Cardiovascular effects of Atenolol, Scopolamine and their combination on healthy men in Finnish sauna baths

Indicators of cardiovascular strain were studied in 12 healthy young men under the influence of drugs affecting the autonomic nervous system during the course of taking a sauna bath. There were four bath sessions: one without a drug (control) and three with drug pretreatment (Atenolol 50 mg or Scopolamine 0.3 mg or their combination taken orally 2 h before the bath). The time spent in the hot room depended on the subjective rating of heat stress. Its mean duration at a temperature of 88°C (dry bulb) was 22 (range 14–33) min and did not differ significantly among the sessions. In the Atenolol experiment the mean resting heart rate before the bath was significantly lower (P < 0.001, ANOVA of repeated measures) than in the other experiments. The increase in heart rate per minute of heat exposure was significantly lower (P < 0.001) in the Atenolol experiment and higher (P=0.017) in the Scopolamine experiment than in the other experiments. The systolic blood pressure increased more slowly (P=0.004) and the diastolic pressure decreased less (P=0.02) in the Atenolol experiment than in the other experiments. Heart rate and blood pressure returned to their initial levels during the 30-min recovery after the heat exposure. The plasma noradrenaline concentrations increased approximately twofold during all of the bath sessions, whereas the plasma adrenaline and serum thromboxane B2 concentrations showed no consistent alterations. A small oral dose of Scopolamine alone or in combination with Atenolol produced no marked cardiovascular strain in healthy men during a sauna bath.     

The role of cyclic nucleotides and prostaglandins in heart function.

A short review of the role of cyclic nucleotides and prostaglandins (PGs) in normal and pathological functions of the heart is given. Possible interrelationships of these two regulatory systems have been studied by using spontaneously beating rat atria preparations. Addition of noradrenaline (NA) to the incubate (1 . 10(-6) M) caused an increase in amplitude and frequency which was preceded and parallelled by an elevation of the tissue cAMP level. A transient increase in cGMP and PGE values was also seen. Propranolol (5 . 10(-6) M) abolished the increase in amplitude and frequency as well as in cAMP and PGE concentrations. Indomethacin (1 . 10(-5) M) inhibited the formation of PGE. The increase in cGMP was blocked by phenoxybenzamine. Interchange between beta- and alpha-receptors according as the temperature is lowered has been described earlier. Hypothermia (20 degrees C) had a positive inotropic effect on the atria and increased the tissue cAMP concentration. Loading of the atria caused an increase in cAMP without any effects on cGMP or PGs. Slight hypoxia did not change the cAMP or PG levels, but elevated the cGMP values. Arrhythmias induced by hypo- or hyperpotassemia did not modify the biochemical parameters measured. PGF2alpha (1. 10(-5) M) normalized the atrial rhythm and increased the amplitude without changing cyclic nucleotide or PG levels. PGE1 (1 . 10(-4) M) increased the amplitude of normorhythmic atria and the tissue concentration of cAMP. PGE2 was the only PG tested which stimulated the heart adenylate cyclase in vitro. There seems to be close but complicated relationships between cyclic nucleotides and PGs in the heart.     

Immunohistochemical detection of c-fos proteins in cultured human glial cells--induction by cyclic AMP and phorbol ester

The expression of c-fos protein in cultured human glial cells derived from the brain and spinal cord was investigated immunocytochemically. Primary cultures of fetal glial cells were maintained in culture for three weeks and deprived of animal sera for 22 h. The glial cell nature of the cells was ascertained by GFAP-immunoreactivity. Incubations with phorbol dibutyrate, 8-Br-cAMP and sodium nitroprusside representing signal transduction pathways of PKC, PKA and cyclic GMP kinase, respectively, were carried out for 60 and 120 min. The control serum-deprived cultures did not display c-fos protein immunoreactivity (c-fos-IR), whereas phorbol dibutyrate incubation for 120 min induced strong c-fos-IR in the nuclei of both brain and spinal cord derived glial cells. Semiquantitative intensity measurements revealed a slight c-fos-IR induction after 8-Br-cAMP as well, but not after sodium nitroprusside. The observations suggest that c-fos protein is involved in PKC and PKA signal transduction in cultured human glial cells.     

Immunohistochemical detection of c-fos proteins in cultured human glial cells — induction by cyclic AMP and phorbol ester

Summary The expression of c-fos protein in cultured human glial cells derived from the brain and spinal cord was investigated immunocytochemically. Primary cultures of fetal glial cells were maintained in culture for three weeks and deprived of animal sera for 22 h. The glial cell nature of the cells was ascertained by GFAP-immunoreactivity. Incubations with phorbol dibutyrate, 8-Br-cAMP and sodium nitroprusside representing signal transduction pathways of PKC, PKA and cyclic GMP kinase, respectively, were carried out for 60 and 120 min. The control serum-deprived cultures did not display c-fos protein immunoreactivity (c-fos-IR), whereas phobol dibutyrate incubation for 120 min induced strong c-fos-IR in the nuclei of both brain and spinal cord derived glial cells. Semiquantitative intensity measurements revealed a slight c-fos-IR induction after 8-Br-cAMP as well, but not after sodium nitroprusside. The observations suggest that c-fos protein is involved in PKC and PKA signal transduction in cultured human glial cells.