Detecting activation of the sympatho-adrenal axis from haemodynamic recordings, in conscious rabbits exposed to acute stress

Roatta, Silvestro; Mohammed, Mazher; Passatore, Magda

doi:10.1111/j.1748-1716.2010.02179.x

Cited by 12 publications

(11 citation statements)

References 49 publications

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“…Trials were considered valid when the maneuvers did not produce stress, as assessed by the absence of relevant changes in ABP, heart rate, and blood flow in the artery under study (36).…”

Section: Methodsmentioning

confidence: 99%

Evidence that the contraction-induced rapid hyperemia in rabbit masseter muscle is based on a mechanosensitive mechanism, not shared by cutaneous vascular beds

Turturici

Mohammed

Roatta

2012

Journal of Applied Physiology

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Turturici M, Mohammed M, Roatta S. Evidence that the contraction-induced rapid hyperemia in rabbit masseter muscle is based on a mechanosensitive mechanism, not shared by cutaneous vascular beds. J Appl Physiol 113: 524 -531, 2012. First published June 7, 2012 doi:10.1152/japplphysiol.00237.2012.-Several mechanisms have been hypothesized to contribute to the rapid hyperemia at the onset of exercise. The aim of the present study was to investigate the role played by the mechanosensitivity of the vascular network. In 12 anesthetized rabbits blood flow was recorded from the exclusively muscular masseteric artery in response to brief spontaneous contractions (BSC) of the masseter muscle, artery occlusion (AO), muscle compression (MC), and muscle stretch (MS). Activation of masseter muscle was monitored by electromyography (EMG). Responses to AO were also recorded from the mostly cutaneous facial and the central ear arteries. Five animals were also tested in the awake condition. The hyperemic response to BSC (peak amplitude of 394 Ϯ 82%; time to peak of 1.8 Ϯ 0.8 s) developed with a latency of 300 -400 ms from the beginning of the EMG burst and 200 -300 ms from the contractioninduced transient flow reduction. This response was neither different from the response to AO (peak amplitude ϭ 426 Ϯ 158%), MC, and MS (P ϭ 0.23), nor from the BSC response in the awake condition. Compared with the masseteric artery, the response to AO was markedly smaller both in the facial (83 Ϯ 18%,) and in the central ear artery (68 Ϯ 20%) (P Ͻ 0.01). In conclusion, the rapid contractioninduced hyperemia can be replicated by a variety of stimuli affecting transmural pressure in muscle blood vessels and is thus compatible with the Bayliss effect. This prominent mechanosensitivity appears to be a characteristic of muscle and not cutaneous vascular beds. muscle stretch; myogenic response; rapid dilatation; reactive hyperemia; muscle compression SKELETAL MUSCLE BLOOD FLOW has long been known to exhibit a rapid increase at the onset of exercise (1,9,12,22,27). The mechanisms behind this phenomenon are still a matter of debate despite the many new insights provided by different research groups in recent years. In particular it has been shown that the contraction-induced compression of venous compartments (muscle pump) cannot fully account for the blood flow increase and that the additional occurrence of a rapid active dilatation is required (18,33,45,46). Other studies have shown that this rapid dilatation is mediated neither by changes in sympathetic neural drive (7, 41), nor by ACh spillover from the motor endplate (6, 33), nor by endothelium-released NO (6), although this last assertion is debated (see DISCUSSION). As early as 1974, Mohrman and Sparks (31) hypothesized that the rapid dilatation could result from the myogenic response of muscle blood vessels to decreased transmural pressure, which in turn results from the increase in intramuscular (extravascular) pressure produced by the contraction. They showed, in fact, that the rapid hypere...

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“…Trials were considered valid when the maneuvers did not produce stress, as assessed by the absence of relevant changes in ABP, heart rate, and blood flow in the artery under study (36).…”

Section: Methodsmentioning

confidence: 99%

Evidence that the contraction-induced rapid hyperemia in rabbit masseter muscle is based on a mechanosensitive mechanism, not shared by cutaneous vascular beds

Turturici

Mohammed

Roatta

2012

Journal of Applied Physiology

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“…Furthermore, radiotelemetry recording requires a substantial economic investment, and there is also the need for surgery to implant the device, neither of which may be warranted for limited measurements (Kurtz et al 2005). Thus, experiments in conscious rabbits in a laboratory setting continue to be of value, as evidenced by a number of recent publications (Kimotsuki et al 2010; Korner et al 2010; Clayton et al 2011; Roatta et al 2011; Guild et al 2012).…”

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confidence: 99%

Comparison of blood pressure and sympathetic activity of rabbits in their home cage and the laboratory environment

Lim

Burke

Armitage³

et al. 2012

Experimental Physiology

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Methodological improvements in measuring cardiovascular parameters have meant that data can be collected from freely moving animals in their home cage. However, experiments in rabbits still often require them to be restrained in a laboratory setting. The aim of this study was to determine whether measurements collected when rabbits were placed in a holding box in the laboratory are representative of values obtained in freely moving conscious rabbits. Nine New Zealand White rabbits received two radiotelemetry implants to monitor mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA). The MAP measured in the laboratory (71 ± 1 mmHg) was similar to that in the home cage (69 ± 1 mmHg), but there was less MAP variability. The RSNA was also similar in both environments. In contrast, laboratory heart rate (HR) was 7% lower than home cage HR (181 ± 4 beats min −1 , P < 0.001), but HR variability was similar. Baroreflex gain, assessed by spectral analysis, was 19% higher in the laboratory than in the home cage due to lower MAP mid-frequency variability in the laboratory. Home cage circadian patterns of MAP and HR were strongly influenced by feeding and activity. Nevertheless, MAP and RSNA laboratory measurements were the same as average 24 h values and remained similar over several weeks. We conclude that while HR is generally lower in the laboratory, a valid representation of MAP and RSNA can be given by laboratory measurements.

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“…The stimulation pattern for single stimuli and doublets consisted of a sequence of 22 alternated single and paired pulses separated by 1-s interval. The paired pulses (doublets) had an interspike interval (ISI) ranging between 4 and 1,000 ms (4,8,12,15,20,30,50,75,100,125,150,175,200,225,250, 300, 400, 500, 750, and 1,000 ms) according to a protocol adopted in previous studies (17,18). This sequence of pulses was followed by four pulse trains of 5 s in duration, separated by 5-s intervals.…”

Section: Methodsmentioning

confidence: 99%

Sympathetic activation by the cold pressor test does not increase the muscle force generation capacity

Roatta

Farina

2011

Journal of Applied Physiology

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A positive inotropic action by the sympathetic nervous system on skeletal muscles has been observed and investigated in animal and in vitro studies. This action provided a theoretical basis for the putative ergogenic action of catecholamines and adrenergic agonists, although there is no clear evidence of this effect in humans. The aim of this study was to investigate the occurrence of inotropic effects associated to physiological sympathetic activation in healthy subjects. The muscle force capacity was investigated in the tibialis anterior (n = 9 subjects) and in the soleus (n = 9) muscles electrically stimulated with single pulses and double pulses with variable interspike interval (4-1,000 ms) and short pulse trains (frequency: 5-14 Hz) before, during, and after sympathetic activation by the cold pressor test (CPT). CPT significantly decreased by 10.4 ± 7.2 and 10.6 ± 4.4% the force produced by single and double pulse stimulation, respectively, and produced smaller decreases in the force obtained by train stimulation in the tibialis anterior, while no significant changes were observed in either type of contraction in the soleus muscle. CPT failed to induce any increase in the force capacity of the investigated muscles. The prevalent decrease in force evidenced in this study supports the concept that the weakening sympathetic action on type I fiber, already shown to occur in humans, prevails over the putative potentiating action.

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Detecting activation of the sympatho-adrenal axis from haemodynamic recordings, in conscious rabbits exposed to acute stress

Abstract: In conscious rabbits, rapid release of adrenaline makes a prominent contribution to vasoconstriction in response to different stressors including box oscillation, muscle pain and air jet but not the nasopharyngeal stimulation.

Cited by 12 publications

References 49 publications

Evidence that the contraction-induced rapid hyperemia in rabbit masseter muscle is based on a mechanosensitive mechanism, not shared by cutaneous vascular beds

Evidence that the contraction-induced rapid hyperemia in rabbit masseter muscle is based on a mechanosensitive mechanism, not shared by cutaneous vascular beds

Comparison of blood pressure and sympathetic activity of rabbits in their home cage and the laboratory environment

Sympathetic activation by the cold pressor test does not increase the muscle force generation capacity

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