Reactivity of the arterial system during vasodilation induced by sodium nitroprusside]

A stepwise decrease in the blood pressure by means of sodium nitroprusside infusion led to progressing diminishing of mesatone pressor effects in anaesthetised rats. Cardiac output changes due to mesatone administration did not depend on the initial blood pressure. The latter being lower than physiological limits, a direct linear correlation occurred between pressor responses and shifts of general peripheral resistance, on one hand, and the degree of the blood pressure initial drop, on the other hand. The constrictor responses under study are discussed in respect to their dependence on initial tone of arterial vessels.     

Effects of testosterone and estradiol on cutaneous vasodilation during local warming in older men

Microvascular vasodilation in humans can become impaired with age, leading to cardiovascular diseases ranging from mild to life-threatening. Reproductive hormones may confer some protection on the vascular system in women; however, it is unclear whether the same is true in men. Our goal was to evaluate the impact of four hormonal conditions (testosterone only, estradiol only, testosterone and estradiol, no testosterone and no estradiol) on microvascular vasodilator responsiveness in the skin of older men. We hypothesized that in older healthy men estradiol promotes cutaneous microvascular dilation during local warming of the skin and that testosterone inhibits this dilation. We measured skin blood flow using laser Doppler flowmetry during 35 min of cutaneous local warming to 42 degrees C in 52 healthy men (average age 67 +/- 1 yr). Subjects were randomized to one of the four hormonal conditions and were studied before and after hormone treatments. The endothelium-dependent vasodilator response to local warming was not different among groups either before or after hormone treatment. For example, with testosterone-only treatment this vasodilator response was 220 +/- 13 AU, and with estrogen only the response averaged 246 +/- 12 AU (P > 0.05). We conclude that, within the doses employed in the present study, testosterone and estradiol did not consistently alter cutaneous vasodilator responsiveness in healthy older men.     

Ethnodemographic processes in the Russian Federation

This is an English translation of the introduction to a textbook on the ethnic demography of the Russian Federation. It explores the intricacies of multiple language groups, ethnic group interspersions, and the existence of small yet self-identifying populations without political territorial status. The political implications of demographic developments affecting ethnic groups, including migration, are also considered.     

Water loss distribution in exercising men under hot conditions

Dynamics of sweating and water loss distribution were studied in 7 exercising men under thermoneutral conditions (Ta, 25 degrees C; Tw, 24 degrees C and RH, 54%) and during moderate heat exposure (Ta, 30 degrees C; Tw, 30 degrees C; RH, 54%). The subjects performed bicycle exercise at intensity of 50% V O2 max. Dynamics of sweating was greater after heat exposure (delay in onset of sweating 3.6 and 1.4 min, p less than 0.05; time constant 10.1 and 7.3 min, p less than 0.02). The dynamics of sweating was related to the net body heat load (r = -0.80, p less than 0.001). Sweat evaporation from the skin (Esk) was significantly higher in heat exposed exercising subjects while dripping sweat (mdrip) did not differ significantly. Water loss distribution in relation to total water loss during control exercise was as follows: (Ediff + Eres) 14.8% (Esk) 59.6%; and (mdrip) 25.6%. During exercise under heat exposure (Ediff + Eres) was 12.1%; (Esk) was 67.5%; and (mdrip) was 20.4%. It is concluded that moderate heat exposure accelerate sweating reaction but does not change significantly water loss distribution in exercising subjects. Dripping sweat seems to be an attribute of sweating not only in hot humid conditions but also under temperate temperature and air humidity.     

Effect of heat stress on cardiac output and systemic vascular conductance during simulated hemorrhage to presyncope in young men

During moderate actual or simulated hemorrhage, as cardiac output decreases, reductions in systemic vascular conductance (SVC) maintain mean arterial pressure (MAP). Heat stress, however, compromises the control of MAP during simulated hemorrhage, and it remains unknown whether this response is due to a persistently high SVC and/or a low cardiac output. This study tested the hypothesis that an inadequate decrease in SVC is the primary contributing mechanism by which heat stress compromises blood pressure control during simulated hemorrhage. Simulated hemorrhage was imposed via lower body negative pressure (LBNP) to presyncope in 11 passively heat-stressed subjects (increase core temperature: 1.2 ± 0.2°C; means ± SD). Cardiac output was measured via thermodilution, and SVC was calculated while subjects were normothermic, heat stressed, and throughout subsequent LBNP. MAP was not changed by heat stress but was reduced to 45 ± 12 mmHg at the termination of LBNP. Heat stress increased cardiac output from 7.1 ± 1.1 to 11.7 ± 2.2 l/min (P < 0.001) and increased SVC from 0.094 ± 0.018 to 0.163 ± 0.032 l·min(-1)·mmHg(-1) (P < 0.001). Although cardiac output at the onset of syncopal symptoms was 37 ± 16% lower relative to pre-LBNP, presyncope cardiac output (7.3 ± 2.0 l/min) was not different than normothermic values (P = 0.46). SVC did not change throughout LBNP (P > 0.05) and at presyncope was 0.168 ± 0.044 l·min(-1)·mmHg(-1). These data indicate that in humans a cardiac output adequate to maintain MAP while normothermic is no longer adequate during a heat-stressed-simulated hemorrhage. The absence of a decrease in SVC at a time of profound reductions in MAP suggests that inadequate control of vascular conductance is a primary mechanism compromising blood pressure control during these conditions.     

Mechanisms of systemic vasodilation by lysozyme-c in septic shock

In septic shock (SS), cardiovascular collapse is caused by the release of inflammatory mediators. We previously found that lysozyme-c (Lzm-S), released from leukocytes, contributed to systemic vasodilation in a canine model of SS. We then delineated the pathway by which this occurs in a canine carotid artery organ bath preparation (CAP). We showed that Lzm-S could intrinsically generate hydrogen peroxide (H(2)O(2)) and that H(2)O(2) subsequently reacted with endogenous catalase to form compound I, an oxidized form of catalase. In turn, compound I led to an increase in cyclic guanosine 3',5'-monophosphate to produce vasodilation. However, it was not clear from previous studies whether it is necessary for Lzm-S to bind to the vasculature to cause vasodilation or, alternatively, whether the generation of H(2)O(2) by Lzm-S in the surrounding medium is all that is required. We examined this question in the present study in which we used multiple preparations. In a partitioned CAP, we found that when we added Lzm-S to a partitioned space in which a semipermeable membrane prevented diffusion of Lzm-S to the carotid artery tissue, vasodilation still occurred because of diffusion of H(2)O(2). On the other hand, we found that Lzm-S could accumulate within the vascular smooth muscle layer (VSML) after 7 h of SS in a canine model. We also determined that when Lzm-S was located in close proximity to vascular smooth muscle cells, it could generate H(2)O(2) to produce lengthening in a human cell culture preparation. We conclude that there are two mechanisms by which Lzm-S can cause vasodilation in SS. In one instance, H(2)O(2) generated by Lzm-S in plasma diffuses to the VSML to cause vasodilation. In a second mechanism, Lzm-S directly binds to the VSML, where it generates H(2)O(2) to produce vasodilation.     

L-arginine availability determines the duration of acetylcholine-induced systemic vasodilation in vivo

In vitro studies have shown that acetylcholine-induced vasorelaxation is mediated by endothelium-derived relaxing factor/nitric oxide (EDRF/NO). EDRF/NO is synthesized from L-arginine by an enzymatic pathway that is inhibited by L-NG-methylarginine. To assess whether EDRF/NO also mediates the vasodilating action of acetylcholine in vivo, we have investigated the effect of L-arginine and L-NG-methylarginine on the hypotensive response to acetylcholine in the anesthetized guinea pig. L-arginine prolonged the duration of the depressor response to acetylcholine and L-NG-methylarginine decreased it. However, neither L-arginine nor L-NG-methylarginine modified the magnitude of acetylcholine's hypotensive effect unless the blood pressure was previously elevated by infusion with norepinephrine. Thus, de novo synthesis of nitric oxide from L-arginine contributes importantly, but not exclusively, to acetylcholine's hypotensive effect in the guinea pig. Furthermore, the concentration of circulating L-arginine may influence the duration and magnitude of acetylcholine-induced depressor responses under normotensive and hypertensive conditions.     

Inhibition of cAMP-dependent protein kinase under conditions occurring in the cardiac dyad during a Ca2+ transient

The space between the t-tubule invagination and the sarcoplasmic reticulum (SR) membrane, the dyad, in ventricular myocytes has been predicted to experience very high [Ca2+] for short periods of time during a Ca2+ transient. The dyadic space accommodates many protein kinases responsible for the regulation of Ca2+ handling proteins of the cell. We show in vitro that cAMP-dependent protein kinase (PKA) is inhibited by high [Ca2+] through a shift in the ratio of CaATP/MgATP toward CaATP. We further generate a three-dimensional mathematical model of Ca2+ and ATP diffusion within dyad. We use this model to predict the extent to which PKA would be inhibited by an increased CaATP/MgATP ratio during a Ca2+ transient in the dyad in vivo. Our results suggest that under normal physiological conditions a myocyte paced at 1 Hz would experience up to 55% inhibition of PKA within the cardiac dyad, with inhibition averaging 5% throughout the transient, an effect which becomes more pronounced as the myocyte contractile frequency increases (at 7 Hz, PKA inhibition averages 28% across the dyad throughout the duration of a Ca2+ transient).     

Dynamics of microevolutionary processes during the use of pigs of various types under conditions at an industrial complex

Breeding of pigs in a closed herd during three generations under industrial complex conditions does not essentially increase the number of animals with homozygous genotypes of polymorphic systems of blood groups. One of the possible causes of this phenomenon is selection favourable to animals with a higher heterozygosity.     

Endothelin produces systemic vasodilation independent of the state of consciousness

The effects of endothelin, ET-1, on pulmonary and systemic hemodynamics were studied in the open chest dog and changes in systemic arterial pressure in dogs under conscious and anesthetized states were compared. Rapid intravenous (IV) bolus injections of ET-1, 100-1,000 nanograms/kg, significantly decreased systemic arterial pressure, and significantly decreased systemic vascular resistance whereas left atrial pressure and pulmonary vascular resistance were not altered. Reductions in systemic arterial pressure in response to bolus injection of ET-1, 100 and 300 nanograms/kg IV, during conscious state and during anesthesia were similar, respectively. The present data suggest that ET-1 dilates the systemic vascular bed independent of the animal's state of consciousness. The present data also suggest that when compared to the systemic vascular bed, the pulmonary vascular bed is less responsive to bolus administration of ET-1.     

Autonomic support of the systemic response under conditions of operator visual-stress activities

The parameters of functioning of muscular, cardiac-respiratory, vegetative and other systems in the organism of healthy persons engaged in the work connected with visual strength have been studied. The optimal limits of system response are determined and thus its realization is shown to be provided with the activation of vegetative regulation apparatus. The structure of the relations between the distinguished parameters is maintained even when new level of functioning is established. Initial activation of vegetative mechanisms is a leading factor of the further rearrangements of visual and somatosensory analyzers with the given kind of activity.