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Rectal temperature changes induced by pulsed electromagnetic field
EPINEPHRINE INTRATHECAL INJECTION IN SAD RATS AND 6HOD TREATED RAT& Ga.__rcia MC, Celuch SM, Taira CA CAtedra de Farmacologia, Fac. de Farmacia y Bioquimica (UBA) and ININFA (CONICET). Junin 956, 5to. piso, (1113) Buenos Aires, ARGENTINA. Previously we have demostrated intrathecal (ith) ir~ection of epinephrine (E) in nomlotensive rats showed a hypotensive effect at dose between 0.03-0.3 ~g while dose at 3-10 ~g induce a pressor response. The aim of this work was to study the hypotensive effect of 0.1 ~g E (ith) in rats with sinoaortic desnervation and in rats with catecholaminergic bulbospinal chemical desnervation. Wistar rats were anesthetized with pentobarbital (40 mg/kg, i.p.). Cannulae were positioned in the femoral artery for blood pressure (BP) measurement and both, in femoral vein and at the spinal level (TI2-L1) for i.v. or ith drug injection. Chemical desnervation were carried out with intracisternal administration of 6-HODA (200 ~tg) seven days before the experiments. In untreated control rats, E (0.03,0.1 and 0.3 ~xg,ith, n=5) showed a dose-dependent decrease in the mean BP (MBP: 7.1_+1.9,-12.K).9 and -15.4_+l.4mmHg, respectively). Hypotensive effect of E (0.1~g, ith) was blocked by the ~-2 antagonist yohimbine (1 rng/kg, i.v.). In 6-HODA treated rats, the hypotensive response to E (0.1 ~t~ ith, n=5) was -15.1_+0.9mmHg and in vehicle treated rats was -9.7+0.7 mmHg (n=5). In sham operated rats, the hypotension to E 0.1 ~ ith) was -13.3:L2mmHg (n=5) and in SAD rats was -19.1+_2mmHg (n=5). These results suggest that both chemical desnervation of catecholaminergic bulbospinal pathways and SAD induce'an increase of hypotensive action of low dose of ith injected E.
INCORPORATION IN AND RELEASE FROM SYMPATHETIC NERVE VARICOSITIES OF ADRENALINE INTRAVENOUSLY
INJECTED F. Brand,o, M.Q. Paiva, A. Albino-Teixeira, P. Serr~loand S. Guimar~es Institute of Pharmacology and Therapeutics, Faculty of Medicine, 4200 Porto, Portugal In incubation experiments it was shown that exogenous adrenaline or noradrenaline does not distribute homogeneously into the adrenergic varicosities and that heterogeneity was more marked in the vas deferens (wall with thick and compact musc!e layer) than in the spleen capsule (with thin and loose muscle layer). One possible explanation for the different distribution of the exogenous amine might be the different thickness and compactness of the muscle layer in the two tissues. To circumvent this mechanical barrier, adrenaline (100 ~g/kg/min, during .90 rain) was intraveneously injected to rats which had received 1 g/kg of pargyline (to inhibit MAO) and 30 mg/kg of tolcapone (to inhibit COMT). At the end of the adrenaline administration, vasa deferentia and spleen capsule were remov6d under pentobarbiml anaesthesia. After a washout period (90 rain) the tissue was exposed to 100 ~xmol/1tyramine for 20 rain. At the end of the exposure to tyramine the noradrenaline/adrenaline ratio was determined in the tissue and in the medium. For the vas deferens, the noradrenaline/adrenaline ratio in the tissue was 26.7~-2.8 and in the medium was 9.1±1.3 (n=7, P<0.01), while for the spleen capsule it was 8.1±1.7 and 6.24-0.9, respectively (n=7, P>0.05). These results confirm that: 1) the incorporated amine is preferentially released by tyramine from the vas deferens but not from the spleen capsule, showing that homogeneity or heterogeneity in amine distribution does not depend on the way of access for the amine. Supported by JNICT (Junta Nacional de Investigag6o Tecnol6gica)
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EFFECTS OF REPEATED NOVEL STRESSORS ON CENTRAL ALPHA-2 ADRENOCEPTOR-MEDIATED MODULATION OF TYROSINE HYDROXYLASE ACTMTY. M.P. Areso, M.T. Giralt. M. Domercq, B. Elorrieta, F.M. G6mez. Dept. Pharmacology. School of Medicine. Univ. of the Basque Country. Leioa, Spain.Chronic stress induces adaptive changes on centralnoradrenergic system. Singe oc2-adrenoceptors regulate tyrosine hydro~lase (TH) activity, the aim of this study was to assess cc2-adren0ceptors sensitivity after a chronic (14 days) novel stressors paradigm. The "in ~Svo" TH activity was evaluated by measuring DOPA accmnulation within 30 rain. after decarboxylase inhibition (NSD 1015, 100 mg/kg, i.p.) and cczadrenoceptors sensitivity was evaluated as clonidine (0.5 mg/kg, i.p., 60 min.) capability to reduce DOPA accumulation. DOPA and NA content were analyzed in hippocampal and h)~othalamic membranes from Sprague-Dawley rats by HPLC-ED. In the hippocampus from chronically stressed rats DOPA basal levels were not different to those found in naive control rats. A clear potentiation in clonidine inhibitory effect (76+5 %~ 13<0.001) was found in hippocampus from chronically stressed rats when compared with clonidine inhibitory effect (45+7 %) in naive control rats. However, in the hypothalamus chronic stress led to a significant loss in clonidine inhibitory effect (24+7 %, p<0.001) when compared with clonidine iultibitory effect in naive control rats (55+3 %). In this brain area DOPA basal levels were significantly reduced (26_+_4%, p<0.05) by chronic stress. In both brain areas NA contents were not modified by the stress paradigm used in this study, The results suggest a different modulation of hippocampal and hypothalamic c,2-adrenoceptors sensitivity induced by chronic stress. While in the hippocampus o¢~.-adrenoceptors supersensitivity may be one mechanism underlying the adaptation to chronic stress, a down-regnlation of hypothalamic cz2-adrenoceptors was found after chronic stress. Supportexl by Basque Government Grant: PI9385.
RECTAL TEMPERATURE CHANGES INDUCED BY PULSED ELECTROMAGNETIC FIELD . . .. M.Matasi6,I.Samar~ija,A.Bobznac-Georglevskl Faculty.of Pharmacy & Bicchem. University of Zagreb, Inst. for physic. & Rehab. Medicine and Rheumat.Hosp."Sveti Duh",Zagreb,Croatia. Pulsed electromagnetic fields (PEMF) are being widely used in therapy of locomotor diseases. Their applications in medicine are rapidly expanding nowadays, but without enough knowledge what exactly happened i n s i d e the body. The goal of this work was to resolve possible mechanisms of PEMF acting. For this purpose rectal temperature of anesthetized rats were measured, during ten-hours exposition to PElF (frequency 9 Hz, strength 3,5 mT) and compared with control group (n= lO). Rats exposed to P E ~ (n=10) showed significantly lower rectal temperature. Maximal difference, reached after the third hour, was 2,2°C (p~0,O1), although the difference became significant already after the first hour (p~0,05) of application of P E ~ . On the basis of these results and literature data about the thermoregulatory pathways (Gilbert et al., J Appl Physiol,43:770-77,1977) and pharmacologicaly induced hypothermia (Quan et al., Am J Physiol,262:i~07-11,1992! Millan et al., J Pharm Exp Ther,264:1364-76,1995) it can be concluded that blocking of sympa. thetic system and consequently appearlng vasodilatation might be reason for significantly higher decrease of rectal temperature at rats exposed to PEMF.
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INCORPORATION IN AND RELEASE FROM SYMPATHETIC NERVE VARICOSITIES OF ADRENALINE INTRAVENOUSLY
INJECTED F. Brand,o, M.Q. Paiva, A. Albino-Teixeira, P. Serr~loand S. Guimar~es Institute of Pharmacology and Therapeutics, Faculty of Medicine, 4200 Porto, Portugal In incubation experiments it was shown that exogenous adrenaline or noradrenaline does not distribute homogeneously into the adrenergic varicosities and that heterogeneity was more marked in the vas deferens (wall with thick and compact musc!e layer) than in the spleen capsule (with thin and loose muscle layer). One possible explanation for the different distribution of the exogenous amine might be the different thickness and compactness of the muscle layer in the two tissues. To circumvent this mechanical barrier, adrenaline (100 ~g/kg/min, during .90 rain) was intraveneously injected to rats which had received 1 g/kg of pargyline (to inhibit MAO) and 30 mg/kg of tolcapone (to inhibit COMT). At the end of the adrenaline administration, vasa deferentia and spleen capsule were remov6d under pentobarbiml anaesthesia. After a washout period (90 rain) the tissue was exposed to 100 ~xmol/1tyramine for 20 rain. At the end of the exposure to tyramine the noradrenaline/adrenaline ratio was determined in the tissue and in the medium. For the vas deferens, the noradrenaline/adrenaline ratio in the tissue was 26.7~-2.8 and in the medium was 9.1±1.3 (n=7, P<0.01), while for the spleen capsule it was 8.1±1.7 and 6.24-0.9, respectively (n=7, P>0.05). These results confirm that: 1) the incorporated amine is preferentially released by tyramine from the vas deferens but not from the spleen capsule, showing that homogeneity or heterogeneity in amine distribution does not depend on the way of access for the amine. Supported by JNICT (Junta Nacional de Investigag6o Tecnol6gica)
Cientifica
e
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EFFECTS OF REPEATED NOVEL STRESSORS ON CENTRAL ALPHA-2 ADRENOCEPTOR-MEDIATED MODULATION OF TYROSINE HYDROXYLASE ACTMTY. M.P. Areso, M.T. Giralt. M. Domercq, B. Elorrieta, F.M. G6mez. Dept. Pharmacology. School of Medicine. Univ. of the Basque Country. Leioa, Spain.Chronic stress induces adaptive changes on centralnoradrenergic system. Singe oc2-adrenoceptors regulate tyrosine hydro~lase (TH) activity, the aim of this study was to assess cc2-adren0ceptors sensitivity after a chronic (14 days) novel stressors paradigm. The "in ~Svo" TH activity was evaluated by measuring DOPA accmnulation within 30 rain. after decarboxylase inhibition (NSD 1015, 100 mg/kg, i.p.) and cczadrenoceptors sensitivity was evaluated as clonidine (0.5 mg/kg, i.p., 60 min.) capability to reduce DOPA accumulation. DOPA and NA content were analyzed in hippocampal and h)~othalamic membranes from Sprague-Dawley rats by HPLC-ED. In the hippocampus from chronically stressed rats DOPA basal levels were not different to those found in naive control rats. A clear potentiation in clonidine inhibitory effect (76+5 %~ 13<0.001) was found in hippocampus from chronically stressed rats when compared with clonidine inhibitory effect (45+7 %) in naive control rats. However, in the hypothalamus chronic stress led to a significant loss in clonidine inhibitory effect (24+7 %, p<0.001) when compared with clonidine iultibitory effect in naive control rats (55+3 %). In this brain area DOPA basal levels were significantly reduced (26_+_4%, p<0.05) by chronic stress. In both brain areas NA contents were not modified by the stress paradigm used in this study, The results suggest a different modulation of hippocampal and hypothalamic c,2-adrenoceptors sensitivity induced by chronic stress. While in the hippocampus o¢~.-adrenoceptors supersensitivity may be one mechanism underlying the adaptation to chronic stress, a down-regnlation of hypothalamic cz2-adrenoceptors was found after chronic stress. Supportexl by Basque Government Grant: PI9385.
RECTAL TEMPERATURE CHANGES INDUCED BY PULSED ELECTROMAGNETIC FIELD . . .. M.Matasi6,I.Samar~ija,A.Bobznac-Georglevskl Faculty.of Pharmacy & Bicchem. University of Zagreb, Inst. for physic. & Rehab. Medicine and Rheumat.Hosp."Sveti Duh",Zagreb,Croatia. Pulsed electromagnetic fields (PEMF) are being widely used in therapy of locomotor diseases. Their applications in medicine are rapidly expanding nowadays, but without enough knowledge what exactly happened i n s i d e the body. The goal of this work was to resolve possible mechanisms of PEMF acting. For this purpose rectal temperature of anesthetized rats were measured, during ten-hours exposition to PElF (frequency 9 Hz, strength 3,5 mT) and compared with control group (n= lO). Rats exposed to P E ~ (n=10) showed significantly lower rectal temperature. Maximal difference, reached after the third hour, was 2,2°C (p~0,O1), although the difference became significant already after the first hour (p~0,05) of application of P E ~ . On the basis of these results and literature data about the thermoregulatory pathways (Gilbert et al., J Appl Physiol,43:770-77,1977) and pharmacologicaly induced hypothermia (Quan et al., Am J Physiol,262:i~07-11,1992! Millan et al., J Pharm Exp Ther,264:1364-76,1995) it can be concluded that blocking of sympa. thetic system and consequently appearlng vasodilatation might be reason for significantly higher decrease of rectal temperature at rats exposed to PEMF.
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