding of the basic biology of the early stages of the syndrome can HF be prevented or at least anticipated. With this in view, we have developed an easily realisable and inexpensive model in the guinea pig, which presents numerous structural, metabolic and biochemical similarities compared with the human heart. Thirty guinea pigs, aged 5 weeks and weighing 300 g were used. After anaesthesia, left Ž . Ž . nephrectomy was performed. After 1 week the guinea pigs were divided into: a control group n s 15 , which received an Ž . Ž . injection of vehicle as well as tap water for 10 weeks; b DOCA-salts group n s 15 , where the animals were treated with an IM injection of 10 mg DOCA 5 days a week for 10 weeks and with drinking water containing 9 grl y1 NaCl and 2 grl y1 KCl. Our results demonstrate that the administration of DOCA-salts to guinea pigs for 10 weeks caused a significant increase in Ž . Ž . Ž . blood pressure BP q 30% associated with left ventricular hypertrophy LVH , evaluated by LV weight q37% , LV wall Ž . Ž . Ž . q36% , by the ratio LV weightrBody weight q23% and by an increase in LV volume q51% . Concerning HF, the latter was clinically evident through an increase in body weight, heart rate and dyspnoea. Indeed, guinea pigs presented pleural andror pericardial effusion often associated with ascite. This model, which combines pressure and volume overload, results in a slow evolution towards HF. This allows a better understanding of the mechanisms in early LV remodelling which has the potential to develop into HF. Some recent studies have emphasised the value of using guinea pigs. The guinea pig heart muscle presents two major regulatory mechanisms of contractility that are closer to those found in humans, the isomyosin pattern which is predominantly V and the phenomenon of Ca 2q -induced Ca 2q -release from the sarcoplasmic reticulum. The 3 DOCA-salts model in the guinea pig is an easy surgical procedure with high post-operative survival, which causes an increase in arterial BP, LVH associated with HF. This model is a useful tool for studying some of the basic mechanisms of cardiovascular diseases. ᮊ