In this experiment we studied the effect of different pedalling rates during cycling at a constant power output (PO) 132±31 W (mean±S.D.), corresponding to 50 % V02 max, on the oxygen uptake and the magnitude of the slow component of V02 kinetics in humans. The PO corresponded to 50 % of V02 max, established during incremental cycling at a pedalling rate of 70 rev.min-1. Six healthy men aged 22.2 ±2.0 years with V02 max 3.89 ±0.92 l.min-1, performed on separate days constant PO cycling exercise lasting 6 min at pedalling rates 40, 60, 80, 100 and 120 rev.min-1, in random order. Antecubital blood samples for plasma lactate [La]pi and blood acid-base balance variables were taken at 1 min intervals. Oxygen uptake was determined breath-by-breath. The total net oxygen consumed throughout the 6 min cycling period at pedalling rates of 40, 60, 80, 100 and 120 rev.min-1 amounted to 7.727± 1.197, 7.705± 1.548, 8.679± 1.262, 9.945± 1.435 and 13.720± 1.862 1, respectively for each pedalling rate. The VO2 during the 6 min of cycling only rose slowly by increasing the pedalling rate in the range of 40-100 rev.min-1. This increase, was 0.142 1 per 20 rev.min-1 on the average. Plasma lactate concentration during the sixth minute of cycling changed little within this range of pedalling rates: the values were 1.83 ±0.70, 1.80 ± 0.48, 2.33 ±0.88 and 2.52 ±0.33 mmoLl-1. The values of [La]pi reached in the 6th minute of cycling were not significantly different from the pre-exercise levels. Blood pH was also not affected by the increase of pedalling rate in the range of 40-100 rev.min-1. However, an increase of pedalling rate from 100 to 120 rev.min-1 caused a sudden increase in the VO2 amounting to 0.747 1 per 20 rev.min-1, accompanied by a significant increase in [La]pj from 1.21 ±0.26 mmol.l-1 in pre-exercise conditions to 5.92±2.46 mmol.l-1 reached in the 6th minute of cycling (P<0.01). This was also accompanied by a significant drop of blood pH, from 7.355 ±0.039 in the pre-exercise period to 7.296 ± 0.060 in the 6th minute of cycling (P<0.01). The mechanical efficiency calculated on the basis of the net VO2 reached between the 4th and the 6th minute of cycling amounted to 26.6 ±2.7, 26.4±2.0, 23.4±3.4, 20.3 ±2.6 and 14.7±2.2 %, respectively for pedalling rates of 40, 60, 80,100 and 120 rev.min-1. No significant increase in the VO2 from the 3rd to the 6th min (representing the magnitude of the slow component of V02 kinetics) was observed at any of the pedalling rates (-0.022±0.056, -0.009±0.029, 0.012±0.073, 0.030±0.081 and 0.122±0.176 l.min-1 for pedalling rates of 40, 60, 80, 100 and 120 rev.min-1, respectively). Thus a significant increase in [La]pi and a decrease in blood pH do not play a major role in the mechanism(s) responsible for the slow component of VO2 kinetics in
humans.
Inflammation and other immune responses are involved in the variety of diseases and disorders. The acute response to endotoxemia includes activation of innate immune mechanisms as well as changes in autonomic nervous activity. The autonomic nervous system and the inflammatory response are intimately linked and sympathetic and vagal nerves are thought to have anti-inflammation functions. The basic functional circuit between vagus nerve a nd inflammatory response was identified and the neuroimmunomodulation loop was called cholinergic anti-inflammatory pathway. Unique function of vagus nerve in the anti-inflammatory reflex arc was found in many experimental and pre-clinical studies. They br ought evidence on the cholinergic signaling interacting with systemic and local inflammation, particularly suppressing immune cells function. Pharmacological/electrical modulation of vagal activity suppressed TNF-α and other proinflammatory cytokines prod uction and had beneficial therapeutic effects. Many questions related to mapping, linking and targeting of vagal-immune interactions have been elucidated and brought understanding of its basic physiology and provided the initial support for development of Tracey's inflammatory reflex. This review summarizes and critically assesses the current knowledge defining cholinergic anti-inflammatory pathway with main focus on studies employing an experimental approach and emphasizes the potential of modulation of va gally-mediated anti-inflammatory pathway in the treatment strategies., I. Zila, D. Mokra, J. Kopincova, M. Kolomaznik, M. Javorka, A. Calkovska., and Obsahuje bibliografii
Neuronal activity in the medulla oblongata and neurogenic inflammation of airways were investigated in a guinea pig model induced by repeated intra-esophageal instillation of hydrochloric acid (HCl) after vagotomy. Unilateral vagotomy was performed in the vagotomy group, while a sham-operation was performed in the sham group. Operation was not conducted in sham control group. Airway inflammation was observed with hematoxylin and eosin (HE) staining. C-fos protein was measured by immunohistochemistry (IHC) and Western blot (WB). Substance P was examined by IHC and enzyme-linked immuno sorbent assay (ELISA). Airway microvascular permeability was detected by evans blue dye (EBD) fluorescence. Inflammation of airway was observed in the trachea and bronchi after chronic HCl perfusion into the lower esophagus, and was alleviated after unilateral vagotomy. C-fos expression in the medulla oblongata
was lower in the vagotomy group compared to the sham control and sham groups. Substance P-like immunoreactivity (SP-li), concentration and microvascular leakage in airway were lower in the vagotomy group than that in the other groups. Our results suggest that vagotomy improved neurogenic inflammation of airways and decreased neuronal activities, the afferent nerves and neurons in medulla oblongata may be involved in neurogenic inflammation of airways mediated by esophageal-bronchial reflex.
In the present study, we investigated the effects of vagus nerve stimulation (VNS), a proposed treatment for patients with intractable epilepsy, on cardiac rhythm following seizures induced by pentylenetetrazole (PTZ) in Wistar rats. After a baselinerecording of electroencephalogram (EEG), electrocardiogram (ECG) and blood pressure (BP), rats in the first group received a single convulsive dose of PTZ (70 mg/kg) (Group 1). In the other
two groups, the Wistar rats were implanted with a cuff electrode on the left cervical vagus nerve. One day after surgery, rats in the second group were treated with VNS (Group 2), whereas rats in the third group were connected to the stimulator but did not receive VNS (Group 3). Ten minutes after VNS onset, 70 mg/kg dose of PTZ was injected. EEG, ECG and BP were continuously recorded during post-injection period. Seizure severity was scored behaviorally. Then, baseline, ictal and postictal periods were analyzed for cardiac rhythms, seizure severity and blood pressure variability. PTZ treatment induced tonic-clonic seizure activity in all animals of Group 1 and Group 3. In these groups a marked increase of mean arterial blood pressure (MABP) but a significant decrease in heart rate and PP interval fluctuations was observed at postictal period. However, in the VNS-treated group the seizure scores and cardiac parameter returned to the baseline level. Present results emphasize that VNS effectively reduces seizure severity and suppress the seizure-induced cardiac rhythm changes.
Two available subspecific names are used interchangeably for the Balkan lynx. In this contribution I demonstrate that the valid name is Lynx lynx balcanicus Bureš, 1941, and L. l. martinoi Mirić, 1978, is its junior synonym. The type locality of L. l. balcanicus is the Šara Mts. in the Republic of Macedonia. In reaching this conclusion, I refrain from infringing upon taxonomic judgment on whether or not the Balkan lynx is a subspecies in its own right. While addressing the Balkan lynx over the last decade, conservationists have largely ignored the older synonym balcanicus and used instead a junior synonym martinoi.