The purpose of the present study was to examine whether excessive CO2 output (V.co2excess) is dominantly attributable to hyperventilation during the period of recovery from repeated cycling sprints. A series of four 10-sec cycling sprints with 30-sec passive recovery periods was performed two times. The first series and second series of cycle sprints (SCS) were followed by 360-sec passive recovery periods (first recovery and second recovery). Increases in blood lactate (ΔLa) were 11.17±2.57 mM from rest to 5.5 min during first recovery and 2.07±1.23 mM from the start of the second SCS to 5.5 min during second recovery. CO2 output (V.co2) was significantly higher than O2 uptake (V.o2) during both recovery periods. This difference was defined as V.co2excess. V.co2excess was significantly higher during first recovery than during second recovery. V.co2excess was added from rest to the end of first recovery and from the start of the second SCS to the end of second recovery (CO2excess). ΔLa was significantly related to CO2excess (r=0.845). However, ventilation during first recovery was the same as that during second recovery. End-tidal CO2 pressure (PETco2) significantly decreased from the resting level during the recovery periods, indicating hyperventilation. PETco2 during first recovery was significantly higher than that during second recovery. It is concluded that V.co2excess is not simply determined by ventilation during recovery from repeated cycle sprints., T. Yano ... [et al.]., and Obsahuje seznam literatury
Inactive forearm muscle oxygenation has been reported to begin decreasing from the respiratory compensation point (RCP) during ramp leg cycling. From the RCP, hyperventilation occurs with a decrease in arterial CO2 pressure (PaCO2). The aim of this study was to determine which of these two factors, hyperventilation or decrease in PaCO2, is related to a decrease in inactive biceps brachii muscle oxygenation during leg cycling. Each subject (n = 7) performed a 6-min two-step leg cycling. The exercise intensity in the first step (3 min) was halfway between the ventilatory threshold and RCP (170±21 watts), while that in the second step (3 min) was halfway between the RCP and peak oxygen uptake (240±28 watts). The amount of hyperventilation and PaCO2 were calculated from gas parameters. The average cross correlation function in seven subjects between inactive muscle oxygenation and amount of hyperventilation showed a negative peak at the time shift of zero (r = -0.72, p<0.001), while that between inactive muscle oxygenation and calculated PaCO2 showed no peak near the time shift of zero. Thus, we concluded that decrease in oxygenation in inactive arm muscle is closely coupled with increase in the amount of hyperventilation., H. Ogata, T. Arimitsu, R. Matsuura, T. Yunoki, M. Horiuchi, T. Yano., and Obsahuje bibliografii a bibliografické odkazy
Previous investigations revealed that most of the fluid regulating hormones showed no consistent relationship to the hypoxic diuretic response (HDR). In this study we examined if adrenomedullin (AM), a hypoxia-mediated diuretic/natriuretic peptide is connected to HDR. Thirty-three persons were examined at low altitude (LA), on the third exposure day at 3440 m (medium altitude, MA) and on the fourteenth day at 5050 m (high altitude, HA). Nocturnal diuresis rose from 460 ml [interquartile range 302 ml] at LA to 560 [660] ml at MA to 1015 [750] ml at HA (p<0.005). Sodium excretion was similar at LA and MA (41.8 [27.0] vs. 41.4 [28.4] mM) and increased to 80.2 [29.1] mM at HA (p<0.005). Urinary AM excretion was 7.9 [3.9] at LA, 7.5 [5.7] pM at MA, and increased to 10.5 [5.1] pM (p<0.05) at HA. Urinary AM excretion was correlated to diuresis (r=0.72, p<0.005) and sodium excretion (r=0.57, p<0.005). Plasma AM concentration rose from 16.4 [3.1] to 18.8 [4.9] pM/l at MA (p<0.005) and to 18.3 [4.3] pM/l at HA (p<0.005). Plasma AM concentration and urinary AM excretion were not correlated, neither were plasma AM concentration and diuresis or natriuresis. Our data suggest the involvement of increased renal AM production in the pathophysiology of high altitude fluid and sodium loss., B. Haditsch, A. Roessler, H. G. Hinghofer-Szalkay., and Obsahuje bibliografii a bibliografické odkazy
Renin-angiotensin system (RAS) plays a key role in the regulation of renal function, volume of extracellular fluid and blood pressure. The activation of RAS also induces oxidative stress, particularly superoxide anion (O2-) formation. Although the involvement of O2- production in the pathology of many diseases is known for long, recent studies also strongly suggest its physiological regulatory function of many organs including the kidney. However, a marked accumulation of O2- in the kidney alters normal regulation of renal function and thus may contribute to the development of salt-sensitivity and hypertension. In the kidney, O2- acts as vasoconstrictor and enhances tubular sodium reabsoption. Nitric oxide (NO), another important radical that exhibits opposite effects than O2-, is also involved in the regulation of kidney function. O2- rapidly interacts with NO and thus, when O2- production increases, it diminishes the bioavailability of NO leading to the impairment of organ function. As the activation of RAS, particularly the enhanced production of angiotensin II, can induce both O2- and NO generation, it has been suggested that physiological interactions of RAS, NO and O2- provide a coordinated regulation of kidney function. The imbalance of these interactions is critically linked to the pathophysiology of salt-sensitivity and hypertension., L. Kopkan, L. Červenka., and Obsahuje seznam literatury
The influence of renal nerves on the effects of concurrent NO synthase inhibition (10 mg kg-1 b.w. i.v. L-NAME) and ETA/ETB receptor inhibition (10 mg kg-1 b.w. i.v. bosentan) on renal excretory function and blood pressure in conscious spontaneously hypertensive rats (SHR) was investigated. L-NAME increased blood pressure, urine flow rate, fractional excretion of sodium, chloride and phosphate in both normotensive Wistar rats and SHR with intact renal nerves (p<0.01). GFR or RBF did not change in any of the groups investigated. The effects of L-NAME on renal excretory function were markedly reduced by bosentan and the values returned to control level in the normotensive rats, while in SHR the values were reduced by bosentan, but they remained significantly elevated as compared to control level (p<0.05). The hypertensive response induced by L-NAME in SHR is partially due to activation of endogenous endothelins, but it does not depend on renal nerves. Chronic bilateral renal denervation abolished the effect of L-NAME on sodium and chloride excretion in normotensive rats, whereas it did not alter this effect in SHR. The participation of endogenous endothelins in changes of renal excretory function following NO synthase inhibition is diminished in SHR as compared to Wistar rats., R. Girchev, P. Markova., and Obsahuje bibliografii a bibliografické odkazy
Antiorthostatic hindlimb suspension (unloading) decreased the resting membrane potential (RMP) of skeletal muscle fibers in fast extensor digitorum longus (EDL) and slow soleus (SOL) muscle of the rat by about 10 % within 7 days and more. Inactivation of the membrane Na+,K+-pump by ouabain brought about similar depolarization as unloading. The increased sodium permeability of the membrane was excluded as the major cause of this depolarization by experiments in which TRIS was substituted for Na+ in the medium. On the other hand, the decrease in the electrogenic participation of the Na+,K+-pump is apparently one of the causes of RMP decrease during hypogravity, in EDL muscle in particular., O. Tyapkina ... [et al.]., and Obsahuje seznam literatury
We present the current state of complex circulatory dynamics model development based on Guyt on’s famous diagram. The aim is to provide an open-source model that will allow the simulation of a number of pathological conditions on a virtual patient including cardiac, respiratory, and kidney failure. The model will also simulate the therapeutic influence of various drugs, infusions of electrolytes, blood transfusion, etc. As a current result of implementation, we describe a co re model of human physiology targeting the systemic circulation, arterial pressure and body fluid regulation, including short- and long-term regulations. The model can be used for educational purposes and general reflection on physiological regulation in path ogenesis of various diseases., J. Kofránek, J. Rusz., and Obsahuje bibliografii
Neonatal exposure to hyperoxia alters lung development in mice. We tested if retinoic acid (RA) treatment is capable to affect lung development after hyperoxic injury and to maintain structural integrity of lung. The gene of vascular endothelial growth factor A (VEGF-A) is one of the RA-responsive genes. Newborn BALB/c mice were exposed to room air, 40 % or 80 % hyperoxia for 7 days. One half of animals in each group received 500 mg/kg retinoic acid from day 3 to day 7 of the experiment. At the end of experiment we assessed body weight (BW), lung wet weight (LW), the wet-to-dry lung weight ratio (W/D) and the expression of mRNA for VEGF-A and G3PDH genes. On day 7 the hyperoxia-exposed sham-treated mice (group 80) weighed 20 % less than the room air-exposed group, whereas the 80 % hyperoxic group treated with RA weighed only 13 % less than the normoxic group. W/D values in 80 and 80A groups did not differ, although they both differed from the control group and from 40 groups. There was a significant difference between 40 and 40A groups, but the control group was different from 40 group but not from 40A groups. The 80 and 80A groups had mRNA VEGF-A expression lowered to 64 % and 41 % of the control group. RA treatment of normoxic and mild hyperoxic groups increased mRNA VEGF-A expression by about 50 %. We conclude that the retinoic acid treatment of newborn BALB/c mice exposed for 7 days to 80 % hyperoxia reduced the growth retardation in the 80 % hyperoxic group, reduced the W/D ratio in the 40 % but not in the 80 % hyperoxic group. Higher VEGF-A mRNA expression in the 80 % hyperoxic group treated with RA was not significant compared to the 80 % hyperoxic group., M. Zimová-Herknerová, J. Mysliveček, P. Potměšil., and Obsahuje bibliografii a bibliografické odkazy
Central administration of losartan effectively blocked the increase of blood pressure and drinking response induced by angiotensin II (Ang II) or carbachol. However, the relationship between angiotensin AT1 receptors and the natriuresis induced by brain cholinergic stimuli is still not clear. The purpose of the study is to reveal the role of brain angiotensin AT1 receptor in the carbachol-induced natriuresis and expression of neuronal nitric oxide synthase (nNOS) in the locus coeruleus (LC) and proximal co nvoluted tubule (PCT). Our results indicated that 40 min after in tracerebroventricular (ICV) injection of carbachol (0.5 μg), urinary sodium excretion was significantly increased to 0.548±0.049 μmol·min-1·100 g-1. Immunohistochemistry showed that carbachol induced an increase of neuronal nitric oxide synthase immunoreactivity (nNOS-IR) in the LC and renal proximal tubular cells. After pretreatment with losartan (20 μg), carbachol-induced urinary sodium excretion was reduced to 0.249±0.067 μmol·min-1·100 g-1. The same was true for carbachol-induced increase of nNOS-IR in the LC and PCT. The present data suggest that ICV cholinergic stimulation could induce a natriuresis and upregulate the activity of nNOS in the LC and PCT. The blockade of AT1 receptors might downregulate the effects induced by carbachol in the LC and PCT. Consequently, we provide a new evidence that brain angiotensinergic pathway and NO-dependent neural pathway contribute to the natriuresis following brain cholinergic stimulation and thus play an important role in the regulation of fluid homeostasis. Furthermore, the final effect of nitric oxide on proximal tubular sodium reabsorption participated in the natriuresis induced by brain cholinergic stimulation., M. Wang, C. L. Jiang, C. Y. Wang, Q. Y. Yao., and Obsahuje bibliografii a bibliografické odkazy