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Animal studies have shown that the rapid hyperemic response to external muscle compression undergoes inactivation upon repetitive stimulation, but this phenomenon has never been observed in humans. The aim of the present study was to determine whether 1) the vascular mechano-sensitivity underlying muscle compression-induced hyperemia is inactivated in an inter-stimulus interval (ISI)-dependent fashion upon repetitive stimulation, as suggested by animal studies, and 2) whether such inactivation also attenuates contraction-induced hyperemia. Brachial artery blood flow was measured by echo Doppler sonography in 13 healthy adults in response to 1) single and repetitive cuff muscle compression (CMC) of the forearm (20 CMCs, 1 s ISI); 2) a sequence of CMC delivered at decreasing ISI from 120 to 2 s; and 3) electrically-stimulated contraction of the forearm muscles before and after repetitive CMC. The peak amplitude of hyperemia in response to CMC normalized to baseline decreased from 2.2 ± 0.6 to 1.4 ± 0.4 after repetitive CMC and, in general, was decreased at ISI < 240 s. The peak amplitude of contraction-induced hyperemia was attenuated after as compared to before repeated CMC (1.7 ± 0.4 and 2.6 ± 0.6, respectively). Mechano-sensitivity of the vascular network can be conditioned by previous mechanical stimulation, and such preconditioning may substantially decrease contraction-induced hyperemia.

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Aim of the present study is to investigate the role of mechano-sensitive channels on basal muscle blood flow and on the compression-induced rapid hyperaemia. To this aim, the mechano-sensitive channel blocker Gadolinium (Gd(3+)) is employed, which already proved to reduce the myogenic response in isolated vessels. Muscle blood flow (MaBF) was recorded from the masseteric artery in 8 urethane-anesthetized rabbits. Rapid hyperemic responses were evoked by 1-s lasting compressions of the masseter muscle (MC) delivered before and after close arterial infusion of Gd(3+) in the masseteric artery. Three infusions were performed at 1-h interval, producing estimated plasma concentration (EPC) of 0.045, 0.45 and 4.5 mM, in the masseteric artery. The amplitude of the hyperaemic response to MC, equal to 195±77% of basal flow in control condition, was reduced by 9.5±19.4% (p=0.18) and 45±28% (p<0.01) while basal MaBf increased by 10±3% (p=0.90) and by 68±30% (p<0.01) at EPC of 0.045 and 0.45 mM, respectively. At EPC of 4.5 mM a strong reduction in both MaBF (by 54±13%, p<0.01) and MC response (75±12%, p<0.01) was instead observed. These effects did not depend on time from infusion. At all doses employed Gd(3+) never affected arterial blood pressure, heart rate and contralateral MaBF. While the effects observed at the highest EPC likely result from blood vessel occlusion due to Gd(3+) precipitation, the effects observed at lower concentrations demonstrate that Gd(3+) affects musculo-vascular function by decreasing both resting vascular tone and responsiveness to mechanical stimuli. The results are compatible with a Gd(3+)-induced blockade of vascular mechano-sensitive channels.

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Mechano-sensitivity of the vascular network is known to be implicated in the rapid dilatation at the onset of exercise, however, it is not known how this mechanism responds to repetitive mechanical stimulation. This study tests the hypothesis that the mechanically-induced hyperaemia undergoes some attenuation upon repetitive stimulation. Muscle blood flow was recorded from 9 masseteric arteries (5 right, 4 left) in 6 anesthetized rabbits. Two mechanical stimuli, masseter muscle compression (MC) and occlusion of the masseteric artery (AO), were provided in different combinations: A) repeated stimulation (0.5 Hz, for 40 s); B) single stimuli delivered at decreasing inter-stimulus interval (ISI) from 4 min to 2 s, C) single AO delivered before and immediately after a series of 20 MCs at 0.5 Hz, and vice-versa. Repetitive AO stimulation at 0.5 Hz produced a transient hyperaemia (378 ±189%) peaking at 4.5 ±1.4 s and then decaying before the end of stimulation. The hyperaemic response to individual AOs progressively decreased by 74 ±39% with decreasing ISI from 4 min to 2 s (p<0.01). Non significant differences were observed between AO and MC stimulation. Decreased response to AO was also provoked by previous repetitive MC stimulation, and vice-versa. The results provide evidence that the mechano-sensitivity of the vascular network is attenuated by previous mechanical stimulation. It is suggested that the mechano-sensitive dilatory mechanisms undergoes some inactivation whose recovery time is in the order of a few minutes.

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The complex interplay of neural, metabolic, myogenic and mechanical mechanisms that regulate blood flow in skeletal muscle (MBF) is still incompletely understood. For the first time, a method is presented for high time-resolution recording of MBF from a purely muscular artery in physiological conditions. Ultrasound perivascular flow probes were implanted (n = 15) mono- or bilaterally around the masseteric branch of the facial artery in nine rabbits and tested up to 16 days after implant. Reliable and stable recordings were achieved in 50% of implants. Blood flow was observed to increase from a resting level of 0.2-0.3 ml min(-1) up to 4.0-6.0 ml min(-1) during spontaneous masticatory activity. In addition, within single masticatory cycles marked back flow transients could be observed (peak flow = -10 ml min(-1)) during powerful masticatory strokes but not during mild mastication. The possibility of (1) surgically removing the sympathetic supply to the relevant vascular bed and of (2) bilaterally monitoring the perfusion of masseter muscles thus allowing to use one side as control side for different types of interventions makes this model a useful tool for disentangling the different mechanisms involved in the control of MBF.

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Mediterranean spotted fever is an infectious disease due to Rickettsia conori transmitted to man by the dog tick Rhipicephalus sanguineus. The review of a consecutive series of 525 cases, admitted to Caltagirone hospital in the last 20 years, permits the classic clinical picture to be identified by fever, maculopapular eruption and tache noire, and any complications to be visualized. Usually the course of the disease is good, but 12.7% of our cases reported complications such as renal failure, myocarditis, pneumonia, encephalitis, anicteric hepatitis, gastrointestinal bleeding, anaemia and impaired glucose tolerance. The development of a systemic vasculite is the main pathogenetic factor in the origin of systemic complications. Early diagnosis and specific antibiotic treatment may reduce the risk of complications.

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Brucellosis is a common zoonosis endemic in many parts of the world. Neurologic involvement is a rare but serious complication and it occurs in 2 - 5% of cases. Neurologic signs can appear during the active phase of disease or later. Six cases of neurobrucellosis are described: meningoencephalitis in 2 cases, meningitis with brain abscess in 1 case, encephalomielitis in 3 cases. Diagnosis was made on the basis of history of the exposure to brucella, of serum and cerebrospinal fluid positive serology, of quantitative change in cerebrospinal fluid, on EEG, CT and MNR and favorable response to specific treatment (rifampin, rolitetracycline tirmethoprim-sulfamethoxazole). Neurobrucellosis should be suspected in case of neurological deficit in brucellosis endemic areas. Treatment of neurobrucellosis remains controversial: we recommend a regimen with rifampin 600 mg x 2 i.v. + tirmethoprim-sulfamethoxazole 2 ff x 2 i.v. for a period of 6-8 weeks.