The major limitation of live donor liver transplantation (LDLT) is the graft size. Grafts from the live donors are likely to be small-for-size for the recipients, especially when the recipient is larger than the donor. Small-for-size graft injuries have been frequently observed, 1–3 but the exact mechanism remains unclear. The majority of previous studies have focused on the hepatic functional analysis and light microscopy, 4,5 but no study has investigated the portal hemodynamics and intragraft gene response at the acute phase after reperfusion in relation to graft size. Although our previous animal study showed that damage of hepatic sinusoids resulted from excessive blood flow and transient portal hypertension at the early phase after reperfusion, 6 the conclusion could not be extrapolated to humans. This is because in the rat model, preexisting portal hypertension is absent, while in the clinical situation, cirrhosis and portal hypertension are usually severe. To clarify the relationship of sinusoidal injury and graft size, we investigated the portal hemodynamics at the early phase after reperfusion together with intragraft gene detection and electron microscope examination in patients receiving right lobe LDLT.

Graft Injury in Relation to Graft Size in Right Lobe Live Donor Liver Transplantation: A Study of Hepatic Sinusoidal Injury in Correlation With Portal Hemodynamics and Intragraft Gene Expression

After receiving information from afferent nerves, the hypothalamus sends signals to peripheral organs, including the liver, to keep homeostasis. There are two ways for the hypothalamus to signal to the peripheral organs: by stimulating the autonomic nerves and by releasing hormones from the pituitary gland. In order to reveal the involvement of the autonomic nervous system in liver function, we focus in this study on autonomic nerves and neuroendocrine connections between the hypothalamus and the liver. The hypothalamus consists of three major areas: lateral, medial, and periventricular. Each area has some nuclei. There are two important nuclei and one area in the hypothalamus that send out the neural autonomic information to the peripheral organs: the ventromedial hypothalamic nucleus (VMH) in the medial area, the lateral hypothalamic area (LHA), and the periventricular hypothalamic nucleus (PVN) in the periventricular area. VMH sends sympathetic signals to the liver via the celiac ganglia, the LHA sends parasympathetic signals to the liver via the vagal nerve, and the PVN integrates information from other areas of the hypothalamus and sends both autonomic signals to the liver. As for the afferent nerves, there are two pathways: a vagal afferent and a dorsal afferent nerve pathway. Vagal afferent nerves are thought to play a role as sensors in the peripheral organs and to send signals to the brain, including the hypothalamus, via nodosa ganglia of the vagal nerve. On the other hand, dorsal afferent nerves are primary sensory nerves that send signals to the brain via lower thoracic dorsal root ganglia. In the liver, many nerves contain classical neurotransmitters (noradrenaline and acetylcholine) and neuropeptides (substance P, calcitonin gene-related peptide, neuropeptide Y, vasoactive intestinal polypeptide, somatostatin, glucagon, glucagon-like peptide, neurotensin, serotonin, and galanin). Their distribution in the liver is species-dependent. Some of these nerves are thought to be involved in the regulation of hepatic function as well as of hemodynamics. In addition to direct neural connections, the hypothalamus can affect metabolic functions by neuroendocrine connections: the hypothalamus-pancreas axis, the hypothalamus-adrenal axis, and the hypothalamus-pituitary axis. In the hypothalamus-pancreas axis, autonomic nerves release glucagon and insulin, which directly enter the liver and affect liver metabolism. In the hypothalamus-adrenal axis, autonomic nerves release catecholamines such as adrenaline and noradrenaline from the adrenal medulla, which also affects liver metabolism. In the hypothalamus-pituitary axis, release of glucocorticoids and thyroid hormones is stimulated by pituitary hormones. Both groups of hormones modulate hepatic metabolism. Taken together, the hypothalamus controls liver functions by neural and neuroendocrine connections.

https://onlinelibrary.wiley.com/doi/pdf/10.1002/ar.a.20086

Neural connections between the hypothalamus and the liver

https://aasldpubs.onlinelibrary.wiley.com/doi/pdf/10.1053/jhep.2003.50044

Vascular mediators in the injured liver.

Exosomes mediate intercellular transfer of pro-fibrogenic connective tissue growth factor (CCN2) between hepatic stellate cells, the principal fibrotic cells in the liver

The role(s) of somatostatin, structurally related peptides and somatostatin receptors in the gastrointestinal tract: a review.

https://www.gastrojournal.org/article/S0016-5085(01)47865-6/pdf

Somatostatin suppresses endothelin-1-induced rat hepatic stellate cell contraction via somatostatin receptor subtype 1.

Previous studies have shown antifibrotic effects of somatostatin Since hepatic stellate cells (HSC) express somatostatin receptors and play a key role in hepatic fibrogenesis, we investigated the in vitro antifibrotic effect of somatostatin on rat HSC At day 12 after isolation, cells were exposed to different concentrations of somatostatin (10(-6)-10(-9) mol l(-1)) mRNA expression of collagen types I and III, and of smooth muscle alpha-actin (alpha-SMA) was analysed by Northern blotting At 10(-9) mol l(-1), somatostatin significantly reduced mRNA expression of collagen I (723 +/- 107%; 95% confidence interval (95% CI): 455-990), collagen III (790 +/- 45%; 95% CI: 676-904) and alpha-SMA (657 +/- 59%; 95% CI: 511-802), as compared to control normalized at 100% These results were confirmed by quantitative RT-PCR Cycloheximide experiments indicated that somatostatin has no direct transcriptional effectUsing immunoprecipitation, we demonstrated that somatostatin also decreased de novo synthesis of collagen I (73 +/-10%; 95% CI: 48-98%), collagen III (65 +/- 13%; 95% CI: 33-97%) and alpha-SMA (47 +/- 9%; 95% CI: 25-69%) Remarkably, at higher concentrations, somatostatin did not suppress collagen mRNA expression nor de novo protein synthesis We ascribe this observation to desensitization of the cells for somatostatin Cell proliferation, as measured by 5-bromo-2'-deoxyuridine labelling, was not altered by somatostatin No significant effect on the intermediate and actin cytoskeleton were detected by immunohistochemistry and Western blotting Our findings imply that in vivo antifibrotic effects of somatostatin could result partially from a direct action of somatostatin on HSC, but other, in vivo effects are probably also involved

https://bpspubs.onlinelibrary.wiley.com/doi/pdf/10.1038/sj.bjp.0706298

Somatostatin at nanomolar concentration reduces collagen I and III synthesis by, but not proliferation of activated rat hepatic stellate cells.

Background/Aims: Somatostatin has been used for over two decades to treat acute variceal bleeding. Although it is assumed that somatostatin lowers portal pressure by constriction of the splanchnic arteries, little is known about the expression of somatostatin receptors (SSTR) in splanchnic blood vessels. In this study we investigated SSTR expression in splanchnic blood vessels from normal and cirrhotic rats.



Methods/Results: Cirrhosis was induced by intraperitoneal injection of 50 mg thioacetamide twice a week for 14 weeks. In portal vein, mesenteric artery and aorta of normal and cirrhotic rats, mRNA for the five known SSTR was measured by quantitative reverse transcriptase-polymerase chain reaction. SSTR subtypes 1, 2, 3 and 4 were expressed, but subtype 5 was undetectable. In the portal vein of cirrhotic animals, SSTR1 was significantly down-regulated as compared with controls. Otherwise, no major differences in receptor expression between normal and cirrhotic animals were observed. Using immunohistochemistry, we identified all five receptors, although the staining of receptor 5 was very weak.



Conclusion: All five SSTR are expressed in splanchnic blood vessels. Our results suggest that cirrhosis reduces expression of SSTR1 in portal vein. In other vessels, no major differences between the normal and cirrhotic state were noted.

Expression of somatostatin receptors in splanchnic blood vessels of normal and cirrhotic rats

Activated rat hepatic stellate cells bear functionally active somatostatin receptors

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Somatostatin suppresses endothelin-1-induced rat hepatic stellate cell contraction via somatostatin receptor subtype 1.

Somatostatin at nanomolar concentration reduces collagen I and III synthesis by, but not proliferation of activated rat hepatic stellate cells.

Expression of somatostatin receptors in splanchnic blood vessels of normal and cirrhotic rats

Activated rat hepatic stellate cells bear functionally active somatostatin receptors