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Biomedical subjects

B T Schjoldager

Publications and source records attributed to B T Schjoldager.

6 recordsLinked to original sources
PubMed2001

[Ogilvie syndrome].

Ogilvie's syndrome is a rare condition with progressive dilatation of the proximal colon without mechanical obstruction. Untreated it can lead to coecal perforation, peritonitis and death. It develops in patients with medical or surgical complications, but can be idiopathic. Caesarean section is the most common preceding surgical procedure. An imbalance between the parasympathetic and the sympathetic innervation of the intestine is thought to be the cause. Trauma to the retroperitoneum, infections, bleeding and electrolyte disturbances, hormonal changes and medicamina are predisposing factors. The syndrome can result in perforation of the coecum as early as the third or fourth day. Therefore a diagnostic abdominal X-ray should not be delayed by the intermittent presence of flatus and stool which is characteristic for this pseudo-obstructive condition. Medical treatment with neostigmine may be successful, coloscopic decompression of the colon is effective as is placing a tube in or close to coecum. If laparotomy is necessary, coecostomy has lower mortality than ileo-coecal resection.

Colon↗
PubMed2001

[Ogilvie syndrome after Cesarean section].

INTRODUCTION: Ogilvie's syndrome, acute pseudo-obstruction of the colon, can lead to perforation of the caecum and death. The syndrome is not well known and diagnosis can be difficult to make in time. METHODS: We analysed seven cases of Ogilvie's syndrome with the aim of improving diagnostics. RESULTS: All had prolonged labour before cesarean section, which was complicated by bleeding. All were treated with syntocinon, a hormone that may influence gastrointestinal motility. All patients developed abdominal meteorism within a few days of operation, which increased despite the passing of flatus and stool. Five cases resulted in caecum perforation before the correct diagnosis and treatment were made. Perforation occurred on days 3-4, day 5, or probably days 8-10 after the operation. One of these patients, who suffered from severe adipositas, died. CONCLUSION: It is very important to make an early diagnosis, as the condition can progress quickly. Diagnosis should be made on the history, clinical assessment, and abdominal X-ray. Intermittent flatus and stool are characteristic of this truly non-obstructive condition and should not therefore delay a diagnostic X-ray.

Adult↗
PubMed1994

Role of CCK in gallbladder function.

Cholecystokinin may play a role in regulation of interdigestive motility, but this still remains to be investigated. CCK constitutes the major hormonal stimulus for postprandial gallbladder emptying. CCK exerts its contractile effects mainly through interaction directly with receptors on the gallbladder smooth muscle cells in the muscle layer, but also through interaction with cholinergic nerves extrinsic and/or intrinsic in nature. Furthermore, CCK can enhance ongoing nicotinic ganglionic transmission occurring in the serosal layer by release of acetylcholine. CCK interaction with the gallbladder smooth muscle CCKA receptor was studied in further detail. CCK contracts strips of gallbladder muscle in a concentration-dependent way with a potency in the nanomolar range in all tested species. The potency is 1,000-fold better than that of gastrin; thus, the receptor is of type CCKA. CCK binding to this receptor is specific and of high affinity, 1,000-fold better than that of gastrin with no differences between the tested species including bovine, porcine, and human. Also, CCK binding affinity was independent of age, gender, or weight of the person and pathology of the human gallbladder. The biochemistry of the CCKA receptor varies between the tested species (bovine and human). Both CCKA receptors are heavily glycosylated, but of different size and carbohydrate content. The bovine CCKA receptor is of apparent size M(r) = 70-85 kD with N-linked complex carbohydrates and sialic acids. The human CCKA receptor is of M(r) = 85-95 kD, with N-linked complex carbohydrates, but no sialic acids. They both have a protein core of apparent size M(r) = 43 kD, with almost identically sized fragments after enzymatic cleavage. Probably the protein cores contain the receptor binding region, which seems well preserved between species. CCK and the CCKA gallbladder muscularis receptor are main regulators of postprandial gallbladder emptying. The biochemistry of the CCKA gallbladder smooth muscle receptor is in accord with newly generated data of purification and cloning of the rat pancreatic CCKA receptor.

Amino Acid Sequence↗
PubMed1989

GLP-1 (glucagon-like peptide 1) and truncated GLP-1, fragments of human proglucagon, inhibit gastric acid secretion in humans.

Glucagon-like peptide 1 amide (GLP-1 amide), a predicted product of the glucagon gene (proglucagon 72-107-amide), and truncated GLP-1 (proglucagon 78-107-amide), recently isolated from porcine small intestine, were infused in doses of 100 and 400 ng/kg/hr and 12.5 and 50 ng/kg/hr, respectively, into eight volunteers to study pharmacokinetics and effects on pentagastrin-stimulated gastric acid secretion (plateau stimulation with pentagastrin at D50: 100 ng/kg/hr). The concentration of GLP-1 in plasma increased from 64 +/- 12 to 189 +/- 23 and 631 +/- 76 pmol/liter, respectively. The concentration of truncated GLP increased from approximately 7 pmol/liter to 28 +/- 3 pmol/liter during the high rate of infusion. A similar increase was seen in response to a mixed meal in eight normal volunteers. The metabolic clearance rate (MCR) of GLP-1 was 2.2 +/- 0.3 and 2.6 +/- 0.3 ml/kg/min, respectively, and the half-life in plasma was 17 +/- 2 min. The MCR of truncated GLP-1 was 13 +/- 2.8 ml/kg/min and the half-life 11.4 +/- 2.1 min. GLP-1 reduced the pentagastrin-stimulated acid secretion 16 +/- 9% during the low-rate infusion and 23 +/- 12% during the high rate (P less than 0.05). Truncated GLP-1 caused a 36 +/- 3% inhibition during the high infusion rate. Thus truncated GLP-1, a naturally occurring peptide, is a potent inhibitor of acid secretion in man and more so than GLP-1.

Adult↗
PubMed1988

Oxyntomodulin: a potential hormone from the distal gut. Pharmacokinetics and effects on gastric acid and insulin secretion in man.

Synthetic oxyntomodulin, a predicted product of the glucagon gene, which is produced in the human lower intestinal mucosa, was infused in doses of 100 and 400 ng kg-1 h-1 into six volunteers to study its pharmacokinetics and effects on pentagastrin-stimulated gastric acid secretion (100 ng kg-1 h-1). The concentration of oxyntomodulin in plasma measured with a cross-reacting glucagon assay increased from 37 +/- 5 to 106 +/- 17 and 301 +/- 40 pmol l-1, respectively. The metabolic clearance rate was 5.2 +/- 0.7 ml kg-1 min-1 and the half-life in plasma was 12 +/- 1 min. Oxyntomodulin reduced the pentagastrin-stimulated acid secretion by 20 +/- 9% during the low-rate infusion (P less than 0.05) and by 76 +/- 10% during the high-rate infusion (P less than 0.05). In accordance with the homology with glucagon, there was a small, significant rise in plasma concentrations of insulin and insulin C-peptide during oxyntomodulin infusion. Oxyntomodulin may therefore be included among the potential incretins and enterogastrones in man.

Gastric Acid↗