[The evaluation of atrial natriuretic peptide and endothelin in serum of the patients with non-atopic bronchial asthma during exacerbation]. / Ocena stezen przedsionkowego peptydu natriuretycznego i endoteliny u chorych na astme oskrzelowa nieatopowa podczas zaostrzenia choroby.

The aim of the study was to evaluate concentrations of atrial natriuretic peptide (ANP) and endothelin in blood serum of the patients with nonatopic bronchial asthma in the exacerbation phase and during non-symptomatic period. The study included 20 patients with nonatopic bronchial asthma (10 women and 10 men, mean age 34.2) treated in the Allergological Outpatient Clinic in Zabrze (Poland). A control group consisted of 5 healthy volunteers without atopy. The study consisted of evaluation of the ANP and endothelin in blood serum by radioimmunoassay and by functional respiratory tests. It was shown that ANP concentrations during bronchial asthma exacerbation were two times lower than in the same group examined in the remission phase (7.8-13.7 pmol/ml, p < 0.05). At the time of bronchospastic symptoms occurrence, the concentrations of endothelin were statistically significant and higher than in the non-symptomatic group (11.6-6.9 pmol/ml, p < 0.05). In the examined group the reverse proportion relation between concentrations of the studied peptides in blood serum was observed r = -0.56, p < 0.05 according to Spearman test.

Effect of enflurane on selected neuropeptides and marker enzymes in rabbit brain.

The aim of this study was to evaluate the effect of 5-, 15-, and 60-min enflurane anesthesia on the levels of Met-enkephalin, Leu-enkephalin and neuropeptide Y in discrete areas of the rabbit brain. We also evaluated the effect of enflurane anesthesia on energetic, transport and catabolic processes by measuring the activities of succinate dehydrogenase, magnesium-dependent adenosine triphosphatase and acid phosphatase in the rabbit striatum and hypothalamus. Induction of anesthesia (5 min) decreased Met-enkephalin levels in the hypothalamus and striatum, and increased them in the hippocampus and mesencephalon. Induction of anesthesia increased Leu-enkephalin levels in all brain areas studied, except for the striatum, and increased neuropeptide Y content in the hippocampus. 15- and 60-min enflurane anesthesia increased Met-enkephalin content in the hypothalamus and hippocampus. After 15- and 60-min anesthesia, and after cessation of anesthesia, Leu-enkephalin levels were increased in the hypothalamus and mesencephalon, and were decreased in the striatum and hippocampus. In the striatum, neuropeptide Y content was significantly decreased during anesthesia and after cessation of anesthesia. Histochemical analysis revealed that enflurane enhanced ATP production, catabolic processes, and the rates of exchange and transport of energetic substrates in the striatum and hypothalamus. In conclusion, enflurane affects the levels of Met, Leu-enkephalins and NPY in a manner depending on the duration of anesthesia and the brain structure. Compared with isoflurane , which was studied in our previous study enflurane produces stronger alterations in the activities of enzymatic marker in the rabbit brain. This suggests that enflurane may be less safe than isoflurane.

Influence of isoflurane on enkephalin levels and on some indicatory enzymes in the central nervous system of rabbits.

The objective of this study was to analyse the effects of isoflurane anesthesia (lasting for 15 or 60 min) and isoflurane anesthesia termination (after 1 or 24 h) on met-enkephalin (MENK) and leu-enkephalin (LENK) levels in discrete brain areas and spinal cord segments in rabbits. Moreover histochemical analysis of activities of succinate dehydrogenase, magnesium-dependent adenosine triphosphatase (Mg++ATP-ase) and acid phosphatase in the striatum and hypothalamus were carried out to evaluate the effects of isoflurane anesthesia on energetic, transport and catabolic processes. Throughout anesthesia (15 and 60 min) and after its termination (1 h) the LENK contents were increased in hypothalamus, hippocampus, mesencephalon and lumbar segment of spinal cord. Moreover, during isoflurane anesthesia and after its termination (1 h) MENK and LENK levels decreased in cervical segment and MENK content dropped in thoracic segment of spinal cord. Histochemical data indicated, that isoflurane enhanced energetic processes as well as exchange processes in neurocytes, glial cells, capillary walls and ependymal cells of the third ventricle. Measurements of acid phosphatase activity provided evidence of no signs of toxicity of isoflurane in the examined areas. The changes in enkephalin levels observed during the isoflurane anesthesia and after its termination depended on the type of examined neuropeptides, as well as on parts of the brain and spinal cord studied. The changes observed after isoflurane administration in enkephalinergic system are discussed with regard to our earlier experiments with halothane and enflurane.

Concentration of enkephalins in cerebrospinal fluid of patients after severe head injury.

We studied head-injured patients treated at the Department of Neurosurgery, Silesian University School of Medicine, Katowice. The patients underwent lumbar puncture on days 1, 4 and 7 for diagnostic reasons. The levels of leu-enkephalin (LENK) and met-enkephalin (MENK) were examined in 4.5 ml of cerebrospinal fluid (CSF). The control group included patients with lumbar discopathy from whom CSF fluid was collected during myelography. Enkephalins were extracted by column chromatography and their levels were assayed radioimmunologically. The results indicate that enkephalins may play a certain role in the pathophysiological response of nervous tissue to traumatic injury. Constantly elevated MENK levels together with decreasing LENK levels in patients with a Glasgow coma scale score < or = 8 may be useful as a poor prognostic factor. It is also suggested that LENK and MENK play different pathophysiological roles.

Leucine enkephalin level in rat hypothalamus, striatum, hippocampus and adrenal glands in experimental rat uremia.

The aim of the study was to analyze the effect of experimental uremia elicited in Wistar rats by 5/6 kidney resection on the leu-enkephalin level in hypothalamus, striatum, hippocampus and adrenal glands. We found, that in uremic rats leu-enkephalin levels decreased in striatum and in adrenal glands. The level of leu-enkephalin in adrenal glands was directly related to plasma creatinine. The weight of uremic rats was significantly lower than that of control rats.

Influence of ketamine and its interactions with morphine and nalbuphine on the level of enkephalins in some parts of the brain and spinal cord.

The aim of this paper was to study the influence of ketamine in a dose of 80 or 160 mg/kg ip on the level of leu-enkephalin (LENK) or met-enkephalin (MENK) in some parts of the brain and spinal cord, as well as to examine the interaction of ketamine with morphine or nalbuphine on this effect. The influence of ketamine on enkephalins release into the brain perfusate was also studied. Ketamine decreased the spinal cord enkephalins concentration mainly in cervical and lumbar part. These effect was antagonized by naloxone. Ketamine administered in a higher dose increased LENK release, and decreased the release of MENK into the brain perfusate. Morphine (20 mg/kg ip) increased the level of LENK in the hypothalamus, decreased the concentrations of MENK in the medulla oblongata and in the cervical part of the spinal cord, and increased the level of this neuropeptide in the thoracic part of the spinal cord. These effects were antagonized by ketamine. Ketamine and morphine administered simultaneously affected the level of enkephalins in some of the studied parts of the brain and spinal cord. Nalbuphine administered in doses ranging from 1 to 20 mg/kg changed the level of enkephalins in some parts of the central nervous system. Ketamine and nalbuphine administered simultaneously changed the level of enkephalins in the spinal cord and in the hypothalamus. It is concluded that: the decrease of the level of enkephalins in the spinal cord is an evident feature of ketamine action mediated probably by opioid receptors. Ketamine affects the release of LENK and MENK from the brain in a different way.(ABSTRACT TRUNCATED AT 250 WORDS)

Chronic treatment with atypical neuroleptics sulpiride and metoclopramide increases striatal enkephalins in rat brain.

The aim of this paper was to study the effect of a single dose of 14, 30 or 90 days' administration of sulpiride (SUL) (50 or 100 mg/kg), metoclopramide (MET) (20 or 40 mg/kg) or haloperidol (HAL) (2 mg/kg) on the level of leu- and met-enkephalin (ENK) in the striatum. A dose and time dependent increase of the striatal ENK level was observed after chronic administration of atypical neuroleptics SUL or MET as well as after chronic treatment with a classical cataleptogenic neuroleptic HAL. The effect of chronic administration of HAL on the striatal level of leu-enkephalin was stronger than after SUL but lower than after MET treatment. It is concluded that: 1) Chronic administration of atypical neuroleptics results in the increased level of striatal ENK similar to that after chronic treatment with classical cataleptogenic neuroleptics; 2) Apparently both more or less selective antagonists of dopaminergic D2 receptors activate the enkephalinergic system in the striatum.

Chronic treatment with chlorpromazine, thioridazine or haloperidol increases striatal enkephalins and their release from rat brain.

The aim of this paper is to study the effect of 1, 2 or 3 months' administration of chlorpromazine (CPZ), thioridazine (TDZ) (2 or 6 mg/kg) or haloperidol (HAL) (0.25 or 1 mg/kg) IP on the level of leu- and met-enkephalin (ENK) in striatum. A dose- and time-dependent increase of striatal ENK level was observed after chronic administration of the neuroleptics (NL), but 8 days after withdrawal of chronically administered NL striatal ENK was decreased. Apomorphine pretreatment significantly attenuated the elevation in ENK produced by chronic injections of NL. In perfusion fluid obtained from the lateral ventricle of animals treated 1 month with HAL a dose-dependent increase of ENK levels was observed, which was augmented by potassium ions. It is concluded that: 1) Chronic administration of neuroleptic drugs that block dopamine receptors increases the level and the release of striatal enkephalins; 2) The results support the hypothesis that activation of dopaminergic neurons tonically inhibits the synthesis of enkephalins in the striatum.

Effect of fluphenazine on the footshock-induced opioid analgesia and leu-enkephalin concentration in the rat brain.

The effect of post-shock injection of 5 mg/kg fluphenazine on stress-induced analgesia (tail immersion test) and leu-enkephalin content in discrete brain areas (radioimmunoassay) was studied in male Wistar rats. The stress-induced analgesia, which was naloxone-reversible, was attenuated and shortened by fluphenazine, the drug also antagonized the stress-induced fall in hypothalamic leu-enkephalin content. Fluphenazine alone depressed the leu-enkephalin content in the medulla oblongata, and this effect was less marked in rats subjected to footshock.