Cutaneous vasoconstriction in conscious rabbits during alerting responses detected by hippocampal theta-rhythm

Yu, Ying; Blessing, W.W.

doi:10.1152/ajpregu.1997.272.1.r208

Cited by 50 publications

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“…Consistent with this, alerting stimuli in humans reliably increase cutaneous sympathetic activity (156). Brief alerting stimuli also evoke variable and often biphasic changes in heart rate (1,8,33,161) due to the fact that there is coactivation of cardiac sympathetic and vagal parasympathetic activity (1,8,33,123).…”

Section: Pattern Of Cardiovascular and Respiratory Responses To Stresmentioning

confidence: 68%

“…In animals, brief alerting stimuli such as an unexpected noise or light will evoke immediate autonomic and respiratory responses, characterized by strong cutaneous vasoconstriction and respiratory activation (17,18,84,109,161). In contrast, such nonnoxious brief stimuli evoke only small and transient increases in arterial pressure and little or no changes in blood flow to the mesenteric, renal, and hindlimb vascular beds (109,162), indicating that the sympathetic outflow to the cutaneous vascular bed is rather selectively activated by mild alerting stimuli.…”

Section: Pattern Of Cardiovascular and Respiratory Responses To Stresmentioning

confidence: 99%

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Central mechanisms regulating coordinated cardiovascular and respiratory function during stress and arousal

Dampney

2015

American Journal of Physiology-Regulatory, Integrative and Comp

127

116

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Actual or potentially threatening stimuli in the external environment (i.e., psychological stressors) trigger highly coordinated defensive behavioral responses that are accompanied by appropriate autonomic and respiratory changes. As discussed in this review, several brain regions and pathways have major roles in subserving the cardiovascular and respiratory responses to threatening stimuli, which may vary from relatively mild acute arousing stimuli to more prolonged life-threatening stimuli. One key region is the dorsomedial hypothalamus, which receives inputs from the cortex, amygdala, and other forebrain regions and which is critical for generating autonomic, respiratory, and neuroendocrine responses to psychological stressors. Recent studies suggest that the dorsomedial hypothalamus also receives an input from the dorsolateral column in the midbrain periaqueductal gray, which is another key region involved in the integration of stress-evoked cardiorespiratory responses. In addition, it has recently been shown that neurons in the midbrain colliculi can generate highly synchronized autonomic, respiratory, and somatomotor responses to visual, auditory, and somatosensory inputs. These collicular neurons may be part of a subcortical defense system that also includes the basal ganglia and which is well adapted to responding to threats that require an immediate stereotyped response that does not involve the cortex. The basal ganglia/colliculi system is phylogenetically ancient. In contrast, the defense system that includes the dorsomedial hypothalamus and cortex evolved at a later time, and appears to be better adapted to generating appropriate responses to more sustained threatening stimuli that involve cognitive appraisal. defensive behavior; sympathetic activity; respiratory activity; hypothalamus; midbrain; sympathetic premotor nuclei AN ANIMAL'S SURVIVAL is dependent on being able to respond appropriately to stressors, which can be categorized into two different groups: interoceptive (also-called physical) stressors and exteroceptive (also-called psychological) stressors (44,133). Physical stressors are those that directly threaten homeostasis, such as hypoxia, hemorrhage, or infection, whereas psychological stressors can be defined as actual or perceived threats in the external environment. Psychological stressors can be further subdivided into conditioned stressors (i.e., ones that are normally innocuous but which are perceived as threatening because of previous experiences) or unconditioned stressors (i.e., ones that are intrinsically threatening, such as the sight, sound, or odor of a predator). Physical and psychological stressors activate different populations of neurons in the brain (44,63,102). Similarly, there is evidence that the autonomic responses to conditioned and unconditioned psychological stressors are also mediated by different pathways in the brain (62). In this review, which is based on my 2013 Carl Ludwig Distinguished Lecture to the American Physiological Society, I consider the brain mec...

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Section: Pattern Of Cardiovascular and Respiratory Responses To Stresmentioning

confidence: 68%

Section: Pattern Of Cardiovascular and Respiratory Responses To Stresmentioning

confidence: 99%

Central mechanisms regulating coordinated cardiovascular and respiratory function during stress and arousal

Dampney

2015

American Journal of Physiology-Regulatory, Integrative and Comp

127

116

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“…In five rabbits additional blood flow probes were implanted around the facial artery (model 1PSB, Transonic Systems), proximal to the origin of the masseteric artery (35) and around the central ear artery (model 1PSL Transonic Systems), which supplies an almost exclusively cutaneous vascular bed (51).…”

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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“…We then used this protocol to demonstrate that the accompanying hypotension was due to the induced bradycardia. Orienting stimuli are usually reported to induce hypotension and bradycardia, but hypertension and bradycardia have also been noted (19)(20)(21)(22)24,(26)(27)(28)(29)(30). Previous studies have been limited by poorly controlled stimuli, such as a hand clap, which rabbits rapidly learn to ignore (21), and these studies did not report beat-to-beat responses.…”

Section: Discussionmentioning

confidence: 99%

“…We considered three possibilities: that the measured hypotension was a factitious finding due to dampened arterial waveforms associated with proximal ear artery vasoconstriction; the measured hypotension is due to vasodilation; and that the measured hypotension simply reflects a reduction in the calculated MAP due to the protracted diastole brought about by the abrupt bradycardia. Yu and Blessing (24,29,30) reported that rabbits exposed to alerting stimuli, such as brief noises, had central ear artery constriction and reduced flow distal to subacutely implanted flow probes. This vasoconstriction suggests that the apparent hypotension we observed might have been caused by dampened traces distal to localized vasoconstriction.…”

Section: Discussionmentioning

confidence: 99%

Mechanism of hypotensive transients associated with abrupt bradycardias in conscious rabbits

Sheldon

Wright

Duff

et al. 2007

Canadian Journal of Cardiology

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T he present study had two purposes: to determine the physiology of an important source of rabbit heart rate variability and to assess whether it may be a model for vasovagal syncope. Given that diminished heart rate variability portends a poor cardiovascular prognosis (1-4), it is important to understand the physiological mechanisms underlying the various constituents of heart rate (5-11). Previously, we showed that RR interval (RR) sequences can be locally interpreted as a linear concatenation of transient, characteristically shaped subsequences, each with its own underlying physiology (10-15). Once recognized, specific RR subsequences can then be induced under controlled conditions so as to further study the underlying physiological, cellular and molecular processes (9-18). Ultimately, this approach facilitates physiological interpretation of RR subsequences in ambulatory heart rate recordings. One of the first RR subsequences described was an abrupt, transient, large-magnitude bradycardia (with associated hypotension) occurring in resting rabbits (5,11,15). Related responses have been noted in several mammalian species, including humans (19-22), and have generally been termed orienting or alerting responses. The association of transient bradycardia and hypotension suggested that this may be a model for human vasovagal syncope, which itself is characterized by transient bradycardia and hypotension (due to vasodepression). Indeed, the predominant finding in vasovagal syncope may be transient vasodepression, given that permanent pacing does not prevent syncopal spells (23). BACKGROUND: Transient bradycardic hypotensive events occur in resting rabbits. If the hypotension is due to vasodepression, these events may be a model for vasovagal syncope. OBJECTIVES: To determine whether these events are responses to brief stimuli and whether the hypotensive episodes are solely due to rapid-onset bradycardia. METHODS: Rabbits were instrumented with subcutaneous electrocardiogram leads, and cannulae were acutely inserted into an ear artery to obtain continuous arterial pressure measurements. Exposure to brief, low-level auditory stimuli at 5 kHz transiently increased the RR interval by approximately 70 ms and decreased mean arterial pressure by approximately 5 mmHg. RESULTS: These evoked bradycardic hypotensive events were almost identical to previously reported spontaneous bradycardic hypotensive events. Intra-aortic telemetric blood pressure monitoring was used to demonstrate that the evoked hypotension reflected prolonged diastole, rather than local ear arterial vasoconstriction. Furthermore, administration of the muscarinic blocker glycopyrrolate abolished not only bradycardia (RR interval 64±14 ms to 1±1 ms; P<0.0001), but also hypotension (-4.1±0.8 mmHg to -0.4±0.3 mmHg; P=0.0055). Finally, cardiac pacing abolished the inducible bradycardia (RR interval 51±10 ms to 2±1 ms; P=0.0006) and its associated hypotension (-4.1±0.7 mmHg to -1.2±0.3 mmHg; P=0.003). CONCLUSIONS: Brief auditory stimuli evoked a transient bradyc...

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Cutaneous vasoconstriction in conscious rabbits during alerting responses detected by hippocampal theta-rhythm

Cited by 50 publications

References 0 publications

Central mechanisms regulating coordinated cardiovascular and respiratory function during stress and arousal

Central mechanisms regulating coordinated cardiovascular and respiratory function during stress and arousal

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

Mechanism of hypotensive transients associated with abrupt bradycardias in conscious rabbits

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