Cardiovascular System Syphilis

Johnson, Sture A. M.; Jansen, G. Thomas; Shapiro, Herman H.

doi:10.1001/archderm.1954.01540240105011

Cited by 9 publications

(16 citation statements)

References 8 publications

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“…In fact, the myogenic response, also called Bayliss effect, is usually described as the increase/decrease in vessel tone in response to the increase/decrease of transmural pressure (3,15,21,52). It has been well characterized in vitro, in cannulated arterial segments subjected to sustained step changes in trans- mural pressure (13,15,21), while the rapid response to short-lasting changes has been comparatively less investigated.…”

Section: The Rapid Hyperemic Response To Brief Spontaneous Contractionsmentioning

confidence: 99%

“…It has been well characterized in vitro, in cannulated arterial segments subjected to sustained step changes in trans- mural pressure (13,15,21), while the rapid response to short-lasting changes has been comparatively less investigated. This is surprising if we consider that the first observation of the phenomenon by Sir William Bayliss was in fact a rapid blood flow increase in the hindlimbs in response to a brief occlusion of the abdominal aorta (3).…”

Section: The Rapid Hyperemic Response To Brief Spontaneous Contractionsmentioning

confidence: 99%

“…The myogenic response is known to be differently expressed by vessels belonging to different tissues and organs (21,30), as well as by the different segments of the same vascular bed (13,17). In this respect, a prominent myogenic reactivity is described for arterial and arteriolar segments of brain, skeletal muscle (5), and kidney while no explicit reference is usually made to skin blood vessels (30,39,40).…”

Section: The Rapid Hyperemic Response To Brief Spontaneous Contractionsmentioning

confidence: 99%

“…For the sake of clarity, it should be emphasized that we here refer to the rapid myogenic response that, as first reported by Bayliss, can be evoked in vivo by a short-lasting arterial occlusion in the form of a rapid (reactive) hyperemia (3,5,38). Different from the "classical" (slow) myogenic response, which develops over a period on the order of 1 min upon sustained changes in transmural pressure and which has been extensively studied and characterized in a variety of experimental conditions, the rapid myogenic response has received much less consideration (15,21) and is still poorly understood.However, a number of intrinsic limitations in the experimental models make the involvement of the mechanosensitive mechanisms in the contraction-induced hyperemia difficult to quantify. First of all, external compression of the forearm is not an unequivocal means to induce a myogenic response since the compression-induced depletion of venous compartments may contribute to the hyperemia according to the muscle pump mechanism (26,45).…”

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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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Section: The Rapid Hyperemic Response To Brief Spontaneous Contractionsmentioning

confidence: 99%

Section: The Rapid Hyperemic Response To Brief Spontaneous Contractionsmentioning

confidence: 99%

Section: The Rapid Hyperemic Response To Brief Spontaneous Contractionsmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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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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Observations on Penicillin Therapy in Cardiovascular Syphilis

Koulumies¹,

Heinivaara²

1957

Journal of Internal Medicine

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Pathophysiological basis of orthostatic hypotension in autonomic failure

Smit

Halliwill²,

Low

et al. 1999

The Journal of Physiology

321

209

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Patients with autonomic failure may be seriously incapacitated in activities of daily living due to orthostatic hypotension. Their low blood pressure is ascribed to a defective increase in arterial resistance and an excessive venous pooling upon standing. Effective pharmacological treatment is now available, but may aggravate supine hypertension and have other undesirable effects. Additionally, pharmacological treatment is less successful for hypotension with physical exercise or in warm surroundings (Bannister & Mathias, 1992). Non-pharmacological measures are regarded as a cornerstone in the treatment of orthostatic hypotension. These measures consist of chronic expansion of the extracellular volume or reducing the vascular volume in which pooling occurs (Bannister & Mathias, 1992). The latter includes protective measures like physical countermanoeuvres which can be applied by those patients with no major additional neurological and musculo-skeletal disorders, and external support garments which can be recommended to all patients. We reasoned that selection and use of appropriate protective measures would be facilitated by understanding the fundamental physiological mechanisms that prevent excessive orthostatic pooling in healthy subjects, why these mechanisms fail in patients with autonomic failure, and how these protective measures work. Therefore we reviewed the literature and summarized the available data about the amount and location of venous pooling in patients with autonomic failure and the effectiveness of physical countermanoeuvres and external support garments.

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Cardiovascular System Syphilis

Cited by 9 publications

References 8 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

Observations on Penicillin Therapy in Cardiovascular Syphilis

Pathophysiological basis of orthostatic hypotension in autonomic failure

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