How Should Human Baroreflexes Be Tested?

Eckberg, D. L.; Fritsch, JM

doi:10.1152/physiologyonline.1993.8.1.7

Cited by 40 publications

(53 citation statements)

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“…The carotid baroreceptor-cardiac reflex responses in the present study could be produced by vagal mechanisms (Eckberg 1993;Fritsch et al 1991) because the duration of the neck pressure ramp was brief (<15 s) and the baroreceptors were stressed with the beat-by-beat stimulus. It is possible that the decrease in vagal tone in the hyperthermic condition reduces the tachycardia response capacity and exaggerates the bradycardia response capacity.…”

Section: Discussionmentioning

confidence: 77%

“…Stimulation of these receptors increases their afferent input to the cardiovascular centers and decreases HR via reduced sympathetic and increased parasympathetic nerve activities. The carotid baroreceptor-cardiac response has been evaluated noninvasively in humans from the beatto-beat HR responses to a change in carotid arterial pressure by application of negative or positive pressures with a neck chamber (Eckberg 1993;Eckberg et al 1992;Fritsch et al 1991). This method can be applied for examination of the effects of hyperthermia on the carotid baroreceptor-cardiac response.…”

Section: Introductionmentioning

confidence: 99%

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Effects of acute hyperthermia on the carotid baroreflex control of heart rate in humans

Yamazaki

Sagawa

Torii

et al. 1997

International Journal of Biometeorology

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The purpose of this study was to examine the effect of hyperthermia on the carotid baroreceptor-cardiac reflexes in humans. Nine healthy males underwent acute hyperthermia (esophageal temperature -38.0 degrees C) produced by hot water-perfused suits. Beat-to-beat heart rate (HR) responses were determined during positive and negative R-were-triggered neck pressure steps from +40 to -65 mm Hg during normothermia and hyperthermia. The carotid baroreceptor-cardiac reflex sensitivity was evaluated from the maximum slope of the HR response to changes in carotid distending pressure. Buffering capacity of the HR response to carotid distending pressure was evaluated in % from a reference point calculated as (HR at 0 mm Hg neck pressure-minimum HR)/HR range x 100. An upward shift of the curve was evident in hyperthermia because HR increased from 57.7 +/- 2.4 beats/min in normothermia to 88.7 +/- 4.1 beats/min in hyperthermia (P < 0.05) without changes in mean arterial pressure. The maximum slope of the curve in hyperthermia was similar to that in normothermia. The reference point was increased (P < 0.05) during hyperthermia. These results suggest that the sensitivity of the carotid baroreflex of HR remains unchanged in hyperthermia. However, the capacity for tachycardia response to rapid onset of hypotension is reduced and the capacity for bradycardia response to sudden hypertension is increased during acute hyperthermia.

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Section: Discussionmentioning

confidence: 77%

Section: Introductionmentioning

confidence: 99%

Effects of acute hyperthermia on the carotid baroreflex control of heart rate in humans

Yamazaki

Sagawa

Torii

et al. 1997

International Journal of Biometeorology

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“…The Oxford method was used to test baroreflex sensitivity (BRS) (6,37). This method involved reflex changes in HR in response to randomized 0.3-ml bolus injections of phenylephrine (1.5-3 g/kg) or sodium nitroprusside (2-5 g/kg) over 10 s. To derive BRS, a least squares linear regression was fit to R-R interval change in response to ramp changes in SBP induced by phenylephrine and sodium nitroprusside.…”

Section: Methodsmentioning

confidence: 99%

Mechanism of cardioventilatory coupling: insights from cardiac pacing, vagotomy, and sinoaortic denervation in the anesthetized rat

Tzeng¹,

Larsen²,

Galletly³

2007

American Journal of Physiology-Heart and Circulatory Physiology

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Cardioventilatory coupling (CVC), a temporal alignment between the heartbeat and inspiratory activity, is a major determinant of breath-to-breath variation in observed respiratory rate (fo). The cardiac-trigger hypothesis attributes this to adjustments of respiratory timing by baroreceptor afferent impulses to the central respiratory pattern generator. A mathematical model of this hypothesis indicates that apparent CVC in graphical plots of ECG R wave vs. inspiratory time is dependent on the heart rate (HR), the rate of the intrinsic respiratory oscillator (f i), and the strength of the hypothetical cardiovascular afferent impulse. Failure to account for HR and fi may explain the inconsistent results from previous attempts to identify the neural pathways involved in CVC. Cognizant of these interactions, we factored in the HR-to-fi ratio in our examination of the role of the vagus nerve and arterial baroreceptors in CVC by cardiac pacing 29 anesthetized Sprague-Dawley rats and incrementally changing the HR. With the assumption of a relatively constant fi, CVC could be examined across a range of HR-to-fo ratios before and after vagotomy, sinoaortic denervation, and vagotomy ϩ sinoaortic denervation. We confirmed the relation between CVC, HR-to-f o ratio, and breath-to-breath respiratory period variability and demonstrated the loss of these relations after baroreceptor elimination. Sham experiments (n ϭ 8) showed that these changes were not due to surgical stress. Our data support the notion that inspiratory timing can be influenced by cardiac afferent activity. We conclude that the putative cardiovascular input arises from the arterial baroreceptors and that the vagus nerve is not critical for CVC. respiratory period variability; respiratory rhythm; arterial baroreceptors; cardiorespiratory synchronization CARDIOVENTILATORY COUPLING (CVC) is a temporal alignment between the heartbeat and inspiratory activity (11-14, 28 -30, 34, 42). Clinical studies show that CVC is a major determinant of breath-to-breath respiratory period variability, and a "cardiactrigger hypothesis" has been proposed to explain the experimental data. It has been hypothesized that CVC reflects breathto-breath adjustments of respiratory timing by afferent impulses to the central respiratory pattern generator arising from the arterial baroreceptors (12,13,26). This hypothesis is supported by modeling studies (13,26,34), as well as experimental observations of CVC under conditions where heart rate (HR) is largely independent of efferent neural modulation, for example, during fixed-rate cardiac pacing (21), in the presence of an artificial pulsatile circulation (1), and during atrial fibrillation (28). It has also been shown that the most consistent relation between inspiration and the heartbeat is the interval between inspiratory onset (I) and the immediately preceding ECG R wave (RI Ϫ1 interval) (28,42). Taken together, these observations suggest that CVC most likely reflects a "triggering" of inspiration by the heartbeat and accounts for the us...

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“…Vagal baroreflex relations were provoked by a stereotyped sequence of 0.6 s pulses of neck pressure and suction (ranging from 40 to -65 mmHg), triggered by successive electrocardiographic R-waves (Eckberg and Fritsch 1993). The upper panel of Fig.…”

Section: Quantifying Reflex Responsivenessmentioning

confidence: 99%

Arterial Baroreflexes and Cardiovascular Modeling

Eckberg

2007

Cardiovasc Eng

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Many cardiovascular models involve prediction of changes that occur when a subject is perturbed in some way, to move from one state to another. A successful, predictive model should involve at least two elements: First, the model should include some index of the intensity of the perturbation that elicits the response; effective responses should, in some fashion, be linearly or nonlinearity related to perturbations. Second, the model should factor in subjects' abilities to meet the challenges posed by the perturbations. This review indicates that these two basic components of a successful model may be difficult to incorporate. In the simple case of passive upright tilt, blood pressure measurements may not accurately indicate the stimulus, because blood pressure reductions are reversed by rapidly occurring reflex blood pressure increases. Since not all subject populations respond identically to hemodynamic challenges, it also may be important to characterize baroreflex responsiveness, and include such a term in a model. Although vagal and sympathetic baroreflex responses to stereotyped challenges can be measured accurately, recent research points to extraordinary variability of baroreflex responsiveness. The complexities discussed in this review should be considered, whether they are, or even can be incorporated into cardiovascular models.

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How Should Human Baroreflexes Be Tested?

Cited by 40 publications

References 0 publications

Effects of acute hyperthermia on the carotid baroreflex control of heart rate in humans

Effects of acute hyperthermia on the carotid baroreflex control of heart rate in humans

Mechanism of cardioventilatory coupling: insights from cardiac pacing, vagotomy, and sinoaortic denervation in the anesthetized rat

Arterial Baroreflexes and Cardiovascular Modeling

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