The cardiac baroreflex constitutes an important mechanism mediating autonomic control of heart activity. Its function can be quantified by applying sequence analysis based on continuous recordings of blood pressure and heart rate. In this study, several indices derived from this method were compared regarding their suitability to estimate baroreflex function at rest and during autonomic stimulation. A cold pressor test was used to induce vagal withdrawal. Changes in the following indices evoked by this procedure were examined: baroreflex sensitivity (the extent of changes in heart period following blood pressure fluctuations), baroreflex effectiveness (the relative frequency in which the reflex responds to blood pressure fluctuations), and baroreflex power (the reflex operations in a defined period). The values of all indices decreased during autonomic stimulation. The strongest and most consistent effect, however, was observed for baroreflex sensitivity, suggesting that this parameter is the most sensitive to changes in parasympathetic tone among the three parameters. Baroreflex sensitivity also proved to differentiate between individuals with higher and lower resting blood pressure. Therefore, this index may best reflect the well-known involvement of the baroreflex in the long-term setting of blood pressure. Midrange correlations between the indices of baroreflex function suggest that they quantify similar, though not identical, aspects of baroreflex function. This study supports the use of sequence analysis as a reliable tool for the quantification of parasympathetic cardiac control. The sensitivity index must be considered the most relevant to quantify baroreflex function among the three parameters.

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A head-down tilt posture, the Trendelenburg position, which could facilitate venous return from the splanchnic organs and lower extremities, is recommended for the treatment of anaphylactic shock. However, few data of animal studies support its effectiveness. We examined the effects of a head-down tilt maneuver on anaphylactic hypotension in BALB/c mice and Sprague-Dawley rats. We measured systemic arterial pressure (Sap) and portal venous pressure (Pvp) in spontaneously breathing anesthetized animals sensitized with ovalbumin. At either supine (control) or a 30-degree head-down tilt position, anaphylactic hypotension was induced by an intravenous injection of antigen. In the control rats, an increase in Sap by 66 mmHg and a decrease in Pvp by 11.5 cmH₂O were observed at 2.5 and 6 min, respectively, after antigen. In contrast, in control mice injected with antigen, Sap decreased similarly, but Pvp increased by only 4 cmH₂O. A head-down tilt maneuver in mice substantially attenuated the antigen-induced decrease in Sap throughout the 60 min measurements, though it aggravated slightly, but significantly, only at the late phase of after 25 min in rats. We conclude that a head-down tilt maneuver attenuates anaphylactic hypotension in anesthetized mice and rats. These beneficial effects were smaller in rats than in mice probably because of substantial portal hypertension, which might prevent the head-down tilt-induced increase in venous return from the splanchnic vascular bed.

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The force-velocity (F-V) relationship of filament sliding is traditionally used to define the inotropic condition of striated muscles. A simple circulation model combined with the Laplace heart was developed to get a deeper insight into the relationship between the F-V characteristics and the cardiac ventricular inotropy. The circulation model consists of a preload and an afterload compartments. The linear F-V relationship for filament sliding in the NL model (Negroni and Lascano 1996) was replaced by the exponential F-V relation observed by Piazzesi et al. (2002). We also modified the NL model to a hybrid model to benefit from the Ca²⁺ cooperativity described by the Robinson model (Robinson et al. 2002). The model was validated by determining the diastolic ventricular pressure-volume relationship of the Laplace heart and the F-V relation of the new hybrid model. The computed parameters of the cardiac cycle agreed well with the physiological data. Computational results showed that the cross-bridge elongation (h in the NL model) temporally undershot the equilibrium h_c during the ejection period and overshot it during the rapid refilling phase. Thereby the time course of ejection and refilling was retarded. In a simulation where the velocity of the mobile myosin head (dX/dt) was varied, the systolic peak pressure of the ventricle varied from a minimum value at dX/dt = 0 to a saturating value obtained with a constant h_c, providing in silico evidence for a functional impact of the cross-bridge sliding rate on the ventricular inotropy.

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Using immunohistochemical and electrophysiological methods, we investigated the role of L-type Ca²⁺ channels in the regulation of the endocochlear potential (EP) of the endolymphatic surface cells (ESC) of the guinea pig stria vascularis. The following findings were made: (1) Administration of 30 μg/ml nifedipine via a vertebral artery significantly suppressed the transient asphyxia-induced decrease in the EP (TAID) and the transient asphyxia-induced increase in the Ca²⁺, referred to as TAIICa, concentration in the endolymph ([Ca]_e). (2) The endolymphatic administration of 1 μg/ml nifedipine significantly inhibited the TAID as well as the TAIICa. The endolymphatic administration of nifedipine (0.001–10 μg/ml) inhibited the TAID in a dose-dependent manner. (3) The endolymphatic administration of (+)-Bay K8644, an L-type Ca²⁺ channel closer, significantly inhibited the TAID, whereas (–)-Bay K8644, an L-type Ca²⁺ channel opener, caused a large decrease in the EP from ∼+75 mV to ∼+20 mV at 10 min after the endolymphatic administration. (4) By means of immunohistochemistry, a positive staining reaction with L-type Ca²⁺ channels was detected in the marginal cells of the stria vascularis. (5) Under the high [Ca]_e condition, we examined the mechanism of the TAIICa and hypothesized that the TAIICa might have been caused by the decrease in the EP through a shunt pathway in the ESC. (6) The administration of nifedipine to the endolymph significantly inhibited the Ba²⁺-induced decrease in the EP. These findings support the view that L-type Ca²⁺ channels in the marginal cells regulate the EP, but not directly the TAIICa.

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Vascular endothelial cell (VEC) responds to wall shear stress that has not only spatial variation, but also temporal gradient. To simplify the problem, we first studied how the calcium dynamics of VEC responded to the steady wall shear stress of varying magnitude in a stenosed artery. We then studied how the VEC responded to the periodic shear stress that had temporal variation, as in the pulsatile blood flow. To investigate the multiphysics model of VEC in vitro, we used a mathematical model for intracellular calcium dynamics and a computational fluid dynamics (CFD) method for arterial wall shear stress, either steady or periodic. The CFD results showed that for the steady stenotic flow, the wall shear stress in the recirculating flow was lower than the threshold value, 4 dyne/cm², at two particular points: flow separation and flow reattachment. For these subthreshold shear stresses, the peak value of the transient calcium response did not hit the normal saturated level, but reached a reduced magnitude. We investigated the effect of severity of stenosis (SOS) of the stenosed artery. For the pulsatile flow, the so-called shear stress slew rate or the temporal gradient of the first upsurge of the periodic flow was an important factor for the VEC calcium dynamics. The calcium response had a finite range of parameter for SOS and shear stress slew rate in which the calcium response was more sensitive than elsewhere, showing a sigmoid pattern.

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Fiber-type distributions, cross-sectional areas, and oxidative enzyme activities of type-identified fibers in the biceps brachii and triceps brachii muscles of 10-week-old male Wistar rats were determined and compared with those in the soleus and plantaris muscles. The soleus and plantaris muscles consisted of two (I and IIA) and three (I, IIA, and IIB) types of fibers, respectively. The deep regions of the biceps brachii and triceps brachii muscles consisted of three types of fibers, while the surface regions of those muscles consisted only of type IIB fibers. The cross-sectional areas of fibers in the deep and surface regions of the plantaris muscle and in the deep regions of the biceps brachii and triceps brachii muscles were in the rank order of type I = type IIA < type IIB, while the oxidative enzyme activities of fibers in the deep and surface regions of the plantaris muscle and in the deep region of the triceps brachii muscle were in the rank order of type IIB < type I = type IIA. These results indicate that fiber-type distributions, cross-sectional areas, and oxidative enzyme activities are muscle type- and region-specific. Therefore, the metabolic and functional significance of the biceps brachii and triceps brachii muscles, especially in the surface regions, where only type IIB fibers are located, in those muscles, appears to be determined by their fibers having larger cells and lower oxidative enzyme activity.

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Peripheral tissue oxygenation has been studied with near-infrared spectroscopy (NIRS) on either the forearm or calf with questionable comparability. The aim was to compare forearm and calf tissue oxygenation in healthy term neonates measured with NIRS. Fractional oxygen extraction, tissue oxygenation index, and mixed venous oxygenation were similar in both extremities, whereas oxygen delivery and oxygen consumption of calf tissue were higher.

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Hyperbaric exposure induces lesions of the CNS in scuba divers. Repeated exposures to hyperbaric air at 0.5 MPa for 30 min with short intervals suppressed NGF-stimulated neurite outgrowth, concomitant with a decrease in the protein expression of ERK in PC12 cells. Hyperbaric exposure most likely causes direct lesions of neural cells.

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