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To determine the hemodynamic mechanisms responsible for the attenuated blood pressure response to mental stress after exercise, 26 healthy sedentary individuals (age 29 ± 8 years) underwent the Stroop color-word test before and 60 min after a bout of maximal dynamic exercise on a treadmill. A subgroup (N = 11) underwent a time-control experiment without exercise. Blood pressure was continuously and noninvasively recorded by infrared finger photoplethysmography. Stroke volume was derived from pressure signals, and cardiac output and peripheral vascular resistance were calculated. Perceived mental stress scores were comparable between mental stress tests both in the exercise (P = 0.96) and control (P = 0.24) experiments. After exercise, the blood pressure response to mental stress was attenuated (pre: 10 ± 13 vs post: 6 ± 7 mmHg; P < 0.01) along with lower values of systolic blood pressure (pre: 129 ± 3 vs post: 125 ± 3 mmHg; P < 0.05), stroke volume (pre: 89.4 ± 3.5 vs post: 76.8 ± 3.8 mL; P < 0.05), and cardiac output (pre: 7.00 ± 0.30 vs post: 6.51 ± 0.36 L/min; P < 0.05). Except for heart rate, the hemodynamic responses and the mean values during the two mental stress tests in the control experiment were similar (P > 0.05). In conclusion, a single bout of maximal dynamic exercise attenuates the blood pressure response to mental stress in healthy subjects, along with lower stroke volume and cardiac output, denoting an acute modulatory action of exercise on the central hemodynamic response to mental stress.

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RESUMO

To determine the hemodynamic mechanisms responsible for the attenuated blood pressure response to mental stress after exercise, 26 healthy sedentary individuals (age 29 ± 8 years) underwent the Stroop color-word test before and 60 min after a bout of maximal dynamic exercise on a treadmill. A subgroup (N = 11) underwent a time-control experiment without exercise. Blood pressure was continuously and noninvasively recorded by infrared finger photoplethysmography. Stroke volume was derived from pressure signals, and cardiac output and peripheral vascular resistance were calculated. Perceived mental stress scores were comparable between mental stress tests both in the exercise (P = 0.96) and control (P = 0.24) experiments. After exercise, the blood pressure response to mental stress was attenuated (pre: 10 ± 13 vs post: 6 ± 7 mmHg; P < 0.01) along with lower values of systolic blood pressure (pre: 129 ± 3 vs post: 125 ± 3 mmHg; P < 0.05), stroke volume (pre: 89.4 ± 3.5 vs post: 76.8 ± 3.8 mL; P < 0.05), and cardiac output (pre: 7.00 ± 0.30 vs post: 6.51 ± 0.36 L/min; P < 0.05). Except for heart rate, the hemodynamic responses and the mean values during the two mental stress tests in the control experiment were similar (P > 0.05). In conclusion, a single bout of maximal dynamic exercise attenuates the blood pressure response to mental stress in healthy subjects, along with lower stroke volume and cardiac output, denoting an acute modulatory action of exercise on the central hemodynamic response to mental stress.

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The aim of the present study was to compare the toxic effects of fluoxetine (F) (8 and 16 mg/kg) and venlafaxine (V) (40 and 80 mg/kg) administered during the third week of pregnancy on early development of rats. Both antidepressants were administered by gavage on pregnancy days 15 to 20 to groups of 10 to 12 animals each. Duration of gestation, food and water consumtion, number of live pups and birth weight were recorded. Litters were culled to six pups at birth (day 1) and followed for growth until weaning (day 25). On day 60, a male and a female from each litter were injected with the 5-HT1 agonist, 5-methoxy-N,N-dimethyltryptamine (6 mg/kg, i.p.) and the serotonergic syndrome was graded. Fluoxetine but not venlafaxine reduced the duration of pregnancy when compared to the control (C) group (F = 21.1 days and C = 21.6 days, mean, P < 0.02: maximum = 22 days and minimum = 21 days in both groups). The highest doses of both fluoxetine, 16 mg/kg (F16), and venlafaxine, 80 mg/kg (V80), reduced the food intake of pregnant rats, resulting in different rates of body weight gain during treatment (from pregnancy day 15 to day 20): F16 = 29.0 g, V80 = 28.7 g vs C = 39.5 g (median). Birth weight was influenced by treatment and sex (P < 0.05; two-way ANOVA). Both doses of fluoxetine or venlafaxine reduced the body weight of litters; however, the body weight of litters from treated dams was equal to the weight of control litters by the time of weaning. At weaning there was no significant difference in weight between sexes. There was no difference among groups in number of live pups at birth, stillbirths, mortality during the lactation period or in the manifestation of serotonergic syndrome in adult rats. The occurrence of low birth weight among pups born to dams which did not show reduced food ingestion or reduction of body weight gain during treatment with lower doses of fluoxetine or venlafaxine suggests that these drugs may have a deleterious effect on prenatal development when administered during pregnancy. In addition, fluoxetine slightly but significantly affected the duration of pregnancy (about half a day), an effect not observed in the venlafaxine treated groups.

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The aim of the present study was to compare the toxic effects of fluoxetine (F) (8 and 16 mg/kg) and venlafaxine (V) (40 and 80 mg/kg) administered during the third week of pregnancy on early development of rats. Both antidepressants were administered by gavage on pregnancy days 15 to 20 to groups of 10 to 12 animals each. Duration of gestation, food and water consumption, number of live pups and birth weight were recorded. Litters were culled to six pups at birth (day 1) and followed for growth until weaning (day 25). On day 60, a male and a female from each litter were injected with the 5-HT1 agonist, 5-methoxy-N,N-dimethyltryptamine (6 mg/kg, ip) and the serotonergic syndrome was graded. Fluoxetine but not venlafaxine reduced the duration of pregnancy when compared to the control (C) group (F = 21.1 days and C = 21.6 days, mean, P<0.02; maximum = 22 days and minimum = 21 days in both groups). The highest doses of both fluoxetine, 16 mg/kg (F16), and venlafaxine, 80 mg/kg (V80), reduced the food intake of pregnant rats, resulting in different rates of body weight gain during treatment (from pregnancy day 15 to day 20): F16 = 29.0 g, V80 = 28.7 g vs C = 39.5 g (median). Birth weight was influenced by treatment and sex (P<0.05; two-way ANOVA). Both doses of fluoxetine or venlafaxine reduced the body weight of litters; however, the body weight of litters from treated dams was equal to the weight of control litters by the time of weaning. At weaning there was no significant difference in weight between sexes. There was no difference among groups in number of live pups at birth, stillbirths, mortality during the lactation period or in the manifestation of serotonergic syndrome in adult rats. The occurrence of low birth weight among pups born to dams which did not show reduced food ingestion or reduction of body weight gain during treatment with lower doses of fluoxetine or venlafaxine suggests that these drugs may have a deleterious effect on prenatal development when administered during pregnancy. In addition, fluoxetine slightly but significantly affected the duration of pregnancy (about half a day), an effect not observed in the venlafaxine-treated groups

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Simple reaction time (RT) to a peripheral visual target is shortened when a non-informative cue is flashed at target location 100-150 ms before target onset (early facilitation). Afterwards, RT to targets appearing at cue location is lengthened (inhibition of return). In the present study we have investigated if these effects arise from the onset and/or from the offset of the cue and the time-dependence of these effects. Twelve subjects were asked not to respond to a non-informative cue (S1) appearing on a computer screen 6 degrees to the right or to the left of a fixation point (FP), but to respond, by pressing a key, to a target (S2) occurring at 4 degrees from the FP in the same hemifield as S1 or in the opposite hemifield. There were two different types of trials. In both, a brief auditory stimulus (W) occurring 700 ms after the onset of FP warned the subject that S2 would appear 100, 200, 300, 500 or 800 ms later. Trials where the onset of S1 coincides with W and S1 remains on until the response to S2 are called ON trials. In OFF trials, S1 onset occurs at the beginning of the trial and its offset coincides with W. We found that in ON trials, RTs to S2 occurring ipsi- or contralaterally to S1 did not differ. In contrast, S1 offset elicited an inhibition of its hemifield beginning at least 100 ms after S1 offset and extending up to 800 ms.

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Simple reaction time (RT) to a peripheral visual target (S2) is shortened when a non-informative cue (S1) is flashed at the S2 location 100-150 ms before target onset (early facilitation). Afterwards, RTs to targets appearing at the S1 location are lengthened (inhibition of return). In the present investigation we studied the spatial distribution of the inhibition elicited by the offset of S1. Twelve subjects were asked not to respond to S1 which appeared on a horizontal meridian located 5.5 degrees above the fixation point (FP), but to respond, by pressing a key, to a target (S2) occurring at 5.5 degrees to the left or to the right. S1 could appear at one of 9 locations along this meridian (5.5, 3.5, 1.5, and 0.5 degrees to the left, 0.0 and 0.5, 1.5, 3.5, and 5.5 degrees to the right) and S2 occurred only at the most eccentric positions. Each trial began with the presentation of FP. Five-hundred ms later, S1 appeared and remained on for 700 ms. One hundred or 800 ms after S1 offset, S2 appeared in the same or in the opposite hemifield. We found that the offset of S1 elicits an inhibition (OFF-inhibition) which has the following features: a) it is maximal at cue's position; b) it spreads to other positions in the cued hemifield, and c) it decreases when the time interval between S1 offset and S2 onset increases from 100 to 800 ms.

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RESUMO

Simple reaction time (RT) to a peripheral visual target is shortened when a non-informative cue is flashed at target location 100-150 ms before target onset (early facilitation). Afterwards, RT to targets appearing at cue location is lengthened (inhibition of return). In the present study we have investigated if these effects arise from the onset and/or from the offset of the cue and the time-dependence of these effects. Twelve subjects were asked not to respond a non-informative cue (S1) appearing on a computer screen 6§ to the right or to the left of a fixation point (FP), but to respond, by pressing a key, to a target (S2) occurring at 4§ from the FP in the same hemifield as S1 or in the opposite hemifield. There were two different types of trials. In both, a brief auditory stimulus (W) occurring 700 ms after the onset of FP warned the subject that S2 would appear 100, 200, 300, 500 or 800 ms later. Trials where the onset of S1 coincides with W and S1 remains on until the response to S2 are called ON trials. In OFF trials, S1 onset occurs at the beginning of the trial and its offset coincides with W. We found that in On trials, RTs to S2 occurring ipsi-or contralaterally to S1 did not differ. In contrast, S1 offset elicited an inhibition of its hemifield beginning at least 100 ms after S1 offset and extending up to 800 ms

Assuntos

RESUMO

Simple reaction time (RT) to a peripheral visual target (S2) is shortened when a non-informative cue (S1) is flashed at the S2 location 100-150 ms before target onset (early facilitation). Afterwards, RTs to targets appearing at the S1 location are lengthened (inhbition of return). In the present investigation we studied the spatial distribution of the inhibition elicited by the offset of S1. Twelve subjects were asked not to respond to S1 which appeared on a horizontal meridian located 5.5§ above the fixation point (FP), but to respond, by pressing a key, to a target (S2) occurring at 5.5§ to the left or to the right. S1 could appear at one of 9 locations along this meridian (5.5, 3.5, 1.5, and 0.5§ to the left, 0.0 and 0.5, 1.5, 3.5, and 5.5§ to the right) and S2 occurred only at the most eccentric positions. Each trial began with the presentation of FP. Five-hundred ms later, S1 appeared and remained on for 700 ms. One hundred or 800 ms after S1 offset, S2 appeared in the same or in the opposite hemifield. We found that the offset of S1 elicits an inhibition (OFF-inhibition) which has the following features: a) it is maximal at cue's position; b) it spreads to other positions in the cued hemifield, and c) it decreases when the time interval between S1 offset and S2 onset increases from 100 to 800 ms

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