Gall‐bladder and sphincter of Oddi response to cholecystokinin in the Australian possumIANNOS, J.; SACCONE, G. T. P.; BUSHELL, M.; BAKER, R. A.; TOOULI, J.
doi: 10.1111/j.1440-1746.1989.tb00853.xpmid: 2491218
ABSTRACT The effects of cholecystokinin octapeptide (CCK‐OP) on the gall‐bladder (GB) and sphincter of Oddi (SO) of the Australian brush tailed possum were examined in 45 anaesthetized animals. CCK‐OP (20–640 ng/kg) consistently caused the GB to contract in a dose‐dependent manner (Kruskal Wallis P<0.05). In 20 animals, the same dose range of CCK‐OP produced an excitatory response in the SO, increasing the SO motility index (MI = frequency of contractions x mean peak amplitude) dose‐dependently (Kruskal Wallis P < 0.05). In five animals, an inhibitory response, that is, a decrease in MI, was recorded, with 640 ng/kg of CCK‐OP producing a 50% decrease in MI. In the remaining 20 animals, variable responses of both excitation and inhibition were elicited within the same animal. The action of CCK‐OP on the SO and GB was not modified by atropine, phentolamine or propranolol. Tetrodotoxin (TTX) reversed the inhibitory responses of the SO to CCK‐OP such that responses were excitatory (sign test P<0.05). TTX did not alter the response of the GB to CCK‐OP. It is concluded that CCK‐OP acts directly on smooth muscle receptors of the GB. In the SO, its action is mediated via non‐cholinergic, non‐noradrenergic inhibitory neurons and also by a direct excitatory action on the smooth muscle of the SO.
Effect of calcitonin on gall‐bladder volume in manJONDERKO, KRZYSZTOF; KOŃCA, ADAM; GOŁAB, TOMASZ; JONDERKO, GERARD
doi: 10.1111/j.1440-1746.1989.tb00854.xpmid: 2491219
ABSTRACT The effect of increasing intravenous doses of synthetic salmon calcitonin (0.0044, 0.0088, 0.0175, and 0.0350 iu/kg per min) versus placebo on the fasted gall‐bladder volume was assessed in seven normal subjects according to a double‐blind study protocol. In addition, the action of calcitonin on meal‐induced gall‐bladder emptying was examined. Gall‐bladder volumes were measured by means of real‐time ultrasonography. Calcitonin evoked a dose‐dependent relaxation of the fasted gall‐bladder. A statistically significant increase of the fasted gall‐bladder volume was observed with 0.0175 (23.4 ± 5.5 cm3 placebo versus 33.9 ± 7.7 cm3 calcitonin, P<0.001) and 0.0350 (21.4 ± 4.6 cm3 placebo versus 36.1 ± 8.4 cm3 calcitonin, P<0.01) iu/kg per min calcitonin, whereas a mean increase of the gall‐bladder volume amounted to 32.1% and 46.5%, respectively. A significant delay of the gall‐bladder emptying after calcitonin was reflected by a decrease of the ejection fraction: 23.2 ± 8.3% calcitonin versus 57.8 ± 6.9% placebo (P<0.02) at 20 min, and 40.5 ± 8.8% calcitonin versus 67.2 ± 3.8% placebo (P<0.02) at 30 min after the test meal. Calcitonin is concluded to have a potent relaxing effect on the human gall‐bladder.
Hepatocellular carcinoma in cirrhotic liver in TriesteMELATO, MAURO; VALENTE, MATTEO; MUCLI, EZIO; MUUSE, MAXAMED MACALLIN; TARAGLIO, STEFANO
doi: 10.1111/j.1440-1746.1989.tb00856.xpmid: 2562353
ABSTRACT One hundred consecutive cases of hepatocellular carcinoma (HCC) in cirrhosis observed at autopsy were studied and their pathological aspects were compared with those reported in the literature. The results, which are representative of HCC epidemiology in a geographical area where cirrhosis is mostly due to alcohol abuse, show that similarities in the architectural pattern of HCC and weight of the liver exist between our material and samples with different aetiology and epidemiology. A relationship between the histological grade of HCC and its propensity to metastasize was demonstrated. The reported better prognosis of clear cells per se could not be confirmed, although clear cell HCC occurred exclusively in grade 2. It was also demonstrated that the relationship between grading and staging was strongly influenced by the association of HCC with cirrhosis, which is a fact that is usually overlooked by the common staging (and grading) methods.
Atrial natriuretic peptide, plasma renin activity, plasma volume, systemic vascular resistance and cardiac output in patients with cirrhosisVINEL, J. P.; DENOYEL, P.; VIOSSAT, I.; CALES, P.; CAUCANAS, J. P.; CHABRIER, P. E.; ESQUERRE, J. P.; BRAQUET, P.; PASCAL, J. P.
doi: 10.1111/j.1440-1746.1989.tb00857.xpmid: 2535241
ABSTRACT The present study aimed to assess relationships between plasma levels of atrial natriuretic peptide (ANP) and plasma volume, systemic vascular resistances, cardiac output and plasma renin activity in patients with cirrhosis. Thirty patients were included: eight with no history of liver disease were used as controls; 22 patients had biopsy‐proven alcoholic cirrhosis without ascites (n=11) and with ascites (n=11). Mean ANP plasma level was significantly higher in both groups of cirrhotic patients than in controls (P<0.05). In the control group, ANP and plasma renin activity were inversely correlated (P<0.05) but no correlation was found in cirrhotic patients. In the group of patients with ascites, ANP plasma levels were inversely correlated to plasma volume (P<0.05) and to cardiac output (P<0.01) and directly correlated to systemic vascular resistances (P<0.01). Using multiple regression analysis, ANP remained correlated only with systemic vascular resistances (P<0.05). These results suggest that cirrhotic patients have high plasma levels of ANP whether or not they have ascites. In the light of current knowledge of ANP actions, the relationships between ANP plasma levels and plasma volume, cardiac output, and systemic vascular resistances are paradoxical in cirrhotic patients with ascites. ANP does not seem to play a critical role in the pathogenesis of sodium and water retention observed in these patients.
Haem in the gut. I. Fate of haemoproteins and the absorption of haemYOUNG, GRAEME P.; ROSE, IAN S.; JOHN, D. JAMES B.
doi: 10.1111/j.1440-1746.1989.tb00858.xpmid: 2491221
ABSTRACT Haem (FeII‐protoporphyrin‐IX) is presented to the gut lumen as haemoproteins derived from exogenous (dietary) and endogenous (mucosal cell desquamation and bleeding) sources. Haemoproteins such as haemoglobin, myoglobin and catalase undergo hydrolysis by luminal proteases to release the haem. Released haem is maintained in a soluble form in the gut lumen by the products of haemoprotein digestion. Chelators of elemental iron do not bind haem‐iron and so haem‐iron is better absorbed than elemental iron. Haem‐iron does not exchange with luminal elemental iron. Mucosal uptake of haem is limited. Less than 10% binds to the brush border of the villus cell. Although the mechanisms by which haem binds to the brush border and is transported to the intracellular environment are poorly understood, it is known that some haem is transferred to secondary lysosomes where the porphyrin ring is split to release iron and form bilirubin. Depending upon the composition of the diet, the iron released from haem within the villus cell can be the major physiological source of iron. In iron‐deficiency in humans, absorption of haem‐iron can increase threefold whereas absorption of elemental‐iron can increase tenfold. These observations indicate that haem‐iron and elemental‐iron are absorbed via different mechanisms which are subject to different regulation. For haem‐iron to be absorbed, the haem itself must be taken up by the mucosa.
SELECTED SUMMARIESdoi: 10.1111/j.1440-1746.1989.tb00862.xpmid: 2562354
CORRECTION OF METABOLIC DEFECT BY GENE TRANSFER INTO ISOLATED HEPATOCYTES Correction of the genetic defect in hepatocytes from the Watanabe heritable hyperlipidemic rabbit. Wilson J.M., Johnston D.E., Jefferson D.M. & Mulligan R.C. BIOCHEMICAL FEMINIZATION OF MALES WITH ALCOHOL‐INDUCED LIVER DISEASE Ethanol‐induced increase in cytosolic estrogen receptors in human male liver: a possible explanation for biochemical feminization in chronic liver disease due to alcohol. Villa E., Baldini G.M., Rossini G.P. et al. PROPHYLACTIC SCLEROTHERAPY Prophylactic sclerotherapy before the first episode of variceal hemorrhage in patients with cirrhosis. Sauerbruch T., Wotzka R., Kopcke W. et al. VARICEAL PRESSURE IN CIRRHOSIS Endoscopic measurement of variceal pressure in cirrhosis: Correlation with portal pressure and variceal hemorrhage. Rigau J., Bosch J., Bordas J.M. et al.