Medical terminology in new age Serbia: Over 150 years of existence

Abstract. The marking of the anniversary in 2022 was of great importance for medical terminology in Serbia. After the first, short-lived institutionalization in the Društvo srpske slovesnosti in 1842 this topic became part of the work assignments and activities of an institution, for the second time. This time it was for the Serbian Medical Society (SMS) right after its foundation in 1872. Every randomness in this area was disabled by very clear and precise attitudes established by the first Constitution of SMS. In this area of our medical science, besides founders and first members of SMS, the special place belongs to physicians Jovan Stejic, Milan Jovanovic-Batut, Radivoje Pavlovic, Aleksandar Kostic, Aleksandar Belic, and others. Nowadays, medical terminology is no longer a part of the Constitution of the SMS. It is not yet clear how this happened, nor who, if any, other institution, has taken this huge obligation and responsibility for the development, improvement, and maintenance of medical terminology in the Serbian language. Its creation needs the cooperation of professionals from different walks of education, first of all, physicians and experts in the Serbian language, because it is a matter of foundation, almost identity values. It is necessary to make proper terms and interpret them precisely. The absence of this inevitably leads, not only to a standstill, but collapsing of the already achieved that would instead of enriching only impoverish the Serbian language

Counterfeit drugs and other products and substances: Review of drugs for influenza prevention and treatment including pandemic influenza A(H1N1) 2009

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Counterfeit drugs and other products and substances: Review of drugs for influenza prevention and treatment including pandemic influenza A(H1N1) 2009

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Total anesthesia, rats brain surgery, nitric oxide (NO) and free radicals

It is expected that clinical recovery after surgically induced brain trauma is followed by molecular and biochemical restitution. Seven days after surgery, we investigated whether the plastic cannula implanted in the left brain ventricle of adult Wistar rats (n = 6-7), performed in pentobarbital anesthesia, could influence oxidative stress elements (superoxide anion and lipid peroxidation), as well as the antioxidative system (superoxide dismuthase-SOD). Also, we investigated whether nitric oxide (NO) is involved in these processes. Biochemical analyses was performed in the forebrain cortex, striatum and hippocampus. Clinical recovery was complete seven days after surgery. Thereafter, thirty minutes before decapitation, through the cannula, one group of rats received saline intracerebroventricularly (control group), and the treated group received Nω-nitro-L-arginine methyl ester (L-NAME). The third group was left unoperated and untreated. Before and after the treatments, rectal body temperature was measured. Compared to the untreated group the index of lipid peroxidation was increased in all three brain structures in the group that received saline (p<0.05 to 0.01). Application of L-NAME deteriorated it in the striatum and hippocampus (p<0.01 compared to the both other groups), but the value in the forebrain cortex was similar to the untreated group. Supeoxide anion level was decreased in the L-NAME treated group only in the striatum (p<0.01 compared to control and untreated groups), but SOD was increased in the hippocampus compared to the saline treated group (p<0.05). Seven days after brain surgery in pentobarbital anesthesia, recovery of biochemical disturbances was not parallel to clinical recovery. Long lasting biochemical changes are rather the consequence of brain injury than to pentobarbital anesthesia. In this experimental model, NO had protective effects, acting against lipid per oxidation in the striatum and hippocampus, but not in the forebrain cortex i. e. NO involvement in the free radical processes strongly depends on the observed brain region.Posle hirurške intervencije na mozgu, očekuje se paralelizam između kliničkog, sa jedne strane, i molekulskog i biohemijskog oporavka, sa druge strane. Da bi to utvrdili, u tri moždane strukture (kora prednjeg mozga strijatum, hipokampus) odraslih Vistar pacova muškog pola, ispitivali smo promene pojedinih prooksidativnih i antioksdativnih parametara, nastalih posle usađivanja plastične kanile u bočnu komoru mozga, kroz koju su ubrizgavane ispitivane supstance (10pi). Kao opšti anestetik korišćen je pentobarbiton natrijum (0,045 g/kg). Eksperiment je nastavljen sedam dana posle operacije, kada su pacovi bili klinički potpuno oporavljeni. Pre ubrizgavanja 0,9% NaCI jednoj grupi (kontrola) i Nω-nitro-L-arginin metil estra (L-NAME, 10 mikrograma, rastvoren u 0,9% NaCI) drugoj grupi, kao i 30 minuta posle toga, merena je rektalna temperatura kod sve tri grupe pacova (treću su činili intaktni pacovi, 6-7 pacova u svakoj grupi). Porast indeksa lipidne peroksidacije u sve tri moždane strukture operisanih pacova koji su dobili NaCI bio je statistički značajan u odnosu na intaktnu grupu. Ubrizgavanjem L-NAME, ove promene su u strijatumu i hipokampusu postale statistički još izraženije u odnosu na grupu koja je dobila NaCI, dok je u kori prednjeg mozga registrovan sasvim slab porast u odnosu na intaktnu grupu. Istovremeno, ometanje sinteze NO bilo je praćeno statistički značajnim padom superoksidnog radikala u strijatumu u odnosu na obe grupe, i porastom superoksid dizmutaze u hipokampusu u odnosu na grupu koja je dobila NaCI. Telesna temperature je bila normalna kod svih pacova u oba vremena merenja. Dokazano je da ne postoji paralelizam između kliničkog i biohemijskog oporavka posle operacije na mozgu pacova, izvedene u opštoj anesteziji uz primenu pentobarbitona. To je ispoljeno pojačanom lipidnom peroksidacijom sedam dana posle operacije u sve tri ispitivane strukture mozga koji su dobili NaCI. Porast lipidne peroksidacije je najverovatnije posledica mehaničkog oštećenja izazvanog operacijom, pre nego same anestezije. U ovim procesima, NO ima značajnu regulatornu ulogu, pri čemu njegovi efekti nisu podjednako ispoljeni u svim delovima mozga. Njegova snažna antioksidativna svojstva registruju se u hipokampusu i strijatumu ali ne i u kori prednjeg mozga, što govori u prilog selektivne osetljivosti mozga.nul

Effects of various nitric oxide synthase inhibitors on AlCl3-induced neuronal injury in rats

The present study was aimed at determining the effectiveness of nitric oxide synthase (NOS) inhibitors: N-nitro-L-arginine methyl ester, 7-nitroindazole and aminoguanidine in modulating the toxicity of AlCl3 on superoxide production and the malondialdehyde concentration of Wistar rats. The animals were sacrificed 10 min and 3 days after the treatment and the forebrain cortex was removed. The results show that AlCl3 exposure promotes oxidative stress in different neural areas. The biochemical changes observed in the neuronal tissues show that aluminum acts as pro-oxidant, while NOS inhibitors exert an anti-oxidant action in AlCl3-treated animals.U eksperimentu je određivana efikasnost inhibitora azot-oksid-sintaze (NOS): metil-estra N-nitro-L-arginina, 7-nitroindazola i aminogvanidina u modulaciji toksičnosti AlCl3 na stvaranje superoksidnog anjona i koncentraciju malondialdehida kod Wistar pacova. Životinje su žrtvovane 10 min i 3 dana nakon tretmana i izolovana je kora velikog mozga. Rezultati pokazuju da izlaganje AlCl3 pokreće oksidativni stres u različitim moždanim regionima. Biohemijske promene opisane u neuronskom tkivu pokazuju da aluminijum deluje kao pro-oksidant, dok inhibitori NOS imaju antioksidativno dejstvo kod životinja tretiranih AlCl3.nul

Nitric oxide (NO) and an NMDA receptor antagonist in pentylenetetrazole-induced convulsions

Controversy about proconvulsant and anticonvulsant nitric oxide (NO) effects and the place of oxidative stress in convulsions, are still a matter of research. We investigated the interaction between 2-amino-5-phosphonovaleric acid (APV), a competitive N-methyl-D-aspartate (NMDA) receptor antagonist and Nw-nitro-L-arginine methyl ester (L-NAME), a nonselective nitric oxide synthase (NOS) antagonist, in pentylenetetrazole (PTZ)-induced convulsions. Pentylenetetrazole was applied to adult Wistar rats intraperitoneally (ip) in a single dose of 80 mg/kg, and L-NAME (10 µg/10 µl) or APV (20 µg/10 µl) intracerebroventricularly (icv), 30 and 10 minutes before PTZ, respectively. In the same manner, another group received both antagonists. Control animals were given 0.9% saline. Nw-nitro-L-arginine methyl ester exerted a weak anticonvulsant effect, preventing generalized clonic (GCC) and clonic-tonic convulsions (CTC) in 17% of cases. With APV protection against GCC and CTC was 100%, forelimb dystonia (FLD) was decreased in 33% of cases, and time to onset of all convulsive patterns was prolonged (p<0.05 to 0.01). All effects of APV, except in CTC, were reversed by L-NAME applied prior to APV. In APV-PTZ treated animals, superoxide anion content was increased in the forebrain cortex, striatum and hippocampus, without an overwhelmed antioxidative superoxide dismutase (SOD) defense system in the other treatments. When the APV-PTZ group was treated with L-NAME, both SOD activity and superoxide anion content were additionally decreased indicating that the NOS-NO system was involved in the metabolism of superoxide anions. It is suggested that clinical and biochemical effects of NO strongly depend upon the pretreatment and might lead to a wrong impression of NO contradictory activity.Kontroverzni nalazi o prokonvulzivnim kao i antikonvulzivnim efektima azot oksida (NO) i značaju oksidativnog stresa u konvulzijama, i dalje su predmet istraživanja. U konvulzijama izazvanim primenom pentilentetrazola (PTZ) ispitivali smo interakciju između 2-amino-5-fosfovalerinske kiseline (APV) kompetitivnog antagoniste N-metil-D-aspartat (NMDA) receptora i Nw-nitro-L-arginin metil estra (L-NAME), neselektivnog antagoniste azot oksid sintaze (NOS). Odraslim pacovima Wistar soja, PTZ je ubrizgavan intraperitonealno (ip) u jednoj dozi od 80 mg/kg. Ostale supstance, L-NAME (10 µg/10 µl) i APV (20 µg/10 µl), primenjivale su se intracerebroventrikularno (icv), i to L-NAME 30, a APV 10 minuta pre PTZ. Po istom vremenskom principu, jedna grupa dobila je oba antagonista, a kontrolna fiziološki rastvor NaCl. Nw-nitro-L-arginin metil estar ispoljio je slabo antikonvulzivno dejstvo, smanjujući incidenciju generalizovanih kloničnih (GCC) i klonično-toničnih konvulzija (CTC) za 17%. Za razliku od L-NAME, APV je sprečila nastanak GCC i CTC kod svih životinja (100%), a incidencija klonusa prednjih nogu (FLD) smanjena je za 33%. Istovremeno primenom APV produženo je vreme od aplikacije PTZ do pojave svih konvulzivnih tipova (p<.05 do 0.01). Primenom L-NAME pre APV, umanjeni su efekti APV, pri čemu je došlo do povećanja incidencije FLD i GCC za 16% odnosno 50%. U kori prednjeg mozga, strijatumu i hipokampusu, životinja koje su dobile APV+PTZ, došlo do povećanja koncentracije superoksidnog anjona. Aktivnost superoksid dizmutaze ne prati ovaj skok. Njen dodatni pad u grupi tretiranoj sa L-NAME pre APV+PTZ, ukazuje da je sistem NOS-NO uključen u metabolizam superoksidnog anjona. Dobijeni rezultati ukazuju da klinički i biohemijski efekti NO u velikoj meri zavise od prethodno primenjenih supstanci i promena izazvanih njima, što može da doprinose sticanju pogrešnog utiska o kontradiktornim dejstvima NO.nul

Influence of NG-nitro-L-arginine methyl ester on clinical and biochemical effects of methylene blue in pentylenetetrazole-evoked convulsions

Background/Aim. Despite years of research in a number of experimental models the question whether nitric oxide (NO) and methylene blue (MB) have pro- or anticonvulsant effects remains to be fully resolved. Methods. In adult Wistar rats the influence of a nonselective inhibitor of nitric oxide synthase NG-nitro-L-arginine methyl ester (LNAME, 10µg) on clinical and biochemical effects of MB (10µg) given before the intraperitoneally administered chemical convulsant pentylenetetrazole (PTZ, 80 mg/kg) was examined. MB and L-NAME were applied intracerebroventricularly. PTZ application was followed by a 4- minute observation time, after which rats were sacrificed and elements of oxido-reductive balance were measured in a crude mitochondrial fraction of forebrain cortex, hippocampus and striatum. Results. Convulsive responses (forelimb dystonia - FLD, generalised clonic- and clonic-tonic convulsions - GCC and GCTC respectively) were observed in all rats received PTZ, together with significantly decreased lipid peroxidation in the forebrain cortex and striatum and increased superoxide dismutase activity in the hippocampus, in comparison to controls (saline treated). It was registered anticonvulsant effects of L-NAME pretreatment. However, these effects were insignificant. In the hippocampus of these animals there was decreased lipid peroxidation (p < 0.01, p < 0.05 vs saline-treated and PTZ-treated rats, respectively) and reverted PTZ-induced increase of superoxide dismutase activity. But MB individually pretreatment significantly decreased the incidence of CTCs and GCCs (FLD: p = 0.0513), prolonged the convulsive latent time for FLD, GCTCs and GCCs, in all the examined brain regions increased lipid peroxidation and decreased the level of superoxide anion. Administration of L-NAME 10 minutes before MB reverted all MB-evoked clinical and biochemical effects. Conclusion. Methylene blue applied individually before PTZ has strong anticonvulsant effects that were eliminated by L-NAME pretreatment. These effects and changed biochemical parameters in the brains of animals treated by L-NAME before MB in comparison to MBtreated group suggest involvement of NO in MB's effects in the animal model of PTZ-evoked convulsions.Uvod/Cilj. I pored višegodišnjeg istraživanja na različitim eksperimentalnim modelima, nije potpuno odgovoreno na pitanje da li azot-oksid (NO) i metilen plavo (MP) deluju konvulzivno ili antikonvulzivno. Metode. Na odraslim pacovima Vistar soja ispitivan je uticaj NG-nitro-L-arginin metil estra (L-NAME, 10 µg), neselektivnog inhibitora azot oksid sintaze, na kliničke i biohemijske efekte metilen plavog (MP, 10 µg) datog intracerebroventrikularno pre hemijskog konvulziva pentilentetrazola (PTZ, 80 mg/kg), primenjenog intraperitonealno. Pacovi su posmatrani četiri minuta posle davanja PTZ-a, posle čega su žrtvovani i u neprečišćenoj mitohondrijskoj frakciji prednjeg mozga, hipokampusa i strijatuma određivani su parametri oksidoreduktivne ravnoteže. Rezultati. Posle primene PTZ-a, konvulzivni odgovor (distonija prednjih nogu - DPN, generalizovane klonične - GKK i generalizovane kloničnotonične konvulzije - GKTK) bio je ispoljen kod svih životinja, kao i statistički značajno sniženje lipidne peroksidacije u kori prednjeg mozga i strijatuma, i povećanje aktivnosti superoksid dizmutaze (SOD) u hipokampusu, u poređenju sa kontrolnom grupom (dobila fiziološki rastvor NaCl). Registrovani su antikonvulzivni efekti L-NAME koji nisu bili statistički značajni. U hipokampusu ovih životinja bila je snižena lipidna peroksidacija (p < 0,01 u poređenju sa kontrolnom grupom, p < 0,05 u poređenju sa životinjama koje su dobile PTZ), kao i aktivnost SOD u poređenju sa životinjama koje su dobile PTZ. Samo metilen plavo dovelo je do statistički značajnog smanjenja incidencije GKK I GKTK (DPN: p = 0,0513), produžilo je latentni period DPN, GKK i GKTK, a u svim ispitivanim strukturama mozga bila je povećana lipidna peroksidacija i smanjen nivo superoksidnog anjona. Svi klinički i biohemijski efekti izazvani primenom MP u potpunosti su odstranjeni primenom L-NAME 10 minuta pre davanja MP. Zaključak. Metilen plavo, dat samostalno pre PTZ, ispoljio je snažne antikonvulzivne efekte. Nestanak ovih efekata i izmenjeni biohemijski parametri u mozgovima pacova koji su pre MP dobili L-NAME, sugerišu da je NO uključen u efekte MP ispoljene na životinjskom modelu konvulzija izazvanih primenom PTZ-a.nul

Antioxidative effect of nerve growth factor (NGF) in rat thalamus after quinolinic acid-induced neurotoxicity

Quinolinic acid (QA) produces a pattern of selective cell loss in the striatum, that closely mimics that of Huntington's disease (HD). The aim of this study was to investigate the antioxidative status in the thalamus after intrastriatal application of QA and the influence of nerve growth factor (NGF) on such neurotoxicity. Wistar rats were treated intrastriatally (coordinates: 8.4A, 2.6L, 4.8V), using a stereotaxic instrument. The first group was treated with QA (150 nmol/l). The second group was treated with QA, followed by NGF (4.5 mg/kg b.w). The control group was treated with 0.9 % saline solution. Seven days after the treatment, we found decreased superoxide dismutase (SOD) activity in mitochondrial fractions of the striatum of both groups. In the thalamus, SOD activity showed no differences. The content of superoxide anion increased in the striatum of QA- treated animals. It was decreased in both structures in the group that was treated with QA and NGF. In the QA+ NGF-treated group, we found increased glutathione peroxidase (GSHPx) and GSH, compared to the group that was treated with QA only, but these values were lower than in the controls. Thus, NGF showed beneficial effects on the oxido-reduction status in the striatum, and also in the thalamus, a structure that is separated from but tightly connected with the striatum.Hinolinska kiselina (HK) prouzrokuje takav selektivni gubitak ćelija u strijatumu, koji veoma dobro imitira onaj kod Huntingtonove bolesti. Cilj ovog istraživanja bio je da se ispita antioksidativni status u talamusu nakon aplikacije HK u strijatum i uticaj NGF na takvu neurotoksičnost. Wistar pacovi su tretirani intrastrijatno, pomoću stereotaksičnog instrumenta (koordinate: 8,4A, 2,6L, 4,8V). Prva grupa je bila tretirana HK (150 nmol/l). Druga grupa je bila tretirana HK, a nakon toga je dobila NGF (4.5 mg/ kg b.w). Kontrolna grupa je bila tretirana fiziološkim rastvorom. Sedam dana nakon tretmana, u mitohondrijskim frakcijama strijatuma, našli smo smanjenu aktivnost SOD u obema grupama. U talamusu, aktivnost SOD se nije promenila. Sadržaj superoksidnog anjona se povećao u strijatumu životinja koje su bile tretirane HK, a smanjio se u obema strukturama, u grupi koja je bila tretirana sa HK i NGF. U HK+ NGF-tretiranoj grupi, našli smo povećanu aktivnost GSHPx i GSH u odnosu na grupu koja je bila tretirana samo sa HK, ali su te vrednosti bile manje u odnosu na kontrolne. NGF je pokazao povoljne efekte na oksido-reduktivni status u strijatumu, ali takođe i u talamusu, strukturi koja je odvojena, ali veoma blisko povezana sa strijatumom.nul

Effect of L-NAME on AlCl3-induced toxicity in rat brain

The present experiment was carried out to determine the effectiveness of nitric oxide synthase (NOS) inhibitor (L-NAME) in elevating the toxicity of AlCl3 on nitrite concentration and acetylcholine esterase activity of Wistar rats. Animals were killed 10 min and 3 days after the treatment and the forebrain cortex and striatum were removed. The results show that AlCl3 exposure promotes oxidative stress in different neural areas. The biochemical changes observed in neuronal tissues show that aluminium acts as a pro-oxidant, while NOS inhibitor exerts as antioxidant action in AlCl3-treated animals. In the present study, active avoidance learning was significantly impaired after AlCl3 injection, while pretreatment with L-NAME prevented the behavioural deficits caused between the 8th and 12th day after intrahippocampal application of neurotoxin. Our data suggest that aluminium may cause learning and memory deficits, while the treatment with L-NAME may decrease the oxidative stress and prevent learning and memory deficits caused by AlCl3.U eksperimentu je ispitivana efikasnost inhibitora azot oksid sintaze (NOS)- L-NAME na toksičnost AlCl3 i određivana koncentracija nitrita i aktivnost acetilholin esteraze kod Wistar pacova. Životinje su dekapitovane 10 minuta ili 3 dana nakon tretmana i izolovani su kora prednjeg mozga i strijatum. Rezultati ukazuju da AlCl3 pokreće oksidativni stres u različitim regionima mozga. Biohemijske promene opisane u neuronskom tkivu ukazuju da aluminijum deluje kao prooksidans, dok inhibitor NOS ima antioksidativno dejstvo kod životinja tretiranih AlCl3. Reakcija aktivnog izbegavanja je bila znatno poremećena nakon aplikacije AlCl3, dok se davanjem L-NAME sprečavaju poremećaji ponašanja uzrokovani između 8. i 12. dana posle intrahipokampusne primene neurotoksina. Naši rezultati ukazuju da aluminijum može dovesti do smetnji u procesima učenja i pamćenja, dok tretman sa L-NAME smanjuje oksidativni stres i sprečava promene u učenju i pamćenju uzrokovane AlCl3.nul

Total anesthesia, rats brain surgery, nitric oxide (NO) and free radicals

It is expected that clinical recovery after surgically induced brain trauma is followed by molecular and biochemical restitution. Seven days after surgery, we investigated whether the plastic cannula implanted in the left brain ventricle of adult Wistar rats (n = 6-7), performed in pentobarbital anesthesia, could influence oxidative stress elements (superoxide anion and lipid peroxidation), as well as the antioxidative system (superoxide dismuthase-SOD). Also, we investigated whether nitric oxide (NO) is involved in these processes. Biochemical analyses was performed in the forebrain cortex, striatum and hippocampus. Clinical recovery was complete seven days after surgery. Thereafter, thirty minutes before decapitation, through the cannula, one group of rats received saline intracerebroventricularly (control group), and the treated group received Nω-nitro-L-arginine methyl ester (L-NAME). The third group was left unoperated and untreated. Before and after the treatments, rectal body temperature was measured. Compared to the untreated group the index of lipid peroxidation was increased in all three brain structures in the group that received saline (p<0.05 to 0.01). Application of L-NAME deteriorated it in the striatum and hippocampus (p<0.01 compared to the both other groups), but the value in the forebrain cortex was similar to the untreated group. Supeoxide anion level was decreased in the L-NAME treated group only in the striatum (p<0.01 compared to control and untreated groups), but SOD was increased in the hippocampus compared to the saline treated group (p<0.05). Seven days after brain surgery in pentobarbital anesthesia, recovery of biochemical disturbances was not parallel to clinical recovery. Long lasting biochemical changes are rather the consequence of brain injury than to pentobarbital anesthesia. In this experimental model, NO had protective effects, acting against lipid per oxidation in the striatum and hippocampus, but not in the forebrain cortex i. e. NO involvement in the free radical processes strongly depends on the observed brain region.Posle hirurške intervencije na mozgu, očekuje se paralelizam između kliničkog, sa jedne strane, i molekulskog i biohemijskog oporavka, sa druge strane. Da bi to utvrdili, u tri moždane strukture (kora prednjeg mozga strijatum, hipokampus) odraslih Vistar pacova muškog pola, ispitivali smo promene pojedinih prooksidativnih i antioksdativnih parametara, nastalih posle usađivanja plastične kanile u bočnu komoru mozga, kroz koju su ubrizgavane ispitivane supstance (10pi). Kao opšti anestetik korišćen je pentobarbiton natrijum (0,045 g/kg). Eksperiment je nastavljen sedam dana posle operacije, kada su pacovi bili klinički potpuno oporavljeni. Pre ubrizgavanja 0,9% NaCI jednoj grupi (kontrola) i Nω-nitro-L-arginin metil estra (L-NAME, 10 mikrograma, rastvoren u 0,9% NaCI) drugoj grupi, kao i 30 minuta posle toga, merena je rektalna temperatura kod sve tri grupe pacova (treću su činili intaktni pacovi, 6-7 pacova u svakoj grupi). Porast indeksa lipidne peroksidacije u sve tri moždane strukture operisanih pacova koji su dobili NaCI bio je statistički značajan u odnosu na intaktnu grupu. Ubrizgavanjem L-NAME, ove promene su u strijatumu i hipokampusu postale statistički još izraženije u odnosu na grupu koja je dobila NaCI, dok je u kori prednjeg mozga registrovan sasvim slab porast u odnosu na intaktnu grupu. Istovremeno, ometanje sinteze NO bilo je praćeno statistički značajnim padom superoksidnog radikala u strijatumu u odnosu na obe grupe, i porastom superoksid dizmutaze u hipokampusu u odnosu na grupu koja je dobila NaCI. Telesna temperature je bila normalna kod svih pacova u oba vremena merenja. Dokazano je da ne postoji paralelizam između kliničkog i biohemijskog oporavka posle operacije na mozgu pacova, izvedene u opštoj anesteziji uz primenu pentobarbitona. To je ispoljeno pojačanom lipidnom peroksidacijom sedam dana posle operacije u sve tri ispitivane strukture mozga koji su dobili NaCI. Porast lipidne peroksidacije je najverovatnije posledica mehaničkog oštećenja izazvanog operacijom, pre nego same anestezije. U ovim procesima, NO ima značajnu regulatornu ulogu, pri čemu njegovi efekti nisu podjednako ispoljeni u svim delovima mozga. Njegova snažna antioksidativna svojstva registruju se u hipokampusu i strijatumu ali ne i u kori prednjeg mozga, što govori u prilog selektivne osetljivosti mozga.nul