Laparoscopic colectomy in idiopathic colonic varices: a safe endeavour

2020 ◽  
Vol 13 (8) ◽  
pp. e235624
Author(s):  
Prakash Kumar Sasmal ◽  
Ankit Sahoo ◽  
Hemanta Kumar Nayak ◽  
Suvradeep Mitra

A 32-year-old man presented to the emergency department with recurrent episodes of haematochezia and haemodynamic instability. He had no complaints of alteration in bowel habits or mucus discharge in the stool. He was a non-smoker and does not consume alcohol. After stabilising the patient, clinical evaluation and investigations with gastrointestinal endoscopy revealed dilated and tortuous submucosal veins involving the entire colon excepting the distal sigmoid. CT angiography and Doppler ultrasonography revealed normal patency and flow in the mesenteric vessels as well as hepatic, portal vein and inferior vena cava. With the exclusion of the secondary causes, we made the diagnosis of the rare entity of idiopathic colonic varices. He underwent a laparoscopic colectomy with ileorectal anastomosis, without any additional technical challenges intra-op and had an uneventful postoperative recovery. Idiopathic colonic varices can be a differential diagnosis of gastrointestinal bleeding and one can safely proceed with laparoscopic colectomy.

Endocrinology ◽  
2008 ◽  
Vol 150 (3) ◽  
pp. 1174-1181 ◽  
Author(s):  
Elisabeth B. Rüttimann ◽  
Myrtha Arnold ◽  
Jacquelien J. Hillebrand ◽  
Nori Geary ◽  
Wolfgang Langhans

Peripheral administration of glucagon-like peptide (GLP)-1 reduces food intake in animals and humans, but the sites and mechanism of this effect and its physiological significance are not yet clear. To investigate these issues, we prepared rats with chronic catheters and infused GLP-1 (0.2 ml/min; 2.5 or 5.0 min) during the first spontaneous dark-phase meals. Infusions were remotely triggered 2–3 min after meal onset. Hepatic portal vein (HPV) infusion of 1.0 or 3.0 (but not 0.33) nmol/kg GLP-1 reduced the size of the ongoing meal compared with vehicle without affecting the subsequent intermeal interval, the size of subsequent meals, or cumulative food intake. In double-cannulated rats, HPV and vena cava infusions of 1.0 nmol/kg GLP-1 reduced meal size similarly. HPV GLP-1 infusions of 1.0 nmol/kg GLP-1 also reduced meal size similarly in rats with subdiaphragmatic vagal deafferentations and in sham-operated rats. Finally, HPV and ip infusions of 10 nmol/kg GLP-1 reduced meal size similarly in sham-operated rats, but only HPV GLP-1 reduced meal size in subdiaphragmatic vagal deafferentation rats. These data indicate that peripherally infused GLP-1 acutely and specifically reduces the size of ongoing meals in rats and that the satiating effect of ip, but not iv, GLP-1 requires vagal afferent signaling. The findings suggest that iv GLP-1 infusions do not inhibit eating via hepatic portal or hepatic GLP-1 receptors but may act directly on the brain. Intrameal hepatic portal and intraperitoneal (IP) infusions of GLP-1 reduce meal size in rats, but only IP GLP-1 requires vagal afferent signaling for this effect.


1990 ◽  
Vol 125 (1) ◽  
pp. 81-88 ◽  
Author(s):  
R. J. Madon ◽  
D. M. Ensor ◽  
D. J. Flint

ABSTRACT An in-vitro perifusion system was devised in order to examine the secretory profiles of isolated islets of Langerhans, derived from different physiological states, when subjected to various stimuli relevant to lactation. Islets from pregnant rats secreted more insulin than did those from virgin animals; however, islets from lactating and virgin animals secreted similar amounts of insulin with all stimuli, including glucose, amino acids, cations and neurotransmitters. When virgin rats were pretreated for 5 days in vivo with GH or prolactin, insulin responses in vitro were unchanged. Cannulation of the hepatic portal vein and inferior vena cava in vivo revealed that both insulin and glucose concentrations were lower in the portal vein of the lactating rat compared with the virgin animal. It was therefore concluded that insulin concentrations are depressed during lactation as a consequence of the pancreas receiving a diminished glycaemic stimulus rather than because of any change in β-cell sensitivity. Journal of Endocrinology (1990) 125, 81–88


Endocrinology ◽  
2014 ◽  
Vol 155 (5) ◽  
pp. 1690-1699 ◽  
Author(s):  
Mukesh Punjabi ◽  
Myrtha Arnold ◽  
Elisabeth Rüttimann ◽  
Mariana Graber ◽  
Nori Geary ◽  
...  

To address the neural mediation of the eating-inhibitory effect of circulating glucagon-like peptide-1 (GLP-1), we investigated the effects of 1) intra-fourth ventricular infusion of the GLP-1 receptor antagonist exendin-9 or 2) area postrema lesion on the eating-inhibitory effect of intrameal hepatic portal vein (HPV) GLP-1 infusion in adult male rats. To evaluate the physiological relevance of the observed effect we examined 3) the influence of GLP-1 on flavor acceptance in a 2-bottle conditioned flavor avoidance test, and 4) measured active GLP-1 in the HPV and vena cava (VC) in relation to a meal and in the VC after HPV GLP-1 infusion. Intrameal HPV GLP-1 infusion (1 nmol/kg body weight-5 min) specifically reduced ongoing meal size by almost 40% (P < .05). Intra-fourth ventricular exendin-9 (10 μg/rat) itself did not affect eating, but attenuated (P < .05) the satiating effect of HPV GLP-1. Area postrema lesion also blocked (P < .05) the eating-inhibitory effect of HPV GLP-1. Pairing consumption of flavored saccharin solutions with HPV GLP-1 infusion did not alter flavor acceptance, indicating that HPV GLP-1 can inhibit eating without inducing malaise. A regular chow meal transiently increased (P < .05) HPV, but not VC, plasma active GLP-1 levels, whereas HPV GLP-1 infusion caused a transient supraphysiological increase (P < .01) in VC GLP-1 concentration 3 minutes after infusion onset. The results implicate hindbrain GLP-1 receptors and the area postrema in the eating-inhibitory effect of circulating GLP-1, but question the physiological relevance of the eating-inhibitory effect of iv infused GLP-1 under our conditions.


2000 ◽  
Vol 278 (3) ◽  
pp. R646-R653 ◽  
Author(s):  
Christa J. Silberbauer ◽  
Denise M. Surina-Baumgartner ◽  
Myrtha Arnold ◽  
Wolfgang Langhans

To investigate the acute effects of lactate on spontaneous feeding, we infused lactate in the hepatic portal vein (0.5, 1.0, and 1.5 mmol lactate/meal) or in the vena cava (1.0 and 1.5 mmol lactate/meal) of ad libitum-fed rats during their first spontaneous nocturnal meal. Infusions (5 min, 0.1 ml/min) were remotely controlled, and a computerized feeding system recorded meal patterns. In separate crossover tests, meal size decreased independent of the infusion route after 1.0 and 1.5 mmol but not after 0.5 mmol lactate. The subsequent intermeal interval (IMI) tended to decrease only after vena cava infusion of 1.0 mmol lactate. The size of the second nocturnal meal increased after the 1.0 mmol lactate infusion. Hepatic portal infusion of 1.5 mmol lactate increased the satiety ratio [subsequent IMI (min)/meal size (g)] by 175%, which was higher than the insignificant 43% increase after vena cava infusion. Hepatic portal infusion of 1.5 mmol lactate also increased systemic plasma lactate but not glucose concentration at 1 min after the end of infusion. The results are consistent with the idea that meal-induced increases in circulating lactate play a role in the control of meal size (satiation). Moreover, the results suggest that lactate also contributes to postprandial satiety and that the liver is involved in this effect. The exact mechanisms of lactate's inhibitory effects on feeding and the site(s) where lactate acts to terminate meals remain to be identified.


1981 ◽  
Vol 46 (1) ◽  
pp. 111-118 ◽  
Author(s):  
J. K. Chesters ◽  
Marie Will

1. Both albumin and transferrin have been suggested as carriers of zinc in plasma. Their relative importance in Zn transport was therefore investigated as a preliminary to a study of the rates of passage of Zn through plasma.2. The apparent log stability constant for Zn binding to human apotransferrin at pH 7·4 was estimated to be approximately 5·9 which is substantially lower than previous reports of 7·0 for the corresponding value for Zn binding to albumin (Giroux & Henkin, 1972).3. When the relative abilities of human albumin and apotransferrin to compete for Zn with low-molecular-weight chelators were compared at the same relative concentrations of these proteins as are found in plasma, albumin retained substantially more Zn than transferrin.4. It seems likely that albumin acts as the major transport protein for Zn in plasma of most species, Zn also being present firmly bound to α2-macroglobulin.5. In porcine plasma or serum however, there were three major Zn-binding proteins, two of which were probably albumin and α2-macroglobulin. The nature of the third component remains unknown but it appeared to have a molecular weight of between 100000–140000, it was precipitated by 2·2 M-ammonium sulphate and by 150 gpolyethylene glycol/l.6. There were no significant differences in Zn distribution in plasma of porcine blood obtained from the aorta, the posterior vena cava or from the hepatic portal vein but use of heparin as an anticoagulant altered the normal pattern of distribution of Zn in plasma.


1993 ◽  
Vol 264 (2) ◽  
pp. R409-R413 ◽  
Author(s):  
D. Greenberg ◽  
G. P. Smith ◽  
J. Gibbs

The satiating effect of intravenous fat infusions was investigated in sham-feeding rats. Intralipid infusions at loads of 2.5-10.0 kcal were administered into either the inferior vena cava or the hepatic-portal vein during sham feeding. Intravenous infusions of Intralipid by either route had no effect on sham feeding during 60-min tests. In earlier work we found that duodenal infusions of Intralipid rapidly inhibited sham feeding and elicited behaviours typical of satiety under test conditions identical to those of the present study. The lack of effect of intravenous infusions of Intralipid on sham feeding is further evidence for a preabsorptive site of action for the satiety effect of Intralipid.


2002 ◽  
Vol 283 (5) ◽  
pp. R1061-R1069 ◽  
Author(s):  
Guus H. M. Schoorlemmer ◽  
Mark D. Evered

Removal of drinking water at the start of the dark period reduced food intake in freely feeding rats within 45 min. Both first and later meals were smaller during 7.5 h of water deprivation, but meal frequency did not change. Ingestion of a normal-sized meal (3 g) rapidly increased plasma tonicity when drinking water was withheld, but intravenous infusions of hypertonic NaCl causing similar increases in plasma tonicity did not reduce feeding. Feeding during 6 h of water deprivation was restored by slowly infusing the volume of water normally drunk into the stomach, jejunum, or cecum, but not in the vena cava or hepatic portal vein. The infusions did not alter water or electrolyte excretion or affect food intake in rats allowed to drink. We conclude that the inhibition of feeding seen during water deprivation is mediated by a sensor that is located in the gastrointestinal tract or perhaps in the mesenteric veins draining the gut, but not the hepatic portal vein or the liver. In the absence of drinking water, signals from this sensor provoke the early termination of a meal.


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