vasoactive-intestinal-peptide and Liver-Diseases

This review has focused on the unique role of radionuclide scintigraphy in characterization of hepatic mass lesions. Radionuclide scintigraphy, unlike most other imaging modalities, is based on specific physiological and biochemical properties of each pathological entity that affects the liver. Hepatic scintigraphy, with its widespread availability, noninvasive nature, and relatively low cost is a powerful adjunct to other imaging techniques in the investigation of hepatic mass lesions. We have reviewed clinical presentation and characteristic findings of most hepatic lesions and have described reported findings with all available imaging modalities with particular emphasis on hepatic scintigraphy (Table 1) as well as a suggested algorithm for workup of solid hepatic masses (Fig 6). Additionally, the role of newer, more specialized techniques including PET scanning, 123I-labeled VIP, and 111In-labeled DTPA-D-Phe-octreotide scanning are reviewed. Hepatic nuclear scintigraphy continues to play an important role in the management of patients with solid hepatic masses.

Topics: Algorithms; Carcinoma, Hepatocellular; Costs and Cost Analysis; Hemangioma, Cavernous; Humans; Indium Radioisotopes; Iodine Radioisotopes; Liver Diseases; Liver Neoplasms; Neuroendocrine Tumors; Octreotide; Pentetic Acid; Terbium; Tomography, Emission-Computed; Vasoactive Intestinal Peptide

Topics: Endotoxins; Humans; Kidney; Kidney Diseases; Kidney Failure, Chronic; Kinins; Liver Diseases; Natriuresis; Plasma Volume; Prolactin; Prostaglandins; Vasoactive Intestinal Peptide; Vasoconstriction; Vasomotor System

The inhibitory effect of different reperfusion periods 45 min following hepatic ischemia on the expression of cholecystokinin (CCK) and vasoactive intestinal peptide (VIP) in the jejunum and the effect of salvia miltiorrhiza pretreatment were investigated, and the possible mechanism and implications were explored. Eighty rats were randomly divided into four groups: normal control group (CO group), sham-operated group (SO group), ischemia/reperfusion (I/R) injury group (IR group) and salvia miltiorrhiza pretreatment group (SM group). The rat model of I/R was established by using a non-invasive artery clamp to clip (45 min) or relax the hepatic pedicle. In the SM group, saline (40 mL/kg) and salvia miltiorrhiza injection (6 g/kg) were injected via the tail vein 30 min before clipping the hepatic pedicle. In the SO group only the porta hepatis was dissected after laparotomy without clamping the hepatic pedicle. At 0, 3, 12, 24 and 72 h post-reperfusion, respectively, upper jejunum samples were taken for immunohistochemistry of CCK and VIP. It was found that 0 h after I/R, the expression of CCK and VIP in the upper jejunum was upregulated. With prolongation of the reperfusion period, the expression of CCK and VIP was also increased, reached the peak at the 24th h, and gradually returned to the normal level at the 72nd h after reperfusion. The levels of both CCK and VIP in the SM group were lower than those in the IR group. It is suggested that the digestive tract congestion injury caused by liver ischemia can upregulate the expression of CCK and VIP in the jejunum following reperfusion. Salviae pretreatment can partly reduce the increased expression of CCK and VIP in the jejunum in the same period, which might contribute to the early recovery of gastrointestinal motility.

Topics: Animals; Cholecystokinin; Gastrointestinal Motility; Intestinal Mucosa; Jejunum; Liver; Liver Diseases; Phytotherapy; Rats; Rats, Sprague-Dawley; Reperfusion Injury; Salvia miltiorrhiza; Vasoactive Intestinal Peptide

Topics: Analysis of Variance; Calcitonin Gene-Related Peptide; Humans; Liver Diseases; Liver Transplantation; Neuropeptide Y; Neuropeptides; Peptide PHI; Peptide YY; Peptides; Substance P; Time Factors; Vasoactive Intestinal Peptide

Innervation of the liver with or without chronic liver disease was immunohistochemically studied. In normal liver tissues, gamma-enolase [neuron-specific enolase (NSE)]- and S-100 protein (S-100)-positive nerve fibers were found around hepatic arteries, portal veins, and bile ductules in the portal area, along the sinusoid, and around central veins inside the hepatic lobule. Neuropeptide Y (NPY)-immunoreactive (IR) nerve fibers were detected in close contact with hepatic arteries and portal veins in the portal area and along the sinusoid in the parenchyma. Vasoactive intestinal polypeptide (VIP)-IR nerve fibers were found in the portal area but were scarce in the parenchyma. VIP-IR nerve fibers were much fewer than NPY-IR fibers. In patients with chronic active hepatitis, NSE- and S-100-positive nerve fibers, as well as NPY-IR nerve fibers, proliferated in the enlarged portal area. In cirrhotic liver, NSE- and S-100-positive nerve fibers and NPY-IR fibers increased remarkably in the fibrous septa, whereas they decreased or vanished inside the pseudolobules. These findings suggest that, in chronic liver disease, intrahepatic nerve fibers change their distribution, accompanying the structural changes in the hepatic lobules.

Topics: Humans; Immunoenzyme Techniques; Liver; Liver Diseases; Microscopy, Electron; Nerve Fibers; Neuropeptide Y; Phosphopyruvate Hydratase; S100 Proteins; Vasoactive Intestinal Peptide

1. The effect of intravenous vasoactive intestinal peptide (VIP, 6 pmol/kg per min) on renal function in six patients with cirrhosis of the liver was examined. 2. VIP caused generalized vasodilation and increased plasma renin activity, but diminished the glomerular filtration rate by about one third. 3. The excretion of water, sodium, potassium and calcium also fell significantly. 4. These results differ from our findings in normal man in whom VIP diminished water and electrolyte secretion largely by increasing tubular reabsorption. 5. It is concluded that the elevated VIP levels present in patients with severe liver disease may affect renal function, but that the presence of liver disease may affect renal responses to VIP.

Topics: Blood Cell Count; Female; Hemodynamics; Humans; Infusions, Intravenous; Kidney; Kidney Function Tests; Liver Cirrhosis, Alcoholic; Liver Diseases; Male; Middle Aged; Vasoactive Intestinal Peptide

Topics: Acute Disease; Animals; Gastrins; Gastrointestinal Hormones; Glucagon-Like Peptides; Liver Diseases; Pancreatic Polypeptide; Swine; Vasoactive Intestinal Peptide

In animals, the effects of vasoactive intestinal polypeptide (VIP) include peripheral vasodilation, hyperdynamic circulation, hyperglycemia, and hyperventilation. Because these phenomena are noted in patients with cirrhosis, it has been postulated that VIP might be escaping hepatic inactivation and entering the systemic circulatory system and contributing to these abnormalities. The major purpose of this study is to establish whether or not VIP levels are elevated in patients with cirrhosis. Additional goals are to determine if VIP levels are elevated in acute liver disease and in chronic illnesses with secondary liver involvement. The data demonstrate that patients with cirrhosis and those with acute liver disease or chronic illnesses with secondary hepatic involvement have a wide range of VIP levels with mean values significantly above that of normal individuals and patients with chronic illness and no liver involvement.

Topics: Acute Disease; Chronic Disease; Gastrointestinal Hormones; Humans; Liver Cirrhosis; Liver Diseases; Liver Neoplasms; Neoplasm Metastasis; Vasoactive Intestinal Peptide

Topics: Amino Acids, Branched-Chain; Animals; Dogs; Gastrointestinal Hormones; Haplorhini; Hepatic Encephalopathy; Liver Diseases; Portacaval Shunt, Surgical; Vasoactive Intestinal Peptide

IN AN EFFORT TO DOCUMENT THE ROLE OF THE LIVER IN THE CATABOLISM OF VASOACTIVE INTESTINAL PEPTIDE, SEVERAL DIFFERENT TYPES OF EXPERIMENTS WERE CARRIED OUT, INCLUDING: 1) simultaneous measurement of portal and systemic immunoreactive vasoactive intestinal peptide, both in the basal state and following calcium stimulation; 2) by measuring plasma concentrations of immunoreactive vasoactive intestinal peptide before and after portacaval shunt; 3) by measuring plasma VIP before and after portacaval shunt following calcium, prostigmine and pentagastrin stimulation; 4) by determining plasma VIP levels in patients with liver disease and in hepatic failure, and in patients with variceal hemorrhage before and serially after portal systemic shunt; 5) by measuring CSF vasoactive intestinal peptide in dogs before and after portacaval shunt and when the animals finally succumb to hepatic failure. The results consistently suggest that the shunting of portal blood away from the liver does not result in significant elevation of basal peripheral plasma levels of vasoactive intestinal peptide. Following stimulation however, increased amounts of peripheral plasma VIP are detected, following calcium, pentagastrin and prostigmine release of VIP. Portal vein levels are always significantly higher than peripheral plasma VIP again, confirming a catabolic role for the liver. In patients, elevation of peripheral plasma VIP is seen in hepatic failure, but not after portacaval shunt. Finally, cerebrospinal fluid VIP is elevated in dogs following hepatic failure, confirming the presence of a neural-gut axis and suggesting an influence of hepatic catabolism of VIP not only in the periphery, but also within the central nervous system.

Topics: Animals; Antigens; Calcium; Dogs; Gastrointestinal Hormones; Hepatic Encephalopathy; Humans; Liver; Liver Diseases; Neostigmine; Pentagastrin; Portacaval Shunt, Surgical; Portal Vein; Stimulation, Chemical; Vasoactive Intestinal Peptide; Veins