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Biomedical subjects

G Strohmeyer

Publications and source records attributed to G Strohmeyer.

At least 109 records · Page 6Linked to original sources
PubMed1990

Motor dysfunction in HIV-infected patients without clinically detectable central-nervous deficit.

Motor tests were performed in 50 HIV-infected patients in all stages according to the current CDC classification, but without any clinically evident central nervous system deficit, and the results compared with an age-matched control group. Patients were excluded from the study if there was alcohol or drug abuse, fever and/or opportunistic cerebral infection. The parameters tested were postural tremor of the outstretched hands, most rapid voluntary alternating index finger movements (MRAM) and rise time of most rapid index finger extensions (MRC). Whereas tremor peak frequencies did not differ significantly in the patients and controls, MRAM and rise times of MRCs showed significant slowing in the patient group. Morphologically, the motor test performance of the HIV-infected patients was similar to that of patients with manifest basal ganglia disease (Parkinson's, Huntington's and Wilson's diseases). MRI scans of all patients were normal. It is concluded that in HIV-infected patients there is a very early subclinical central nervous system affection, especially of the basal ganglia, which is detectable with appropriate, quantitative motor function tests. These functional abnormalities precede the structural alterations in the MRI scans.

Adult↗
PubMed1990

Pancreatic exocrine secretion in acute experimental pancreatitis.

Little is known about exocrine pancreatic secretory function in patients with acute pancreatitis, in particular during the early phase of the disease. Therefore, this study evaluates basal and stimulated pancreatic secretion in vivo and in vitro in four different models of acute pancreatitis which reflect its clinical spectrum of severity: (a) edematous pancreatitis induced in the rat by seven IP injections of 50 micrograms/kg cerulein at hourly intervals; (b) edematous pancreatitis with cellular necrosis induced in the mouse by seven IP injections of 50 micrograms/kg cerulein at hourly intervals; (c) hemorrhagic pancreatitis induced in the mouse by feeding an ethionine-supplemented, choline-deficient diet for 66 hours; and (d) hemorrhagic pancreatitis induced in the rat by retrograde infusion of 0.6 mL 5% sodium taurocholate into the pancreatic duct. Secretory studies were performed in vivo and in vitro at various times after onset of pancreatitis. The results show that the exocrine pancreas gradually became resistant to cholecystokinin stimulation after the onset of acute pancreatitis in all four animal models. Cholecystokinin-stimulated secretion was almost abolished in vivo and in vitro at the time of maximal histological damage. In vivo basal secretion was also reduced. In vitro there was an increase in basal release of amylase from isolated acini that was not caused by an increase in luminal secretion but by enzyme release from damaged cells. The time course of improvement of secretory function after acute experimental pancreatitis depended on the severity of the pancreatitis. Recovery of secretory capacity took longer after severe necrotizing pancreatitis than after edematous pancreatitis. However, the ultimate resolution of secretory function was remarkable, in particular after severe hemorrhagic pancreatitis. In all four models, secretory capacity became indistinguishable from normal before the morphological alterations had completely resolved. The present experimental data suggest that pancreatic secretion, and particularly pancreatic secretory response to cholecystokinin, may also be reduced in patients early after the onset of acute pancreatitis.

Acute Disease↗
PubMed1990

Does acute consumption of large alcohol amounts lead to pancreatic injury? A prospective study of serum pancreatic enzymes in 300 drunken drivers.

Blood samples of 300 consecutive subjects suspected for drunken driving were prospectively analyzed for concentrations of pancreatic and hepatic enzymes. Mean alcohol concentration was 1.5 +/- 0.8 0/00 (+/- SD; range 0-3.7 0/00). Increased enzyme concentrations were found in 25/300 subjects for amylase, in 43/300 for trypsin, in 49/300 for gamma-glutamyl transferase and in 82/300 for glutamic oxaloacetic transaminase. Subjects with alcohol concentrations greater than 1 0/00 had abnormal pancreatic and hepatic enzymes more frequently than subjects with alcohol concentrations smaller than 1 0/00. However, pancreatic enzyme levels were higher than twice the upper normal limit only in 3/300 subjects, whereas hepatic enzyme levels exceeded twice the upper normal limit in 31/300 subjects. Therefore, other factors in addition to alcohol are necessary to initiate acute pancreatitis. The liver is more susceptible to acute injury by alcohol than the pancreas.

Acute Disease↗
PubMed1990

Effects of long-term CCK stimulation and CCK blockade on pancreatic and intestinal growth, morphology, and function.

This study evaluated the effects of long-term cholecystokinin (CCK) stimulation and blockade on pancreatic and intestinal growth, function, and morphology. CCK release was induced by feeding of the protease inhibitor camostate and CCK blockade by feeding of the CCK antagonist CR 1409. Four groups of NMRI-mice received the following diets for 9 months (each group consisting of 36 mice): (1) chow (control); (2) chow + 100 mg/kg/day camostate; (3) chow + 50 mg/kg/day CR 1409; (4) chow + 100 mg/kg/day camostate + 50 mg/kg/day CR 1409. Long-term feeding of camostate greatly increased pancreatic weight by induction of marked hypertrophy (increase in protein content) and moderate hyperplasia (increase in DNA content). Camostate feeding also increased secretory capacity of the exocrine pancreas. Despite camostate-induced growth neither hyperplastic nor neoplastic nodules developed. The CCK-antagonist CR 1409 markedly inhibited the effects of camostate which are therefore mainly mediated by CCK. Neither long-term CCK stimulation nor CCK blockade altered morphology or composition of duodenal mucosa. Feeding of CR 1409 alone (i.e., without camostate) slightly but significantly decreased pancreatic content of protein and secretory capacity of enzymes when compared to the chow-fed control; pancreatic weight and DNA content remained unchanged after long-term administration of CR 1409. Thus, long-term, continuous and effective blockade of the CCK-receptor only slightly inhibited pancreatic growth and secretory capacity. CCK is, therefore, not an essential growth factor for the pancreas, although increases of endogenous CCK stimulate pancreatic growth and secretory capacity.

Animals↗
PubMed1990

Gene and haplotype frequencies of HLA antigens in 269 patients with Crohn's disease.

Evidence of strong genetic markers in Crohn's disease (CD) is still absent. Many investigations have focused on HLA antigens, with conflicting results. To obtain more detailed information on the relation of HLA to the disease, we used the HLA data from 269 CD patients to compute the maximum-likelihood estimates of HLA gene and haplotype frequencies. These results provide further evidence that HLA B44 and Cw5 do indeed play a role in the development of CD. Furthermore, it is conceivable from our results that HLA Cw7 may protect against being affected with this disease.

Chi-Square Distribution↗
PubMed1990

[Extra-cardiac risk factors in heart surgery evaluated by the gastroenterologist].

The present review analyzes the main gastroenterologic and hepatologic risk factors that influence the risk of cardiosurgical operations, as well as the prognosis. Gastroenterological or hepatic diseases are only rarely a contraindication for open-heart surgery, but sometimes require further preoperative diagnostic investigations and treatment. Although gastroenterological or hepatic complications of open-heart surgery are present in less than 1% of all cases, up to 30-40% are lethal. The severe complications often require other surgical interventions, especially in case of perforation of ulcer, gastrointestinal bleeding or intestinal ischemia. The postoperative jaundice of unknown origin is a very difficult clinical problem. Its pathogenesis is still incompletely understood.

Gastrointestinal Diseases↗
PubMed1990

[T-lymphocyte subpopulations in the peripheral blood of patients with Crohn disease].

Immunological disorders seem to be of considerable relevance to the pathogenesis of Crohn's disease (CD). T-cells play a central role in immunoregulation. The T-cell subpopulations of 70 patients with CD were compared to those of age- and sex-matched healthy controls. The suppressor-inducer subpopulations were found to be reduced in CD patients irrespective of wether they were taking steroids or not. In contrast to other subpopulations suppressor-inducer cells remained unchanged during follow-up. The results point to a disturbance in the regulation of suppressor T-cells in patients with Crohn's disease.

Adrenal Cortex Hormones↗
PubMed1990

Crohn's disease: what about the pancreas?

Crohn's disease (CD) is now accepted as a systemic illness. The importance of extraintestinal manifestations is underlined by the fact that such "complications" can be more prominent and even more difficult to control than the intestinal disease itself. Lately, evidence for a more than accidental association of pancreatitis and exocrine pancreatic insufficiency with CD is growing. This might have a significant impact on the treatment of abdominal pain and diarrhea in CD, symptoms which have so far been attributed exclusively to the intestinal rather than the extraintestinal manifestations of the disease.

Crohn Disease↗
PubMed1990

Crohn's disease in four members of a family, two of whom are dizygotic twins.

Familial occurrence of Crohn's disease (CD) is well known, but the disease is rarely reported to occur in dizygotic twins. We present an additional case of dizygotic twins, both of whom developed CD, from a family in which two other members are affected. The 16-year-old son contracted the disease 2 years before his 50-year-old father, and 13 years before his twin sister. Another sister was affected 6 years after the onset of the disease in the propositus. HLA haplotyping of the three children matched the Mendelian ratio. The multiple occurrence of CD in blood relatives, especially in siblings, emphasizes the importance of genetic factors in the development of this disease. This family history, however, could point to psychic influences promoting the occurrence of CD on the basis of a polygenic disease susceptibility.

Adolescent↗
PubMed1989

[Noncirrhotic liver fibrosis after chronic arsenic poisoning].

A 67-year-old woman with portal hypertension, splenomegaly without portal vein thrombosis, leucopenia and thrombocytopenia of splenic origin had repeated episodes of life-threatening haemorrhage from esophageal varices. Since childhood she had suffered from psoriasis and had been treated over a period of 15 years with Fowler's solution (in all about 25 g of arsenic trioxide). She had the characteristic skin lesions of arsenical poisoning-palmar hyperkeratoses and two basal cell carcinomas on the trunk. Histological examination of a wedge biopsy from the liver showed definite structural changes with fibrosis around the central veins and in the portal tracts. There was no evidence of cirrhotic alteration. The hepatocytes were normal by light microscopy and electron microscopy. This case of noncirrhotic hepatic fibrosis is considered to have been caused by chronic arsenical poisoning.

Aged↗
PubMed1989

[Virus-associated hemorrhagic colitis in the differential diagnosis of peracute rectal bleeding].

Severe anal bleeding together with increasing abdominal discomfort occurred in an 81-year-old woman previously hospitalized numerous times because of decompensated type II B diabetes. A suspected rectal cancer was excluded by biopsy from the lower to middle rectum, but the biopsy revealed histologically indurated and bleeding ulcerations. Typical nuclear inclusion bodies provided the diagnosis of virus-associated proctocolitis. Serological tests supported the diagnosis of infection with herpes simplex and cytomegalic virus. Laser coagulation stopped the bleeding. At the same time a Guillain-Barré syndrome was noted which improved after administration of cortisone and high parenteral doses of acyclovir.

Acute Disease↗
PubMed1989

Intestinal motor activity in experimental hyperthyroidism in conscious dogs.

The small intestinal motor effects of experimental hyperthyroidism were studied in 8 conscious dogs to reveal possible mechanisms of accelerated small bowel transit in hyperthyroidism. Six strain gauge transducers were implanted on the small intestine of each dog. Long-term hyperthyroidism was induced by subcutaneous administration of 100 and 200 micrograms/kg.day of thyroxin. Application of thyroxin did not interrupt the cyclic fasting motor activity. Thyroxin (100 micrograms/kg.day) caused a slight increase in the period of the migrating motor complex (p less than 0.05). The maximum contractile frequency rose dose-dependently up to 11% (p less than 0.05). During phase 2 and the digestive state the contraction frequency increased up to 29% and 27%, respectively (p less than 0.05). More contractions occurred in groups during the digestive state in hyperthyroidism. Half of the dogs showed giant migrating contractions during thyroxin administration, whereas those contractions were not observed during the control period. We conclude that fasted and postprandial intestinal motility is changed in experimental hyperthyroidism. Acceleration of small bowel transit may be caused by changes in contractile pattern of phase 2 and the digestive state or by the increased frequency of giant migrating contractions.

Animals↗
PubMed1989

Effects of loxiglumide on gallbladder emptying in healthy volunteers.

This study evaluates the effects of the specific cholecystokinin receptor antagonist loxiglumide on gall-bladder emptying after a meal or after intravenous infusion of caerulein in humans. Ten healthy male volunteers were studied five times on separate days. The following five studies were performed in randomized order: (a) caerulein was intravenously infused at doses increasing from 7.5 to 120 ng/kg.h without the antagonist; (b) in addition to increasing doses of caerulein, loxiglumide was given intravenously at doses of 0.2, 1.0, or 5.0 mg/kg.h; (c) a solid-liquid 800-kcal meal was given without loxiglumide; (d) the 800-kcal meal was given with simultaneous infusion of 1 or 5 mg/kg.h loxiglumide; and (e) loxiglumide (5 mg/kg.h) was given. without caerulein or the test meal. Gallbladder volume was measured by ultrasound. Loxiglumide dose-dependently inhibited gallbladder emptying induced by caerulein or the meal. High doses of the antagonist did not only abolish meal-induced gallbladder emptying but increased gallbladder volume after administration of caerulein or the meal when compared with prior fasting values. The antagonist given alone markedly increased gallbladder volumes compared with prior fasting values. In conclusion, given alone markedly increased gallbladder volumes compared with prior fasting values. In conclusion, cholecystokinin is the hormone primarily and mainly responsible for mediation of gallbladder emptying after a regular meal. Cholecystokinin might also play a physiologic role in the regulation of the fasting tone of the gallbladder.

Adult↗
PubMed1989

Comparative effects of CCK receptor antagonists on rat pancreatic secretion in vivo.

The present experiments evaluate in vivo effects of recently described cholecystokinin (CCK) receptor antagonists on rat pancreatic secretion. Pancreaticobiliary secretion was studied after bile duct cannulation in anesthetized rats. After two basal 10-min fractions were selected, secretion was stimulated by intravenous caerulein (0.1-30.0 micrograms/kg) or secretin, and collected for seven further 10-min fractions. Peptide antagonists (CR 1409, CR 1392, and CR 1505) and nonpeptide antagonists (asperlicin and L364,718) were given intravenously 10 min before agonists. Increasing doses of antagonists gradually reduced secretion of protein and enzymes stimulated by submaximal and maximal doses of caerulein. The antagonists did not alter nonstimulated or secretin-stimulated secretion, indicating their specificity for the CCK receptor. Except for proglumide and asperlicin, all antagonists were able to abolish caerulein-stimulated pancreatic secretion, as evaluated by the mean integrated 1-h response to a near-maximal dose of caerulein. The caerulein dose-response curve was gradually shifted to the right by increasing doses of CR 1409, indicating competitive-like kinetics. Inhibition of secretion due to supramaximal doses of caerulein, however, could be reversed by doses of CR 1409 smaller than expected from extrapolating truely competitive kinetics from an in vitro situation to the in vivo situation. The rank order of potency of the compounds to antagonize caerulein-stimulated secretion in vivo agreed with their relative potencies to antagonize caerulein-stimulated amylase secretion from pancreatic acini in vitro as well as with their affinity to bind to peripheral CCK receptors in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)

Amylases↗