Interactions between behavior and the cardiovascular system.

Cohen, David H.; Obrist, Paul A.

doi:10.1161/01.res.37.6.693

Cited by 108 publications

(44 citation statements)

References 74 publications

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“…As can be seen in Figure 5, the QX-314 injection procedure produced only a transient increase in blood pressure and heart rate, similar to that observed after restraint or saline injection. Effects of varying levels of halothane anesthesia on the pressor response Since concomitant formalin-evoked behaviors could contribute to autonomic changes (Sokolov, 1963;Cohen and Obrist, 1975;Hilton and Redfern, 1986;Taylor et al, 1994) we next measured formalin-induced cardiovascular responses in the absence of behavioral activity, that is, in lightly-anesthetized animals. Table 1 illustrates that prepinch baseline arterial pressure [F(3,9) = 7.0, p < O.Ol] and heart rate [F(3,7) = 42.2, p < O.OOl] were inversely proportional to halothane concentration, as were preformalin arterial pressure and heart rate (p < 0.05).…”

Section: Formalin Dose Dependency Of Cardiovascular Responsesmentioning

confidence: 99%

Persistent cardiovascular and behavioral nociceptive responses to subcutaneous formalin require peripheral nerve input

1995

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Hindpaw injection of formalin produces acute (Phase 1) and persistent (Phase 2) nociceptive behaviors. This model has provided critical evidence supporting a contribution of central sensitization (hyperexcitability of spinal neurons) to the expression of persistent pain. Here, we evaluated the contribution of ongoing peripheral nerve inputs to Phase 2 pain responses. In addition to pain behavior (flinching), we measured formalin-evoked increases in arterial pressure and heart rate; these cardiovascular responses were also biphasic in nature. The arterial pressure response correlated highly with behavior, and was dependent on formalin concentration (0.625–5.0%), indicating that it was largely driven by noxious input. Lightly anesthetized (0.7% halothane) rats exhibited robust increases in blood pressure in the absence of pain behavior, indicating cardiovascular responses did not reflect somatomotor-cardiovascular coupling. Animals obtained from Charles River exhibited slightly larger Phase 2 flinching and heart rate responses compared to those obtained from Bantin and Kingman, suggesting cardiovascular-related pain responses can vary with the source of animal. We next evaluated the contribution of ongoing peripheral nerve activity to the expression of the Phase 2 pressor, tachycardia, and flinch responses. After Phase 1 subsided, but before Phase 2 began, we locally anesthetized the ipsilateral or contralateral (control) hindpaw with a hydrophilic lidocaine derivative, QX-314 (2%). Intraplantar QX-314 blocked Phase 2 pressor, tachycardia and behavioral responses only when injected into the paw that received formalin (2.5% or 10.0%). We conclude that persistent ongoing activity in peripheral afferent fibers during Phase 2 is required for the persistent pain evoked by formalin.

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Section: Formalin Dose Dependency Of Cardiovascular Responsesmentioning

confidence: 99%

Persistent cardiovascular and behavioral nociceptive responses to subcutaneous formalin require peripheral nerve input

1995

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“…A large body of data dealing with heart-rate alterations caused by psychological stress in higher vertebrates is available (see review by Cohen & Obrist, 1975), and even a cause-effect relationship between psychological factors and sudden cardiac death in man and animals has been suggested by some authors (Henry, 1973;Lown et al, 1977;Obrist et al, 1970) who seek new insights into cardiopathy by examining the role of the higher nervous system in chronotropic modifications of heart activity. The experimental paradigms used by most of the authors are concerned with chronic stress, or its effects, and include conditioning, avoidance tasks, anticipation (Cohen, 1974b;Cohen & Obrist, 1975;Gantt, 1960), maternal separation (Seiler et al, 1979), and social status (Candland, Bryan, Nazar, Kopf, & Sendor, 1970).…”

Section: Experimental Data From Vertebratesmentioning

confidence: 99%

“…The experimental paradigms used by most of the authors are concerned with chronic stress, or its effects, and include conditioning, avoidance tasks, anticipation (Cohen, 1974b;Cohen & Obrist, 1975;Gantt, 1960), maternal separation (Seiler et al, 1979), and social status (Candland, Bryan, Nazar, Kopf, & Sendor, 1970). The physiological meaning of heart arrests concomitant with startle could be absolutely different from that of cardiovascular adaptations over a period of hours or days.…”

Section: Experimental Data From Vertebratesmentioning

confidence: 99%

Behavioral determinants of severe cardiac inhibition

Cuadras

1981

Psychobiology

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“…It has also been claimed that increased reactivity to behavioral challenges such as mental arithmetic is more characteristic of hypertensive individuals than increased reactivity to physical challenges such as exercise. 9 The evidence of Ravogli et al 1 appears to refute both of these claims.…”

Section: G Pickeringmentioning

confidence: 96%

Inheritance of hypertension and blood pressure reactivity.

Pickering¹

1990

Hypertension

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A lthough there is general agreement that there / \ is a strong genetic component to essential A. \ -hypertension, it is not clear exactly what is inherited. A popular but largely unsubstantiated view is that sustained hypertension may be preceded by a period of increased reactivity to noxious stimuli. In this issue of Hypertension, Ravogli et al 1 provide important new data that help'to resolve this question. By using four different tests of blood pressure reactivity, they found that normotensive young adults with one or both parents hypertensive do not show any increased reactivity when compared with subjects with normotensive parents, although they did show slightly higher blood pressures during casual measurement and 24-hour monitoring, with a proportional increase in left ventricular mass.The reactivity hypothesis was first proposed more than 50 years ago by Hines and Brown, 2 who claimed that "prehypertensive" individuals show an exaggerated pressor response to a cold pressor test. In its stronger form, this hypothesis states that increased reactivity plays a causal role in the development of hypertension and that the repeated transient pressor episodes the increased reactivity engenders eventually lead to a sustained elevation of pressure. In its weaker form, the hypothesis proposes that the reactivity is merely a marker for future hypertension, without necessarily having any direct causal role.A recent review of 39 studies comparing reactivity in hypertensive and normotensive individuals concluded that although the majority do show an increased reactivity, it is by no means a universal finding.3 If it is accepted that the positive studies outweigh the negative ones, the question is raised as to whether the increased reactivity is a cause or a consequence of the hypertension.By studying individuals who are still normotensive but who have a family history of hypertension, it should be possible to answer this question. A review of studies of reactivity in subjects with and without a family history claimed that increased reactivity is typical of individuals with a positive family history,

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Interactions between behavior and the cardiovascular system.

Cited by 108 publications

References 74 publications

Persistent cardiovascular and behavioral nociceptive responses to subcutaneous formalin require peripheral nerve input

Persistent cardiovascular and behavioral nociceptive responses to subcutaneous formalin require peripheral nerve input

Behavioral determinants of severe cardiac inhibition

Inheritance of hypertension and blood pressure reactivity.

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