Biomedical subjects
Publications and source records attributed to K Wiśniewski.
A group of 62 patients treated with schizophrenia for the first time was examined. Connection between the IQ, the type or interests, Bleulers' primary symptoms and Schneider's criteria was analyzed. A number of dependence factors were discovered, what allowed to draw conclusions about the role of intelligence and interest in patients' first manifestation of schizophrenia.
We investigated the effects of 2R,4R-APDC, a selective group II metabotropic glutamate receptor (II mGluR) agonist, on certain behaviors in rats subjected and non-subjected to hypoxia. Short-term hypoxia was used as a model of experimentally induced amnesia. 2R,4R-APDC given intracerebroventricularly (icv) at doses of 1 mumol and 100 nmol decreased the number of crossings and rearings in the open field, impaired acquisition and consolidation but improved retrieval in the passive avoidance tests. It also shortened the time spent in open arms and prolonged the time spent in closed arms, reduced the number of open and closed arms entries in an elevated "plus" maze, which is a measure of anxiety. Four-minute hypoxia (2% O(2), 98% N(2)) retrieval of conditioned responses, and exhibited an anxiogenic effect in the elevated "plus" maze in rats, i.e. it reduced the time spent in open arms and the number of entries to closed and open arms. 2R,4R-APDC effect on locomotor and exploratory activity was not changed after hypoxia, i.e. we observed inhibition of motility. This agonist of II mGluRs used at both doses before hypoxia significantly improved acquisition and retrieval, and had dual effect on consolidation, viz. at a dose of 1 mumol, it impaired this process and at a dose of 100 nmol it improved it. In the elevated "plus" maze, rats pretreated with 2R,4R-APDC and then subjected to hypoxia shortened the time spent in open arms and prolonged the time spent in closed arms, reduced the time spent in open arms, i.e. the drug exhibited anxiogenic effect. We conclude, therefore, that 2R,4R-APDC itself impaired acquisition and consolidation, enhanced retrieval but in rats undergoing hypoxia, it improved acquisition, retrieval and when used at the dose of 100 nmol enhanced consolidation. 2R,4R-APDC had beneficial effect in hypoxia-induced memory impairment in passive avoidance test.
An effect of somatostatin on arterial blood pressure, isolated heart, and its interaction with adrenergic system have been studied in rats. It was found, that somatostatin does not exert any significant effect on blood circulation. It modifies however catecholamines action. Somatostatin decreases the activity of alpha-adrenergic receptors agonist (norepinephrine), and potentiates the activity of beta-adrenergic receptors agonist (isoprenaline).
Our recent studies have shown that facilitating effect of angiotensin II (AII) on recall is mediated by dopaminergic systems. In this study the influence of bilateral destruction of dopaminergic endings in the entorhinal cortex on improving recall intracerebroventricular injection of AII was tested. Since this lesion did not abolish the facilitating influence of AII, it may be suggested that the dopaminergic projection to the entorhinal cortex is not responsible for the facilitating effect of AII on recall in a passive avoidance situation.
The role of peptides such as fibrinogen degradation products (FDP), albumin degradation products (ADP), globulin degradation products (GDP), Bradykinin (BRS) and Angiotensin II (A) in CNS function is presented. Peptides change the activity of the CNS, of the centrally acting drugs and of some neuromediators. The mechanism of the phenomena observed is discussed.
The paper reviews the functions of proteolytic enzymes in processing intracellular peptides. The enzymes may "activate" precursors of active peptides, "inactivate" active peptides by their degradation to biologically inactive forms, and "change" the peptides degrading biologically active forms to smaller peptides of different biological activity. The results of own studies on angiotensin II and its fragments are quoted to illustrate how various fragments of the peptide may display various biological activity.
The effect of collagen degradation products (CDP I--molecular weight circa 3000 D and CDP II--molecular weight circa 1200 D) on the central dopaminergic system was studied. Differences in the action of both these fractions in the apomorphine stereotypy test were noted; CDP I administered to rats in a dose of 5 micrograms just before application of the drug inducing the stereotypy enhanced the stereotypic behaviour of the animals whereas a dose of 40 micrograms significantly inhibited such behaviour. CDP II, on the other hand, had no effect on this type of stereotypy. Both fractions given in doses of 15 and 40 micrograms enhanced the stereotypy induced by amphetamine. CDP I and CDP II (15 and 40 micrograms) administered 30 min before observation of the animals intensified the cataleptic action of haloperidol, whereas both fractions (CDP I and CDP II) when administered 45 min before observation reduced the catalepsy.
Suprofen is a new non-steroidal anti-inflammatory drug administered intragastrically 90 min before roentgen irradiation in a dose of 20 mg/kg and then daily for 10 days in a dose of 10 mg/kg exerts the radioprotective effect evaluated according to a 30-day survival rate and an average life expectancy of the deceased animals as well as according to a decrease of postirradiation leukopenia incidence. A single administration of suprofen following roentgen irradiation exerts no radioprotective effect. Suprofen was found to enhance the radioprotective action of cysteamine.
The effect of cholecystokinin (CCK-33) and its fragments, C-terminal octapeptide (CCK-8) and C-terminal tetrapeptide (CCK-4), on arterial blood pressure and on the function of the isolated rat heart was studied in three groups of animals: normal (C group), rats with streptozotocin-induced diabetes of one month's duration (DM group) and with diabetes treated with insulin (DMI group). CCK-33 (5.0, 10.0 and 20.0 U/kg iv) raised dose-dependently systolic and diastolic arterial blood pressure but did not change the heart rate in the group of normal rats. CCK-33 administered in doses of 1.0, 2.0, 5.0 U/0.1 ml) increased the amplitude of the isolated heart contraction and reduced heart rate but had no effect on coronary outflow in this group. In the diabetic rats, CCK-33 in dose 20.0 U/kg iv reduced the arterial blood pressure and had no effect on heart rate in vivo. CCK-33 increased the cardiac contraction amplitude and lowered heart rate of the isolated heart from the diabetic rats. In the group of insulin-treated diabetic rats, CCK-33 did not change the blood pressure, increased the heart rate in vivo. This peptide increased the cardiac contraction amplitude, no lowering of the heart rate of the isolated heart was noted. CCK-8 and CCK-4 had no effect on arterial blood pressure and the function of the isolated heart in any of the groups of animals studied. The results indicate that shortening of CCK-33 to CCK-8 and CCK-4 eliminates the circulatory effect of this peptide and that in diabetes CCK-33 produces circulatory effects opposite to those observed in normal animals. Insulin partially normalizes the action of CCK-33 on the circulation in diabetes.
Our earlier experiments have shown that the facilitating action of angiotensin II (AII) on recall of passive avoidance is mediated by dopaminergic systems. In an attempt to find the site of action of AII on memory in the brain, bilateral lesions of the two structures belonging to the limbic system, receiving efferentation from A 10 dopaminergic neurons, were made in 32 male rats before behavioral testing of the influence of intracerebroventricular AII injection on recall in a passive avoidance situation. 32 additional rats served as sham operated controls. Bilateral lesions to the dentate gyrus of the hippocampus and olfactory tubercle did not significantly change the facilitating effect of AII on recall. The results may suggest that dopaminergic projections from A 10 neurons of the ventral tegmental area to the dentate gyrus and olfactory tubercle are not responsible for the enhancing effect of AII on recall of passive avoidance.
The interaction of cholecystokinin (CCK-33) and its fragments, C-terminal octapeptide (CCK-8) and C-terminal tetrapeptide (CCK-4) with norepinephrine (NE) was studied in rats with streptozotocin (STZ)-induced diabetes. The rats, male Wistar, were divided into three groups: control, diabetic and insulin-treated diabetic. Twenty-eight days after STZ administration, the systolic and diastolic arterial blood pressure, heart rate and the function of the heart isolated by the Langendorff method were studied. NE caused a rise in systolic blood pressure in the control and insulin-treated diabetic rats, the opposite effect of NE was observed in diabetic rats. NE had no effect on heart rate in any of the groups studied. CCK-33 potentiated the hypertensive effect of NE in the control rats reduced the hypertensive effect of this amine in diabetic rats treated with insulin and its hypotensive effect in the diabetic rats. CCK-8 did not change the NE effect on arterial blood pressure in the control and insulin-treated diabetic rats but did reduce the hypotension caused by NE in diabetic rats. CCK-4 did not change the effects of NE in any of the groups. NE induced an increase in cardiac contraction amplitude in all rats but its positive inotropic action was found to be the weakest in the diabetic rats. Administration of CCK-33 did not change the positive inotropic effect of NE in any of the groups but did, however, weaken its influence on heart rate in diabetic rats and insulin-treated diabetic rats. CCK-8 reduced the positive inotropic action of NE but did not affect its chronotropic effect. CCK-4 had no effect on the action of NE in any of the groups. Diabetes can change the response of alpha-adrenergic system to CCK-33 and NE. Insulin partially normalized the circulatory system response in the diabetic rats.
Rats with impaired retrieval of passive avoidance behavior induced by chronic (9 weeks) administration of ethanol were studied. Angiotensin II (AII) and its fragments: AII(3-8) and AII(4-8), administered (icv, 2.0 micrograms) on the third day after ethanol withdrawal, neutralized the toxic effect of ethanol. Furthermore, the peptide AII(3-8) also gave an improvement in retrieval of the capability to perform simple behavioral tasks as it did in the control group in rats chronically pretreated with alcohol.
Kallikrein given in combination with acetylcholine (ACh) increased the central inhibitory action of ACh as measured in the Lat's test, duration of thiopental sleep and inhibition of electrogenic convulsions. Indomethacin aboished the potentiating effect of kallikrein on these actions of ACh, PGE1 did not play a significant role in the influence of kallikrein on the central action of ACh. However, inhibition of prostaglandin synthesis with indomethacin plays an important role in the interaction of kallilkrein and ACh.
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The participation of prostaglandins (PGs) E2 and F2 alpha administered icv in the action of fibrinopeptides A and B (FAB) on the central dopamine neurons was investigated. PGE2 and PGF2 alpha (0.5 microgram) attenuated the intensity of apomorphine (APO)-induced stereotypy and completely abolished the stimulatory action of FAB. PGE2 given together with FAB attenuated, while PGF2 alpha did not affect the amphetamine-induced stereotypy and haloperidol-induced catalepsy. The investigated PGs did not affect or normalized the level of dopamine depressed by peptides in some parts of the brain. The results indicate that PGE2 alpha and PGF2 alpha do not participate in the mechanism of the central action of FAB.
Pretreatment of rats with paracetamol (200 mg/kg po) abolished the enhancement of apomorphine and amphetamine stereotypy evoked by angiotensin II (0.5 microgram icv). The effect of angiotensin II was restored by an icv administration of 1 microgram of PGE1 X PGF2 alpha abolished the enhancement of stereotypy evoked by angiotensin II. PGE1 increased, while PGF2 alpha did not change the basic stereotypy induced by apomorphine and amphetamine. A specific radioimmunoassay of E-type prostaglandins (PGE1 + PGE2) revealed an increase by 136% in the level of PGE in the striata of rats pretreated with angiotensin II. These results suggest that stimulatory effects of angiotensin II in the central nigrostriatal system are, at least in part, mediated by the release of the E type of prostaglandins.
The effect of kallikrein was studied on the acquisition and extinction of conditioned reactions in rats. It was demonstrated that kallikrein in doses of 50 and 100 mu/kg i.p. accelerated the process of learning in these animals. The observed effect might be connected with a rise in the activity of kininogenic enzymes in the central nervous system.
Fibrinopeptides A and B (FAB) stimulate central dopamine neurons. Inhibition of prostaglandin synthesis by administration of indomethacin potentiated the stimulatory action of FAB on apomorphine stereotypy, while induced inhibitory action of FAB on amphetamine stereotypy. Results of studies on the level and turnover of dopamine do not explain the changes in the stereotyped behavior. The data suggest that prostaglandins may to some extent participate in the mechanism of the central action of FAB.