Biomedical subjects
Publications and source records attributed to R Brus.
It was shown that central chemical sympathectomy by 6-hydroxydopamine and central chemical serotoninectomy by 5,6-dihydroxytryptamine diminish the level of gamma-aminobutyric acid in discrete areas of rat brain.
The effects of paracetamol and indomethacin on the action of centrally administered noradrenaline (NA) on the blood pressure, heart rate and rectal body temperature were studied in rats. It was demonstrated that both these substances increased NA effect on the arterial blood pressure and heart rate but caused no changes in NA effect on body temperature. These results suggest a modulating action of prostaglandins in the central nervous system on the functions of the centres regulating cardiovascular functions.
In male Wistar rats PGD2 was injected introcerebroventricularly in a dose of 1, 10 or 50 microgram. PGD2 did not produce change in rat behavior and did not change the body temperature, blood pressure and respiration. PGD2 potentiated slightly the catalepsy elicited by chloropromazine or haloperidol, and in high dose had weak cataleptogenic effect. PGD2 changed the level of GABA i some brain areas. In general, however, the central effects of PGD2 are almost negligible.
Thyrotropin releasing hormone (pGlu-His-Pro-NH2-TRH) is a hypothalamic peptide that exerts pharmacological actions on the mammalian central nervous and circulatory systems independent of hormonal activity. In rats TRH produces an increase in blood pressure, heart rate and respiratory rate, following its intracerebroventricular (icv) administration. Because of a suspected role of the central dopamine (DA) system in these effects, we examined the influence of assorted DA receptor agonists and antagonists on the central cardiovascular and respiratory effects of TRH. Adult male Wistar rats were anesthetized with urethane (1.5 g/kg ip), implanted with an intracranial cannula for icv injections, and continuously monitored for (a) mean arterial blood pressure via an indwelling catheter in the right carotid artery, (b) heart rate via an ECG lead II signal and (c) respiratory rate via a photoelectric transducer. TRH (100 nmol) produced a sustained increase in blood pressure (ca. 20 mm Hg), heart rate (ca. 60 beats per min-bpm) and respiratory rate (< or = 200 breaths per min) during a 30 min observation period. The DA D1 receptor agonist SKF 38393 HCl (0.3 or 3.0 mg/kg ip) attenuated the effects of TRH on blood pressure and heart rate by > 50%, while the DA D2 receptor agonist quinpirole HCl (1.0 mg/kg ip) potentiated the chronotropic response to TRH by > 50%. The predominant DA D2 receptor antagonist haloperidol lactate (1.0 mg/kg ip) potentiated the effects of TRH on blood pressure and heart rate by > 50%, with the latter effect on heart rate being mimicked by the D2 receptor antagonist spiperone HCl (1.0 mg/kg ip). Chlorpromazine HCl (5.0 mg/kg ip), a low potency non-selective D2 receptor antagonist, had effects opposite to that of haloperidol. The effect of TRH on respiration was potentiated by quinpirole but not modified by other DA receptor agonists or antagonists. These findings indicate that the DA system is involved in a complex manner in the central cardiovascular actions of TRH, while DA D2 receptors alone appear to be involved in modulating respiratory effects of TRH.
5-hydroxydopamine, unspecific centrally acting false neurotransmitter. Acta Physiol. Pol., 1977, 28 (1): 13-22. 3,4,5-trihydroxyphenetylamine-5-hydroxydopamine (5-OHDA) injected intracerebro-ventricularly decreases the level of noradrenaline, 5-hydroxytryptamine and 5-hydroxyindoleacetic acid in different parts of the rat brain. It does not affect acetylcholine level. 5-OHDA causes dose-dependent hypothermia, transient hypertension and depression of locomotor and exploratory activity in rats. This behavioral phenomena are reversed by central chemical sympathectomy elicited by 6-hydroxydopamine. It is concluded that 5-OHDA is an unspecific centrally acting false transmitter.
Ethanol abuse in pregnancy is known to produce serious damage to the developing central nervous system of mammalian species. As with several other classes of nerves, the ontogenetic influence of ethanol on dopamine (DA) nerves is long-lived. To test whether reactivity of DA receptors might be altered by prenatal ethanol administration, rats were given 10% (v/v) ethanol in their drinking water, starting 10 days before mating and continuing to the end of pregnancy. Male offspring were tested at 3 months for behavioral effects known to be induced by DA agonists acting at specific subtypes of DA receptors. The oral activity dose-effect curve for SKF 38393, a DA D1 agonist, was not altered from control. However, quinpirole-induced yawning behavior, reputedly a DA D3-associated event, was markedly impaired in the male rats that had been exposed in utero to ethanol. These findings indicate that prenatal ethanol exposure may predominately produce diminished reactivity of the DA D3, but not DA D1 subtype of DA receptor.
The insect myotropic octapeptide leucopyrokinin Glp-Thr-Ser-Phe-Thr-Pro-Arg-Leu-amide (LPK or Lem-PK) (1) and its truncated analogues without the first N-terminal amino acids [2-8]-LPK (2) as well as devoid of the first, second and third N-terminal amino acids [4-8]-LPK (3) were prepared together with a series of the following modified [2-8]-LPK heptapetides such as: [Ala2] (4)-, [Ala3] (6)-, [D-Phe4] (7)-, [Ala5] (8)-, [D-Ala5] (9)-, [D-Thr5] (10)-, [Ser5] (11)-, [D-Pro6] (12)-, [Ala6] (13)- and [D-Arg7]-[2-8]-LPK (14) and [Pro1]-LPK (5). Bioassays were carried out by means of a hot-plate and a tail immersion tests in rats after i.c.v. and i.p. injections. Peptides 1 and 2 revealed prolonged high antinociceptive effects, while other peptides were practically inactive. [2-8]-LPK (2) probably crosses the blood-brain barrier in rats.