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T W Frick

Publications and source records attributed to T W Frick.

33 records · Page 2Linked to original sources
PubMed1994

A rat model to study hypercalcemia-induced acute pancreatitis.

Hypercalcemia causes acute pancreatitis in humans, a phenomenon reproduced experimentally in cats and guinea pigs. Because the rat is the most frequently used animal for the study of experimental pancreatitis, the present studies were performed to evaluate the effects of hypercalcemia in the rat. In in vitro studies, pancreatic lobules were prepared from fasted Wistar rats (200-250 g) and incubated in HEPES bicarbonate-buffered medium (pH 7.4) containing 0, 0.6, 1.2, 2.5, 5, and 10 mM CaCl2 with or without carbachol 10(-6) M. Amylase was measured in the medium after 30 min to 3 h, and expressed as percent of total amylase. In in vivo studies, fasted male Wistar rats (300-400 g) received calcium (CaCl2; 0.6 mmol/kgh) into the tail vein for 12 h. Control animals received NaCl 0.9% infusion. Histologic slides (H&E-stained) were evaluated in a blinded fashion. Pancreatic lobules showed a higher basal amylase output when incubated in higher calcium medium. The largest, significant difference (2.6-fold) was between 0.6 and 5 mM medium CaCl2 (p < 0.05). Carbachol-stimulated amylase release was again higher with increasing medium calcium with the most pronounced difference (1.3-fold) between 0.6 and 2.5 mM CaCl2 (p < 0.05). In vivo calcium-treated animals showed accumulation of zymogen granules in the cytoplasm, cytoplasmic vacuolization, focal acinar cell depolarization, acinar necrosis, and edema. Calcium causes amylase release from rat pancreatic lobules in vitro. Higher medium calcium levels both significantly increase amylase release from unstimulated and carbachol stimulated lobules. Twelve-hour in vivo calcium infusion leads to accumulation of zymogen granules in acinar cells and acinar injury.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1993

Drug-induced acute pancreatitis: further criticism.

A comprehensive literature search was performed to collect all available data on drug-induced pancreatitis. Strong evidence for an association with acute pancreatitis has been described for anticholinesterases, calcium 2',3'-dideoxyinosine, estrogen, L-asparaginase, salicylates, thiazide-diuretics, valproic acid, and vinca alkaloids. Weak evidence has been found for antituberculous agents, azathioprine, biguanides, cisplatinum, cyclosporine A, H2-blocking agents, loop diuretics, 6-mercaptopurine, metronidazole, pentamidine, steroids, sulfonamides, sulindac and tetracycline. Many cases were associated with underlying conditions known to induce acute pancreatitis themselves. It is concluded that for none of the drugs studied the available data are consistent enough to support a definite association with acute pancreatitis. Nevertheless, the data suggest that drugs may be a trigger or a cofactor in inducing pancreatitis.

Acute Disease↗
PubMed1993

[Results of surgical therapy of ulnar sulcus syndrome. Submuscular anterior transposition versus simple decompression of the ulnar nerve].

The operative treatment of the ulnar neuropathy at the elbow is controversial. We studied the course of 79 patients who had been operated for the first time, either by simple decompression (31 cases) or by submuscular anterior transposition (48 cases) of the ulnar nerve. Our results show that the simple decompression can be recommended in all patients without cubital (sub)luxation of the ulnar nerve. The submuscular anterior transposition should be preferred if a tendency of cubital (sub)luxation of the ulnar nerve has been found.

Adult↗
PubMed1992

Intestinal infarction after nonabdominal trauma; association with cerebral trauma.

Nonocclusive bowel infarction in nonabdominal trauma has been ascribed to periods of hypotension. However, to our knowledge only 17 cases have been reported, and hypotension was not always found. We studied the frequency and possible causes of intestinal infarction in all patients treated at our traumatologic intensive care unit from 1977 through 1986 (n = 2350). Intestinal infarction was diagnosed at the time of surgery or autopsy; patients with pre-existing vascular disease were excluded. We found 12 patients (incidence: 0.5%) of age 45 +/- 20 years (mean +/- SD). All had severe cerebral trauma [Head and Neck Abbreviated Injury Scale (AIS) score: 4-5, admission Glasgow Coma Scale (GCS) score: 6.5 +/- 3.8]. Eight patients suffered from additional injuries. The Injury Severity Score (ISS) was 27 +/- 7. All patients received ventilator assistance continuously before the diagnosis of intestinal infarction or death. The leading symptom of intestinal infarction was sepsis and multiple organ failure with abdominal distention. Five patients with favorable cerebral prognosis underwent surgery: one survived with good cerebral and gastrointestinal recovery. Four patients did not have surgery because of a poor cerebral prognosis. Three patients died of their cerebral trauma before intestinal infarction was clinically manifested. The data show that early diagnosis in ventilated patients with head injuries is extremely difficult because of the heterogenicity of this group of patients, the low frequency of the complication, and the complexity of the clinical picture. Although patients inevitably were exposed to several agents or situations associated with intestinal infarction, the ubiquitous causes were dehydration and diuretic therapy.

Adolescent↗
PubMed1992

Ultrastructure of the guinea pig pancreas in acute hypercalcemia.

The effect of acute hypercalcemia on pancreatic ultrastructure and the ultrastructural localization of calcium during hypercalcemia were studied in the guinea pig pancreas. After 3 h of i.v. calcium infusion (0.6 mmol/kg/h), hypertrophy and distention of the Golgi apparatus and an increased number of condensing vacuoles were seen. At 6 h, vacuolar fusion and displacement of zymogen granules occurred. At 9 h, irregular distribution of zymogen granules, indentation of the nucleus with chromatin clumping, and inclusion of intact cell organelles were present. Disruption of the plasma membrane and release of cell organelles into the interstitial space were seen. Control animals receiving saline solution (0.9% NaCl) revealed normal pancreatic ultrastructure. The serum ionized calcium values were 0.65 +/- 0.36 mM in controls and 0.71 +/- 0.14, 0.79 +/- 0.21, and 1.22 +/- 0.50 mM at 3, 6, and 9 h of calcium infusion, respectively. The ultrastructural localization of calcium was performed with the pyroantimonate staining technique after 3 h of calcium and saline infusion. Large calcium deposits were found in calcium-treated animals along the plasma membrane and in the Golgi region. The findings indicate that calcium exerts a strong stimulatory effect that eventually leads to the degeneration of the pancreatic acinar cell.

Acute Disease↗
PubMed1992

Hypercalcaemia and pancreatic ultrastructure in cats.

OBJECTIVE: To study the effects of local and systemic infusions of calcium on the ultrastructure of the pancreas in cats. DESIGN: Controlled study. INTERVENTIONS: Three groups of four cats each had local infusions (into the splenic artery) of calcium gluconate 0.6 mmol/kg.hour or potassium chloride 1.1 mmol/kg.hour, or sodium chloride 0.9%, for three hours. Two groups of eight cats each had systemic infusions (into the jugular vein) of either calcium gluconate 0.6 mmol/kg.hour or sodium chloride 0.9%, for twelve hours. In the group that was given calcium, the infusion rate was reduced after three hours to 0.3 mmol/kg.hour to maintain the hypercalcaemic state for a further nine hours. RESULTS: Local infusion of calcium caused destruction of acinar cells with hydropic degeneration of nuclei, discharge of cell organelles into the interstitial spaces, and extravasation of red blood cells but no apparent damage to the capillaries. There were no ultrastructural changes of any importance in the groups that received potassium or sodium chloride. Systemic infusion of calcium resulted in a 1.8 fold increase in the ionised calcium concentration in the serum, progressive signs of overstimulation of the Golgi apparatus with hypertrophy, fusion of condensing vacuoles, and disruption of the acinar cell polarization. This was followed by clumping of nuclear chromatin and destruction of acinar cells. CONCLUSION: Acute pancreatitis in cats can result from stimulation and destruction of acinar cells by hypercalcaemia.

Acute Disease↗
PubMed1992

[Acute pancreatitis in the rat following experimental microembolism with cholesterol crystals].

Several case reports exist which demonstrate cholesterol crystals to be the cause of acute pancreatitis in humans. The crystals have been found intravascularly in the pancreas and at least in one case the origin of the crystals was known. We have undertaken to experimentally reproduce this pathogenetic mechanism in the rat. 30 rats were subjected to the following procedures: under anaesthesia the splenic artery was distally ligated and proximally cannulated; 16 control animals were injected via the cannula with saline (8 rats), particle free cholesterol saturated physiologic saline (3 rats) or nothing (5 rats). 14 rats were injected with ca. 400 microliters of a dilute suspension of cholesterol crystals of 5-40 microns diameter in cholesterol saturated physiologic saline. The abdomen was closed and after 24 h all animals were killed. Acute pancreatitis was diagnosed in all animals that received cholesterol microcrystals and in none of the controls. The diagnosis was based on macroscopic and histological findings. Acute pancreatitis was of focal, disseminated, necrotic type with oedema and moderate haemorrhage and fat necrosis. Only those parts of the pancreas were affected which were supplied by branches of the distal splenic artery used for retrograde injections of cholesterol crystals. This model supports the notion that microembolic or microthrombotic events play a pivotal role in the pathogenesis of spontaneous acute pancreatitis.

Acute Disease↗
PubMed1990

Acute hypercalcemia induces acinar cell necrosis and intraductal protein precipitates in the pancreas of cats and guinea pigs.

The effect of local and systemic calcium administration was tested on the pancreas of cat and guinea pig. After 3 h of local calcium infusion (0.6 mmol/kg x h) via the splenic artery of the cat hemorrhagic pancreatitis could be shown. Control animals treated with potassium (1.1 mmol/kg x h) or 0.9% NaCl alone showed no morphological change in the pancreas. Intravenous administration of calcium (0.6 mmol/kg x h) led to a 1.8-fold increase in serum ionized calcium levels in the cat and a 1.6-fold increase in levels in the guinea pig. The cat showed necrosis of acinar and ductal cells throughout the gland at 12 h. In the guinea pig, acinar cell vacuolisation and cell necrosis started at 3 h, and at 9 h degeneration of entire acini, hydropic swelling and degeneration of ductal cells, and perivascular leukocytic infiltration was present. In both species, a significant increase in the number of intraductal precipitates and a significant increase in urinary amylase output was present in calcium treated animals. The findings suggest that hypercalcemia has a deleterious effect on the pancreas that causes acinar and ductal cell necrosis and eventually pancreatitis.

Amylases↗
PubMed1990

Obstructive ileus and acute pancreatitis.

A 48-year-old patient presented with a 24 hour history of diffuse abdominal pain and diarrhea. Based on elevated serum amylase and lipase levels, a CT-scan, and a history of chronic alcohol intake, acute alcoholic pancreatitis was diagnosed. The patient clinically improved under conservative therapy, but after restarting enteral nutrition on the fourth day, he developed full blown mechanical ileus. Intraoperatively, an adhesive band and acute edematous pancreatitis and fat necrosis was found. Retrospectively, the initial clinical symptoms and plain abdominal x-ray findings suggest coincidence of obstructive ileus and acute pancreatitis. We hypothesize that obstructive ileus had triggered pancreatitis.

Acute Disease↗
PubMed1987

Hypercalcemia associated with pancreatitis and hyperamylasemia in renal transplant recipients. Data from the Minnesota randomized trial of cyclosporine versus antilymphoblast azathioprine.

The incidence and possible etiologic factors of acute pancreatitis and hyperamylasemia were statistically evaluated in renal transplant recipients. Two hundred twenty-four patients were randomized in a prospective trial of cyclosporine and antilymphoblast azathioprine immunosuppressive regimens. They had a median follow-up of 20 months. Pancreatitis developed in 8 patients and hyperamyl asemia developed in 20 patients. There were no statistical relationships between the incidences of pancreatitis and hyperamylasemia and the immunosuppressive drugs or viral infections. However, pancreatitis developed in 11 percent of the transplant patients with repeatedly elevated serum calcium levels (37 patients, p less than 0.01) and hyperamylasemia developed in 19 percent (p less than 0.025). Other etiologic factors, such as gallstones, alcoholism, and corticosteroids, played a minor role in this patient population. These results suggest that hypercalcemia is a major etiologic factor for pancreatitis in renal transplant recipients.

Acute Disease↗
PubMed1987

Effect of the organophosphate iso-OMPA on amylase release by pancreatic lobules of dog, guinea pig, and cat.

Organophosphates (OPs) cause irreversible inhibition of cholinesterases (ChEs) and profound cholinergic stimulation. There are major differences in the response of the dog and cat pancreas to the in vivo administration of Diazinon (O,O-diethyl O-2-isopropyl-4-methyl-6-pyrimidyl phosphothioate), a butyrylcholinesterase (BuChE) inhibitor. Acute edematous pancreatitis is found in the dog but not in the cat. The present experiments were designed to see what effect OP had in vitro on pancreatic exocrine function of dog, cat, and guinea pig, and whether the effects were consistent with an anti-ChE activity. A water-soluble OP agent, tetraisopropyl pyrophosphoramide (iso-OMPA) at 10(-3) M, which like Diazinon inhibits BuChE, was used. Minced pieces of fresh whole pancreata 3 mm in size were taken from 3 dogs, 4 guinea pigs, and 2 cats. The tissues were placed in flasks containing Eagle's solution and gassed with 100% O2. Cumulative amylase release was measured by Phadebas method up to 3 h. At half-maximal acetylcholine (ACH) concentration (10(-5) M), the canine pancreas pretreated with iso-OMPA (10(-3) M) showed a 42-87% greater release of amylase than tissues receiving ACH alone (p less than 0.001). The same potentiated response to ACH was seen in guinea pig pancreas pretreated with iso-OMPA (p less than 0.001), but iso-OMPA pretreatment did not augment the ACH response in the cat. Atropine pretreatment effectively blocked all ACH responses, and there was no effect seen with iso-OMPA alone. In the dog, iso-OMPA in combination with half-maximal carbachol (10(-6) M), or in combination with half-maximal cholecystokinin (CCK-8) stimulation (10(-9) M), provided no potentiated amylase release.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMedDate not supplied

Electrohydraulic extracorporeal non-water bath shock-wave lithotripsy of gallstones: two years' experience.

A prospective study was performed to evaluate the effectiveness of extracorporeal shockwave lithotripsy (ESWL) using a non-water bath lithotripter in combination with oral chemolitholysis on gallstone clearance. Patients were treated without general anesthesia or parenteral analgesia. We treated 74 patients selected according to the widely accepted criteria. Only 2 patients could not be sufficiently treated because of pain. After a 2 year period, 24 (32%) patients showed complete stone clearance, 35 (47%) patients had residual fragments, 5 (7%) patients underwent cholecystectomy, 2 (3%) patients were lost to follow up, and 8 (11%) patients discontinued the treatment before fragment clearance. According to the life-table estimate, 77% of our patients with successful ESWL and uncomplicated oral chemolitholysis are stonefree after 1 year. We consider the major advantage of this nonsurgical treatment of gallstone disease is that general anesthesia or parenteral analgesia has become unnecessary.

Adult↗
PubMedDate not supplied

Effects of insecticide, diazinon, on pancreas of dog, cat and guinea pig.

The organophosphate insecticide Diazinon has been reported to cause acute pancreatitis in dogs. Based on histochemical examination of the acinar tissue, it was suggested that pancreatic tissue-fixed butyrylcholinesterase (BuChE) is the target enzyme of organophosphate toxicity. To further evaluate this theory, we exposed dogs, cats, and guinea pigs to a single sublethal dose of the organophosphate insecticide Diazinon (75 mg/kg). In cats, which lack pancreatic BuChE, no pathological changes occurred after two, three, and six hours, whereas in the guinea pigs as in dogs, both having abundant pancreatic BuChE, vacuolization of the acinar cells, interstitial edema and vasculitis indicate acute edematous pancreatitis as early as two hours. Atropine pretreatment (0.2 mg/kg) gave complete protection against pancreatitis. It was concluded that inhibition of pancreatic BuChe leads to cholinergic hyperstimulation of the acinar cell, which results in acute pancreatitis, and that pancreatic BuChE is essential for dogs and guinea pigs to downregulate cholinergic excitation. The insecticide pancreatitis model is considered a simple, non-invasive, reproducible, and cheap and useful method to evaluate early changes and methods of treatment in acute pancreatitis. Pancreatitis in humans has also been reported after accidental insecticide exposure.

Animals↗