During sympathetic activation in normal humans, there is a predominance in the LF oscillation of blood pressure, RR interval, and sympathetic nerve activity. During sympathetic inhibition, the HF component of cardiovascular variability predominates. This relationship is best seen when power spectral components are normalized for total power. Synchronous changes in the LF and HF rhythms of both RR interval and MSNA during different levels of sympathetic drive are suggestive of common central mechanisms governing both parasympathetic and sympathetic cardiovascular modulation.

Background-Low-dose atropine causes bradycardia either by acting on the sinoatrial node or by its effects on central muscarinic receptors increasing vagal activity. Any central muscarinic effects of high-dose atropine on RR interval are masked by peripheral muscarinic blockade at the sinoatrial node, which causes tachycardia. Effects of central parasympathetic activation on sympathetic activity are not known. Methods and Results-Using power spectral analysis of RR interval, intra-arterial blood pressure, respiration, and muscle sympathetic nerve activity (MSNA), we examined the effects of both low (2 g/kg IV) and high (15 g/kg IV) doses of atropine. After low-dose atropine, RR increased by 9Ϯ1% (PϽ0.0001), the low-frequency (LF) component (in normalized units, NU) of RR variability decreased by Ϫ32Ϯ8%, and the high-frequency (HF) NU component increased (ϩ74Ϯ19%); hence, LF/HF of RR variability fell by 52Ϯ10% (all PϽ0.01). Although overall MSNA did not change, LF NU of MSNA decreased (Ϫ15Ϯ5%), HF NU of MSNA increased (ϩ31Ϯ3%), and LF/HF of MSNA fell (Ϫ41Ϯ8%) (all PϽ0.01). After high-dose atropine, LF NU of MSNA decreased (Ϫ17Ϯ12%), HF NU of MSNA increased (ϩ22Ϯ3%), and LF/HF of MSNA fell (Ϫ51Ϯ21%) (all PϽ0.02). Conclusions-Increasing central parasympathetic activity with low-dose atropine is associated with an increase in the HF and a decrease in the LF oscillations of both RR interval and MSNA variability. High-dose atropine similarly induces an increase in the HF and a decrease in the LF components of MSNA variability. Thus, central parasympathetic activation is able to modulate the oscillatory characteristics of sympathetic nerve traffic to peripheral blood vessels.

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SUMMARYLike all spiders, tarantulas (family Theraphosidae) synthesize silk in specialized glands and extrude it from spinnerets on their abdomen. In one species of large tarantula, Aphonopelma seemanni, it has been suggested that silk can also be secreted from the tarsi but this claim was later refuted. We provide evidence of silk secretion directly from spigots (nozzles) on the tarsi of three distantly related tarantula species: the Chilean rose, Grammostola rosea; the Indian ornamental, Poecilotheria regalis; and the Mexican flame knee, Brachypelma auratum, suggesting tarsal silk secretion is widespread among tarantulas. We demonstrate that multiple strands of silk are produced as a footprint when the spider begins to slip down a smooth vertical surface. The nozzle-like setae on the tarsi responsible for silk deposition have shanks reinforced by cuticular thickenings, which serve to prevent the shanks' internal collapse while still maintaining their flexibility. This is important as the spigots occur on the ventral surface of the tarsus, projecting beyond the finely divided setae of the dry attachment pads. We also reveal the structure and disposition of the silk-secreting spigots on the abdominal spinnerets of the three tarantula species and find they are very similar to those from the earliest known proto-spider spinneret from the Devonian period, giving another indication that silk secretion in tarantulas is close to the ancestral condition.

Sequential overlapping pulse shock waveforms facilitate defibrillation compared with single pulse shocks of the same total energy. This is due at least in part to the changing orientation of the electrical vector during the multiple pulse shock.

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