Biomedical subjects

Janez Rozman

Publications and source records attributed to Janez Rozman.

6 recordsLinked to original sources

PubMed2005

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↗

PubMed2002

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↗

PubMed2002

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↗

PubMed2002

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↗

PubMed2002

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↗

PubMed2002

Nicardipine diminished equinatoxin II-induced decrease of coronary flow in isolated rat and pig hearts.

Equinatoxin II (EqT II) is a basic, cardiotoxic polypeptide. The vasoconstrictory effect of the toxin on isolated porcine coronary arteries was diminished by nicardipine, an L-type calcium channel antagonist. A comparison was made of the effects of EqT II alone and EqT II in the presence of nicardipine on the coronary flow in porcine and rat hearts isolated according to Langendorff's method. In both models EqT II decreased coronary flow in a dose-dependent manner and there were no statistically significant differences between the two models (p>0.05). However, 1 M nicardipine diminished the effects of EqT II on coronary flow in isolated porcine hearts more than in isolated rat hearts (p<0.05). The results suggest that the activation of L-type calcium channels is one of the mechanisms involved in the lowering of coronary flow induced by EqT II.

Animals↗