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Matjaz Bunc

Publications and source records attributed to Matjaz Bunc.

At least 19 recordsLinked to original sources

Immediate oxygen therapy prevents brain cell injury in carbon monoxide poisoned rats without loss of consciousness.

In CO-poisoned patients without loss of consciousness no significant long-term functional differences in outcome have been shown in any hyperbaric versus normobaric oxygen studies. Since brain histology changes cannot be studied in CO-poisoned patients we evaluated the efficacy of normobaric and hyperbaric oxygen therapy in preventing brain cell injury in CO-poisoned animals without loss of consciousness. Wistar rats without loss of consciousness after exposure to 3000ppm of CO for 60min were exposed to ambient air (group 1), 100% oxygen at a pressure of 1bar (group 2) and 100% oxygen at a pressure of 3bar (group 3). The rats were sacrificed after two weeks, brain samples were stained with hematoxylin-eosin and a percentage of pyknotic cells in hippocampus was reported. Analyses of differences in percentage of pyknotic cells between different kinds of therapy showed that the percentage of pyknotic cells of the second group (2.3+/-1.2%) treated with normobaric oxygen and the third group (4.5+/-4.0%) treated with hyperbaric oxygen were similar, and both of them were significantly different, with a much lower percentage of pyknotic cells, from the first group left on ambient air (47.7+/-10.0%). In conclusion, immediate normobaric and hyperbaric oxygen therapy equally prevents hippocampal cell injury in CO-poisoned rats without loss of consciousness.

Animals↗

Prolonged psychosis after Amanita muscaria ingestion.

Amanita muscaria has a bright red or orange cap covered with small white plaques. It contains the isoxazole derivatives ibotenic acid, muscimol and muscazone and other toxins such as muscarine. The duration of clinical manifestations after A. muscaria ingestion does not usually exceed 24 hours; we report on a 5-day paranoid psychosis after A. muscaria ingestion. A 48-year-old man, with no previous medical history, gathered and ate mushrooms he presumed to be A. caesarea. Half an hour later he started to vomit and fell asleep. He was found comatose having a seizure-like episode. On admission four hours after ingestion he was comatose, but the remaining physical and neurological examinations were unremarkable. Creatine kinase was 8.33 microkat/l. Other laboratory results and brain CT scan were normal. Toxicology analysis did not find any drugs in his blood or urine. The mycologist identified A. muscaria among the remaining mushrooms. The patient was given activated charcoal. Ten hours after ingestion, he awoke and was completely orientated; 18 hours after ingestion his condition deteriorated again and he became confused and uncooperative. Afterwards paranoid psychosis with visual and auditory hallucinations appeared and persisted for five days. On the sixth day all symptoms of psychosis gradually disappeared. One year later he is not undergoing any therapy and has no symptoms of psychiatric disease. We conclude that paranoid psychosis with visual and auditory hallucinations can appear 18 hours after ingestion of A. muscaria and can last for up to five days.

Amanita↗

S100B protein in conscious carbon monoxide-poisoned rats treated with normobaric or hyperbaric oxygen.

OBJECTIVE: To evaluate S100B, an astroglial structural protein, during normobaric and hyperbaric oxygen therapy of conscious carbon monoxide (CO)-poisoned rats. So far, the usefulness of hyperbaric oxygen therapy in conscious CO-poisoned patients has been shown with neuropsychological testing. The S100B protein has been demonstrated as a possible biochemical marker and prognostic parameter in CO-poisoned rats. DESIGN: Randomized, controlled interventional trial. SETTING: University laboratory. SUBJECTS: : Male Wistar rats weighing 254 +/- 14 g. INTERVENTIONS: The rats were exposed to a mixture of 3,000 ppm CO in air for 60 mins. After CO exposure, the first group of eight conscious rats was exposed to ambient air for 30 mins, the second group of six conscious rats was exposed to 100% normobaric oxygen for 30 mins, and the third group of six conscious rats was exposed to 100% hyperbaric oxygen at 3 bars for 30 mins. Blood samples were taken from the jugular vein just before CO exposure and immediately after oxygen therapy. The level of consciousness was evaluated at the end of exposure, and the survival rate was monitored for 14 days. The S100B concentrations were measured with a commercial immunoluminometric assay. MEASUREMENTS AND MAIN RESULTS: Analyses of differences in S100B levels between different kinds of therapy before and after treatment showed a global significant difference (p = .002). The post hoc test results showed that S100B levels after therapy of the first group treated with ambient air (0.16 +/- 0.07 microg/L) and the second group treated with normobaric oxygen (0.19 +/- 0.05 microg/L) were similar (p = .741), and both of them were significantly different, with much higher values of S100B levels after therapy, from the third group treated with hyperbaric oxygen (0.06 +/- 0.03 microg/L; p = .018 and p = .002, respectively). All the rats survived. CONCLUSIONS: S100B is elevated in conscious CO-poisoned rats left on ambient air or treated with normobaric oxygen, but not in conscious CO-poisoned rats treated with hyperbaric oxygen.

Animals↗

Prolonged hypoglycaemia after insulin lispro overdose.

Insulin lispro has a more rapid onset and a shorter duration of hypoglycaemic action than regular insulin. We report a 39-year-old woman, with no previous medical history, who injected 300 U of the insulin lispro (Humalog) in an attempted suicide. Half an hour later, she was found comatose and brought to our emergency department. On arrival, she was comatose, with capillary glucose of 0.4 mmol/L. She awoke after a 50 ml intravenous bolus of 50% glucose. A continuous infusion of 10% glucose was started. Intermittent hypoglycaemia with neurological signs requiring treatment with 50% glucose was recorded three times during subsequent hospitalization, the last episode being 11 h after insulin injection. The plasma insulin level 4 h after injection was 1465 mU/L, and 18 h after injection was 11 mU/L. Hypoglycaemia after an insulin lispro overdose may last for more than 11 h. Repeated hypoglycaemia after an insulin overdose could be avoided with a glucose infusion rate equivalent to the maximal glucose disposal rate.

Adult↗

Modulation of a dog's internal organ function by selective stimulation of the splanchnic nerve.

The superficial regions of the dog splanchnic nerve were selectively stimulated with 33-electrode spiral cuffs in 11 circumferential groups of three electrodes to modulate the function of the innervated internal organs and glands. In two adult Beagle dogs under general anaesthesia, the cuffs were chronically implanted on the nerve trunks before the celiac ganglion. Superficial regions of the nerves were selectively stimulated for 15 s with biphasic, rectangular, current pulses (2 mA intensity, 200 micros duration, and 20 Hz frequency) which were delivered sequentially to the corresponding group of three electrodes. The results showed that Group no. 8 of three electrodes elicited the highest influence on pressure within the bladder. Namely, a decrease in pressure starting from 34.97 mmHg at the beginning of stimulation to 34.92 mmHg at the end of stimulation was observed. It was also shown that only Group no. 4 of three electrodes significantly modified the endocrine function of the pancreas. A considerable increase in glucagon secretion with a peak value of 47 pg/ml and an insignificant change in insulin secretion were also observed. The results of histological observations demonstrated that the use of the cuff was associated with a buildup of connective tissue encapsulation around the cuff as well as within it. However, functional deficits were not observed in the animal, and most of the fibers appeared to be histologically normal after stimulation. The results of this study clearly demonstrate that internal organs and glands can be selectively stimulated through the selective stimulation of innervating superficial regions of the autonomous peripheral nerve.

Animals↗

Acute poisoning with autumn crocus (Colchicum autumnale L.).

INTRODUCTION: Colchicum autumnale, commonly known as the autumn crocus or meadow saffron, contains the antimitotic colchicine, which binds to tubulin and prevents it forming microtubules that are part of the cytoskeleton in all cells. CASE REPORT: A 71-year-old woman ate a plant she thought to be wild garlic (Allium ursinum). Ten hours later she arrived at the emergency department complaining of nausea, vomiting and watery diarrhea. Ingestion of a poisonous plant was suspected and she was treated with gastric lavage, oral activated charcoal and an infusion of normal saline. Toxicology analysis with gas chromatography and mass spectrometry revealed colchicine in the patient's gastric lavage, blood (5 microg/l) and urine (30 microg/l). She developed arrhythmias, liver failure, pancreatitis, ileus, and bone marrow suppression with pancytopenia. Alopecia began in the third week. Treatment was supportive only. Five months later she had no clinical or laboratory signs of poisoning. DISCUSSION: The patient mistakenly ingested autumn crocus instead of wild garlic because of their great similarity. Colchicine primarily blocks mitosis in tissues with rapid cell turnover; this results in gastroenterocolitis in the first phase of colchicine poisoning, bone marrow hypoplasia with pancytopenia in the second and alopecia in the third, all of which were present in our patient. Colchicine toxicity in tissues without rapid cell turnover caused arrhythmias, acute liver failure and pancreatitis. CONCLUSION: Colchicine poisoning can result in gastroenterocolitis followed by multi-organ dysfunction syndrome. In unexplained gastroenterocolitis after ingestion of wild plants as a salad or spice, especially when wild garlic is mentioned, we should always consider autumn crocus. Diagnosis could be confirmed only by toxicology analyses. Management of colchicine poisoning is restricted to supportive therapy.

Aged↗

Case report: fatal poisoning with Colchicum autumnale.

INTRODUCTION: Colchicum autumnale, commonly known as the autumn crocus, contains alkaloid colchicine with antimitotic properties. CASE REPORT: A 76-year-old man with a history of alcoholic liver disease and renal insufficiency, who mistakenly ingested Colchicum autumnale instead of wild garlic (Aliium ursinum), presented with nausea, vomiting and diarrhea 12 hours after ingestion. On admission the patient had laboratory signs of dehydration. On the second day the patient became somnolent and developed respiratory insufficiency. The echocardiogram showed heart dilatation with diffuse hypokinesia with positive troponin I. The respiratory insufficiency was further deteriorated by pneumonia, confirmed by chest X-ray and later on by autopsy. Laboratory tests also revealed rhabdomyolysis, coagulopathy and deterioration of renal function and hepatic function. The toxicological analysis disclosed colchicine in the patient's urine (6 microgram/l) and serum (9 microgram/l) on the second day. Therapy was supportive with hydration, vasopressors, mechanical ventilation and antibiotics. On the third day the patient died due to asystolic cardiac arrest. DISCUSSION AND CONCLUSION: Colchicine poisoning should be considered in patients with gastroenterocolitis after a meal of wild plants. Management includes only intensive support therapy. A more severe clinical presentation should be expected in patients with pre-existing liver and renal diseases. The main reasons for death are cardiovascular collapse, respiratory failure and leukopenia with infection.

Aged↗

S100B protein in carbon monoxide poisoning: a pilot study.

Carbon monoxide (CO) poisoning is the most common form of lethal poisoning. The aim of this prospective clinical study was to assess the possible role of S100B, the structural protein in the astroglia, as a biochemical marker of brain injury in carbon monoxide poisoning. Serum S100B determination was performed in 38 consecutive patients poisoned by carbon monoxide who were admitted to the Emergency Department (ED) in Ljubljana. All three unconscious patients had elevated S100B levels. The patient with the highest S100B died. S100B was elevated in two of the six patients with initial transitory unconsciousness at the scene. All 29 patients without loss of consciousness had normal S100B levels. Carbon monoxide poisoning appears to be associated with elevated S100B levels.

Adolescent↗

Polydipsia as another mechanism of hyponatremia after 'ecstasy' (3,4 methyldioxymethamphetamine) ingestion.

Acute symptomatic hyponatremia after ecstasy (3,4 methyldioxymethamphetamine; MDMA) ingestion is well documented and has been attributed to the syndrome of inappropriate antidiuretic hormone (SIADH). We report the case of an 18-year-old woman who took five tablets of ecstasy in a suicide attempt and drank 1700 ml water at the Emergency Department (ED). The laboratory findings obtained 5 h after ingestion showed a serum sodium concentration of 130 mmol/l, plasma osmolality of 264 mOsm/kg, urinary osmolality of 335 mOsm/kg and natriuresis of 101 mmol/l. The plasma arginine vasopressin level by radioimmunoassay was 33.7 pmol/l 5 h after ingestion. A gas chromatography-mass spectrometry assay confirmed MDMA in blood samples, with serum concentrations of 0.87 mg/l on arrival. This case report strongly suggests that MDMA reduces serum sodium levels through the dual pathways of SIADH and polydipsia. Accordingly, we believe that hyponatremia may be prevented in ED patients after MDMA ingestion by the early restriction of water intake.

Adolescent↗

Prognostic value of S100B protein in carbon monoxide-poisoned rats.

OBJECTIVE: To assess the possible role of S100B, a structural protein of astroglial cells, as a biochemical marker in acute carbon monoxide-poisoned rats and to compare its prognostic value with consciousness level, which is one of the major parameters for treatment decision in acute carbon monoxide poisoning. DESIGN: Nonrandomized, controlled interventional trial. SETTING: University laboratory. SUBJECTS: Male Wistar rats weighing 263 +/- 18 g. INTERVENTIONS: The rats were exposed to a mixture of 3000 ppm carbon monoxide in air for 60 mins (group 1) and a mixture of 5000 ppm carbon monoxide in air for 30 mins (group 2). Blood samples were taken from the jugular vein just before and immediately after the carbon monoxide poisoning. The level of consciousness was evaluated at the end of the exposure, and the survival rate was monitored for 7 days. The S100B concentrations were measured with a commercial immunoluminometric assay. MEASUREMENTS AND MAIN RESULTS: In the first group, the unconscious rats after carbon monoxide exposure had significantly higher S100B levels compared with the rats without loss of consciousness. In the second group, the unconscious rats that later died had significantly higher S100B levels compared with the unconscious rats that survived. The S100B levels of all conscious and unconscious surviving rats were not significantly different. The serum level of S100B below 0.44 microg/L predicted survival of carbon monoxide-poisoned rats, with a sensitivity of 100% and a specificity of 86%. CONCLUSIONS: Acute carbon monoxide poisoning is associated with elevated S100B levels. S100B is a better predictor of final outcome than the consciousness level, so it could be used as a prognostic parameter for acute carbon monoxide poisoning in rats.

Animals↗

The potential value of the protein S-100B level as a criterion for hyperbaric oxygen treatment and prognostic marker in carbon monoxide poisoned patients.

Carbon monoxide (CO) poisoning resulting in diffuse tissue hypoxia. Cerebral hypoxia is a major cause of morbidity and mortality after CO poisoning. There are some clinical criteria that could help a physician to make a decision concerning the application of hyperbaric oxygenation therapy. However, it would be convenient to discover an objective biochemical serum marker that could help in the grade evaluation of CO poisoning and indication of therapy in CO-poisoned patients. We present two case reports where the established criteria for the CO poisoning were not optimum for the decision regarding therapy. It seems that the S-100B protein could be used as a biochemical marker of CO induced brain injury. S-100B values could perhaps help us to select patients for hyperbaric oxygen therapy and to predict the short and long term outcome.

Adult↗

Toxic effects of head-to-tail 3-alkylpyridinium polymers isolated from the marine sponge Reniera sarai in rat.

Toxic water soluble polymeric 3-alkylpyridinium salts (poly APS; MW 18900 and 5520Da) were isolated from the marine sponge Raniera sarai. In vitro they strongly inhibited acetylcholinesterase. In order to evaluate the role of acetylcholinesterase inhibition in toxin lethality, and to assess other possible lethal effects, in vivo experiments were performed on male Wistar rats, and ECG, blood pressure and breathing pattern were monitored. The results showed that none of the animals died due to the acetylcholinesterase inhibitory action of poly-APS. Doses lower than 1mg/kg caused only transient bradycardia and transient prolongation of expirium. At doses above 2.7mg/kg of poly-APS all treated animals died, but signs were not typical of acetylcholinesterase inhibition. Arterial blood pressure fell to mid-circulatory pressure, and breathing stopped after a few breaths with an increase of the residual volume. Autopsy of the experimental animals that died due to the effects of the toxin revealed that mid-size and small sized blood vessels in the heart and lungs were filled with granular brownish material with inclusions of red blood cells and platelets. Data obtained on blood samples from animals treated with poly-APS also revealed numerous thrombocyte aggregates. In vitro poly-APS induced thrombocyte aggregation in a dose dependent manner. The acetylcholinesterase-inhibitory effects were most pronounced only at lower doses of poly-APS. With higher doses those effects were masked or covered by other, more pronounced and faster developing lethal effects of the toxin such as platelet aggregation. Therefore it is reasonable to assume that acetylcholinesterase inhibitory effects are not responsible for the lethal activity of the toxin.

Animals↗

Stimulation of nerves innervating the dog's pancreas.

Our aim was to modulate secretion of insulin and glucagon into the blood of a diabetic but otherwise healthy dog with stimulation of nerves innervating the pancreas. The 33 electrode spiral cuffs were implanted in an adult beagle canine. The first cuff was installed on the vagus nerve, the second one on the splanchnic nerve, and the last one on the pancreatic nerve. To cause insulin-dependent Type I diabetes, partial dysfunction of the pancreas was induced. Nerves were stimulated using biphasic, rectangular current pulses (10 mA, 200 micros, 20 Hz). Samples from the femoral artery were drawn before the experiment, after 5 min, and 5 min after the stimulation stopped. The results of radioimmunological assay of blood samples showed that in the intact pancreas, stimulation of the vagus nerve caused a considerable increase in insulin secretion, no significant change in glucagon secretion, and a decrease in C-peptide secretion. Splanchnic nerve stimulation did not cause considerable change in insulin and C-peptide secretion while considerable increase in glucagon secretion was noticed. Pancreatic nerve stimulation did not considerably change the secretion of any of the three hormones. In the dysfunctioned pancreas, vagal nerve stimulation caused an increase in insulin and glucagon secretion and a minor increase in C-peptide secretion. Splanchnic nerve stimulation caused a minor decrease in insulin secretion, a considerable increase in glucagon secretion, and a small increase in C-peptide secretion. Pancreatic nerve stimulation did not cause a considerable change in insulin secretion while a minor increase in glucagon and C-peptide secretion was observed.

Animals↗

Recording of ENGs from the nerves innervating the pancreas of a dog during the intravenous glucose tolerance test.

Electroneurograms (ENGs) from the vagus nerve (VN), the splanchnic nerve (SN) and the pancreatic nerve (PN) innervating the pancreas of a dog, were recorded with chronically implanted 33-electrode spiral cuffs (cuff) before and after the pancreas were stimulated with intravenously (i.v.) administered glucose. In the cuffs platinum electrodes were arranged in three parallel spiral groups containing 11 electrodes on the inner surface. The cuffs had an inner diameter of 2 mm and a length of 18 mm. In a two-year study, the cuffs were implanted into two Beagle dogs and were also used for pancreatic stimulation, although this is not described in this paper. In the VN, the cuff was installed on the nerve at the neck, whilst in the SN, the cuff was installed on the nerve before the celiac ganglion, and in the PN, the cuff was installed on the nerve just before it enters the pancreas. Six months after implantation, when the model of interpretation of the results was developed, three recordings of ENG in each animal were conducted. The first one was conducted in the unstimulated pancreas while the second and the third were conducted 1 and 8 min after a known amount of glucose was i.v. administered. Since the results obtained in both animals were actually quite similar, we present the results obtained in one animal. To evaluate the changes in superficial activity of the nerves, elicited by the administration of glucose, the power spectra corresponding to ENGs, recorded from the nerves before and after the administration of glucose, were integrated within the band of frequencies ranging from 1 to 5 kHz. Accordingly, the magnitude of the integrated power spectrum (MIPS), corresponding to the ENG recorded from the SN before administration of glucose, was 2.863 au. One minute after glucose was administered the value fell to 2.795 au while 8 min after the administration the value returned to 2.8 au. The MIPS corresponding to the ENG recorded from the PN before the administration of glucose was 3.236 au. One minute after the administration the value fell to 2.901 au while 8 min after the administration the value rose to 3.009 au. The MIPS, corresponding to the ENG recorded from the VN before the administration of glucose, was 3.656 au. One minute after the administration the value fell to 3.565 au. Eight minutes after the administration the value rose to 3.689 au. The results show that 1 min after glucose was administered superficial activity in all three nerves was reduced while 8 min after administration the activity in the nerves returned to the same level of activity before the glucose was administered. This information could be effectively used in a further study of pancreatic innervation and its function. Moreover, the results suggest that cuffs could also be useful in recording the ENGs from other nerves of the autonomic nervous system that innervate various glands and internal organs.

Animals↗

Intravascular plug formation induced by poly-APS is the principal mechanism of the toxin's lethality in rats/rat tissues.

Toxic water soluble polymeric 3-alkylpyridinium salts isolated from the sponge Raniera sarai strongly inhibited AChE in vitro. In vivo, experimental animals died due to plugs formed in microcirculation. The mechanism of this plug formation is unknown. In vitro, the toxin did not affect the coagulation rate, but the rate of platelet aggregation was accelerated in a dose-dependent manner. The hemolytic activity of poly-APS was diminished by the addition of serum proteins in a dose-dependent manner. These results support the conclusion that non-specific binding to proteins is the underlying mechanism of the lethality of poly APS.

Animals↗

Equinatoxin II-induced lysis Of the cultured endothelial cell line ECV-304.

Equinatoxin II (EqT II) is a pore-forming actinoporin. Its lethality in rat tissue is due to cardio-respiratory effects. The toxin contracts the vascular smooth muscle only in the presence of intact endothelium. In our study, its effects on the endothelial cell culture ECV-304 were tested. The EqT II effects were dose-dependent and were influenced by calcium ions and sucrose. The obtained results support the conclusion that calcium ions are the intracellular messengers of the EqT II effects on the isolated endothelial cells.

Cell Line↗