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Notes: 1. To investigate the participation of both vagal cardiopulmonary baroreceptor activity and efferent renal sympathetic nerve activity (ERSNA) in the natriuretic response to saline volume expansion (SVE), three series of experiments were undertaken in anaesthetized rats.2. In the first two series of experiments, the natriuretic (series A) and ERSNA (series B) responses to SVE were evaluated in both sham operated and cervical bilateral vagotomized rats. The acute experiment consisted of two baseline (BL) periods, treatment (sham control (CTR) or real cervical bilateral vagotomy), a volume expansion phase (Ringer’s solution, 10% bodyweight) and a postexpansion phase. The results of these two series indicate that vagotomy significantly enhances basal ERSNA (37±8%; P 〈 0.05 vs BL) and significantly attenuates the renal sympathoinhibitory response (by approximately 50%; P 〈 0.05 vs CTR) but not the natriuretic response to SVE, suggesting the potential expression of a vagotomy induced compensatory natriuretic mechanism.3. To assess this, the natriuretic response to SVE was evaluated in chronic sham operated or renal denervated groups of rats in which vagotomy was or was not performed (series C). There were no differences among groups in either systemic haemodynamics or plasma protein concentration. Vagotomy plus chronic renal denervation induced a supranormal natriuretic and diuretic response (approximately 30%; P 〈 0.01) to SVE when compared with similar natriuretic and diuretic responses of the remaining groups.4. These data support the idea that, in intact rats on a normal sodium diet, neither cardiopulmonary baroreceptors nor renal nerves are necessary for the elimination of an acute intravenous isotonic sodium load and indicate that during SVE the activation of vagal cardiopulmonary baroreceptors exerts an inhibitory effect on both ERSNA and the expression of a natriuretic mechanism. Such a natriuretic mechanism is expressed only when SVE is induced in vagotomized rats (compensating for the vagotomy mediated antinatriuretic effects of an enhanced ERSNA), but is unmasked only when, in addition, renal nerves are chronically transected. All of this offers an efficient element of safety in eliminating an acute isotonic sodium load when cardiopulmonary baroreceptors are severed.

Notes: Objectives: To systematize a procedure that allows one to characterize the perfusion response pattern of attached gingiva to the topical and transitory compression of alveolar mucose, using laser-Doppler flowmetry.Material and methods: A cross-sectional study was carried out, in 20 healthy adult subjects of either sex, with teeth in antero-mandibular sextant but without periodontitis at the lower left lateral incisor (LLLI). Sample was selected by convenience non-probability sampling. Gingival perfusion was evaluated at labial LLLI attached gingiva using a specially designed gingival tray. Two perfusion recordings were carried out 5 min. apart, each one consisting of a 40 s control phase, a 22 s compression phase and a 40 s post-compression phase. During compression phase, LLLI alveolar mucose was compressed with a wood-mounted cotton swab until the perfusion decreased to about 1/5 of its control perfusion value.Results: Integrated primary basal flow (IPBF) during control phase was of 14,210±1075 perfusion units (PU), whereas integrated flow during compression phase was of 1651±202 PU (p〈0.05). After compression was released, integrated total secondary real flow was 13,322±1513 PU (p〈0.05) which represented a 91.3±3.8% of IPBF. Gingival compression propitiated an induced flow debt (IFD) of 6478±781 PU, which increased in 980±482 PU after compression was released, representing 18% of the IFD (Debt index).Conclusions: A hypoaemic response in reaction to topical and transitory LLLI alveolar mucose compression was observed. Debt index and the ITSRF% are reproducible indices of microvascular perfusion response whose validation under pathological circumstances remains to be evaluated.