The effects of serosally added 5-hydroxytryptamine (5-HT, 100 μM) on the short circuit-current (Isc) across jejunum and ileum taken from fed, starved and undernourished (Gerbillus cheesmani) were investigated. The effects of the neurotoxin, tetrodotoxin (TTX, 10 μM) on the basal Isc as well as on the maximum increase in Isc induced by 5-HT were also studied. There were regional variations in the basal Isc as well as in the way by which the small intestine responds to 5-HT. The basal Isc was greater in jejunum than in ileum and such differences were TTX-sensitive. The maximum increase in Isc, which results from addition of 5-HT, was higher in jejunum than in ileum under all three feeding conditions. TTX reduced the maximum increase in Isc induced by 5-HT across stripped and intact intestine of the two regions in the three nutritional states. The 5-HT-induced Isc in the jejunum of both starved and undernourished gerbils and in the ileum of starved animals was the function of both submucosal and myenteric plexus. In jejunum and ileum taken from starved and undernourished gerbils the 5-HT-induced Isc was both chloride- and bicarbonate-dependent. Thus the results indicated that both starvation and undernourishment increase that response and such increases were TTX-sensitive and both chloride- and bicarbonate-dependent., F. Y. Al-Balool., and Obsahuje bibliografii a bibliografické odkazy
Several diseases induce hypermetabolism, which is characterized by increases in rest ing energy expenditures (REE) and whole body protein loss. Exaggerated protein degradation is thought to be the driving force underlying this response. The effects of caspase and calpain inhibitors on REE in physiological and hypermetabolic conditions, how ever, are unknown. Thus, we studied whether MDL28170 (calpain inhibitor) or z-VAD-fmk (caspase inhibitor) affect REE under physiological conditions and during hypermetabolism post -burn. Rats were treated five times weekly and observed for 6 weeks. Treatmen t was started 2 h (early) or 48 h ( late) after burn. In normal rats, MDL28170 transiently increased REE to 130 % of normal during week 2-4. z-VAD-fmk reduced REE by 20-25 % throughout the observation period. Within 14 days after burns, REE increased to 13 0±5 % . Whereas MDL28170/ early treatment did not affect REE, MDL28170/ late transiently increased REE to 180±10 % of normal by week 4 post- burn. In contrast, with z -VAD -fmk/ early REE remained between 90-110 % of normal post- burn. z-VAD-fmk/ late did not affect burn-induced increases in REE. These data suggest that caspase cascades contribute to the development of hypermetabolism and that burn-induced hypermetabolism can be pharmacologically modulated. Our data point towards caspase cascades as po ssible therapeutic targets to attenuate hypermetabolism after burns, and possibly in other catabolic disease processes., P. G. Vana, H. M. LaPorte, R. H. Kennedy, R. L. Gamelli, M. Majetschak., and Obsahuje bibliografii
The present study examined the effects of a free radical scavenger, N-tert-butyl-alfa-phenylnitrone (PBN) on lithium-pilocarpine-induced status epilepticus (SE) and its short-term consequences in rats 12 (P12) or 25 (P25) days old. PBN (2 x 100 mg/kg i.p.) was injected according to the following schedules: 1) PBN-pretreated animals received the first dose 30 min prior to pilocarpine, the second dose was given 1 min after SE onset, and 2) PBN-treated animals received the first dose of PBN 1 min after SE onset and the second one 60 min later. Paraldehyde was administered to decrease mortality. Effects of PBN were highly age-dependent. In P25 group, PBN-pretreatment increased latency to SE onset and significantly suppressed the severity of motor manifestation of SE. Both PBN pretreatment and treatment improved recovery after SE. In contrast, administration of PBN in P12 animals did not affect SE pattern or recovery after SE.
Administration of PBN had no effects on the motor performance of animals 3 and 6 days after SE. Neuronal damage was examined 24 h and 7 days after SE using Fluoro-Jade B staining. Mild neuroprotective effects of PBN in hippocampal fields CA1 and CA3 occurred in P25 rats in both experimental schedules. In contrast, administration of PBN aggravated neuronal injury in the hippocampus in P12 rats. Administration of PBN to intact rats did not induce neurodegeneration in either age group.
With the aim to contribute to the elucidation of the role of phytohormones in response of plants to adverse environmental conditions, seedlings of Phaseolus vulgaris, Nicotiana tabacum, Beta vulgaris, and Zea mays were supplied with water, 100 µM abscisic acid (ABA), or 10 µM N6-benzyladenine (BA) immediately before imposition of water stress (WS). In all four species, contents of chlorophylls (Chls) and carotenoids were markedly decreased during WS and after rehydration only in plants pre-treated with water but not in those pre-treated with ABA or BA. Contents of pigments of xanthophyll cycle increased during WS more in plants pre-treated with ABA or BA than in those pre-treated with water, but the degree of their de-epoxidation was highest in the later. Similarly, the efficiency of photosystem 2, determined as variable to maximal Chl fluorescence ratio, was not markedly decreased in bean plants pre-treated with ABA or BA in contrast to those pre-treated with water. The imposed WS was not severe enough to damage chloroplast ultrastructure. However, different changes in a size of starch inclusions were observed. In bean plants, the amount of starch increased considerably in plants pre-treated with water, while it decreased in BA pre-treated plants and no change was found in ABA pre-treated ones. The starch content declined under WS in sugar beet and tobacco plants but only moderate changes were found in ABA or BA pre-treated plants. Thus the application of BA and especially of ABA reduced the negative effects of subsequent WS. and D. Haisel ... [et al.].
Spontaneous activity of cortical neurons exhibits alternative fluctuations of membrane potential consisting of phased depolarization called "up-state" and persistent hyperpolarization called "down-state" during slow wave sleep and anesthesia. Here, we examined the effects of sound stimuli (noise bursts) on neuronal activity by intracellular recording in vivo from the rat auditory cortex (AC). Noise bursts increased the average time in the up-state by 0.81±0.65 s (rang e, 0.27-1.74 s) related to a 10 s recording duration. The rise times of the spontaneous up-events averaged 69.41±18.04 ms (range, 40.10-119.21 ms), while those of the sound-evoked up-events were significantly shorter (p<0.001) averaging on ly 22.54±8.81 ms (range, 9.31- 45.74 ms). Sound stimulation did not influence ongoing spontaneous up-events. Our data suggest that a sound stimulus does not interfere with ongoing spontaneous neuronal activity in auditory cortex but can evoke new depolarizations in addition to the spontaneous ones., Y. Zhang ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
In a previous study we demonstrated that acute footshock stress increased glutathione peroxidase activity in the prefrontal cortex and striatum of adult male rats. Adolescents may respond differently to stress as life stressors may be greater than at other ages. The present study examined the effects of the acute footshock stress on superoxide dismutase (SOD) and glutathione peroxidase (GPx) enzyme activities and thiobarbituric acid reactive substances (TBARS) levels in adolescent male and female rat brains. We demonstrated that acute footshock stress increased SOD activity in the prefrontal cortex, and increased GPx activity in the hippocampus in female rats. In males, acute footshock stress increased GPx activity in the prefrontal cortex and hippocampus. Footshock stress did not change TBARS levels. These results indicate a strong role of gender in the response of adolescent subjects to various aspects of stress.
Anaerobic threshold which describes the onset of systematic increase in blood lactate concentration is a widely used concept in clinical and sports medicine. A deflection point between heart rate-work rate has been introduced to determine the anaerobic threshold non-invasively. However, some researchers have consistently reported a heart rate deflection at higher work rates, while others have not. The present study was designed to investigate whether the heart rate deflection point accurately predicts the anaerobic threshold under the condition of acute hypoxia. Eight untrained males performed two incremental exercise tests using an electromagnetically braked cycle ergometer: one breathing room air and one breathing 12 % O2. The anaerobic threshold was estimated using the V-slope method and determined from the increase in blood lactate and the decrease in standard bicarbonate concentration. This threshold was also estimated by in the heart rate-work rate relationship. Not all subjects exhibited a heart rate deflection. Only two subjects in the control and four subjects in the hypoxia groups showed a heart rate deflection. Additionally, the heart rate deflection point overestimated the anaerobic threshold. In conclusion, the heart rate deflection point was not an accurate predictor of anaerobic threshold and acute hypoxia did not systematically affect the heart rate-work rate relationships.
The purpose of this study was to investigate the validity of non-invasive lactate threshold estimation using ventilatory and pulmonary gas exchange indices under condition of acute hypoxia. Seven untrained males (21.41.2 years) performed two incremental exercise tests using an electromagnetically braked cycle ergometer: one breathing room air and other breathing 12 % O2. The lactate threshold was estimated using the following parameters: increase of ventilatory equivalent for O2 (VE/VO2) without increase of ventilatory equivalent for CO2 (VE/VCO2). It was also determined from the increase in blood lactate and decrease in standard bicarbonate. The VE/VO2 and lactate increase methods yielded the respective values for lactate threshold: 1.910.10 l/min (for the VE/VO2) vs. 1.890.1 l/min (for the lactate). However, in hypoxic condition, VE/VO2 started to increase prior to the actual threshold as determined from blood lactate response: 1.670.1 l/min (for the lactate) vs. 1.370.09 l/min (for the VE/VO2) (P=0.0001), i.e. resulted in pseudo-threshold behavior. In conclusion, the ventilatory and gas exchange indices provide an accurate lactate threshold. Although the potential for pseudo-threshold behavior of the standard ventilatory and gas exchange indices of the lactate threshold must be concerned if an incremental test is performed under hypoxic conditions in which carotid body chemosensitivity is increased.
Mechanical circulatory support (MCS) with an implantable left ventricular assist device (LVAD) is an established therapeutic option for advanced heart failure. Most of the currently used LVADs generate a continuous stream of blood that decreases arterial pulse pressure. This study investigated whether a change of the pulse pressure during different pump speed settings would affect cerebral autoregulation and thereby affect cerebral blood flow (CBF). The study included 21 haemodynamically stable outpatients with a continuous-flow LVAD (HeartMate II, Abbott, USA) implanted a median of 6 months before the study (interquartile range 3 to 14 months). Arterial blood pressure (measured by finger plethysmography) was recorded simultaneously with CBF (measured by transcranial Doppler ultrasound) during baseline pump speed (8900 rpm [IQR 8800; 9200]) and during minimum and maximum tolerated pump speeds (8000 rpm [IQR 8000; 8200] and 9800 rpm [IQR 9800; 10 000]). An increase in LVAD pump speed by 800 rpm [IQR 800; 1000] from the baseline lead to a significant decrease in arterial pulse pressure and cerebral blood flow pulsatility (relative change −24 % and −32 %, both p < 0.01), but it did not affect mean arterial pressure and mean CBF velocity (relative change 1 % and −1.7 %, p=0.1 and 0.7). In stable patients with a continuous-flow LVAD, changes of pump speed settings within a clinically used range did not impair static cerebral autoregulation and cerebral blood flow.
We compared the effects of adaptation to intermittent high altitude (IHA) hypoxia of various degree and duration on ischemia-induced ventricular arrhythmias in rats. The animals were exposed to either relatively moderate hypoxia of 5000 m (4 or 8 h/day, 2-3 or 5-6 weeks) or severe hypoxia of 7000 m (8 h/day, 5-6 weeks). Ventricular arrhythmias induced by coronary artery occlusion were assessed in isolated buffer-perfused hearts or open-chest animals. In the isolated hearts, both antiarrhythmic and proarrhythmic effects were demonstrated depending on the degree and duration of hypoxic exposure. Whereas the adaptation to 5000 m for 4 h/day decreased the total number of premature ventricular complexes (PVCs), extending the daily exposure to 8 h and/or increasing the altitude to 7000 m led to opposite effects. On the contrary, the open-chest rats adapted to IHA hypoxia exhibited an increased tolerance to arrhythmias that was even more pronounced at the higher altitude. The distribution of PVCs over the ischemic period was not altered by any protocol of adaptation. It may be concluded that adaptation to IHA hypoxia is associated with enhanced tolerance of the rat heart to ischemic arrhythmias unless its severity exceeds a certain upper limit. The opposite effects of moderate and severe hypoxia on the isolated hearts cannot be explained by differences in the occluded zone size, heart rate or degree of myocardial fibrosis. The proarrhythmic effect of severe hypoxia may be related to a moderate left ventricular hypertrophy (27 %), which was present in rats adapted to 7000 m but not in those adapted to 5000 m. This adverse effect can be overcome by an unknown protective mechanism(s) that is absent in the isolated hearts., G. Asemu, J. Neckář, O. Szárszoi, F. Papoušek, B. Ošťádal, F. Kolář., and Obsahuje bibliografii