Posthæmorrhagic Fainting

Barcroft, H.; Edholm, O. G.; McMichael, J.; Sharpey‐Schafer, E. P.

doi:10.1016/s0140-6736(00)74173-0

Cited by 262 publications

(34 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…was measured along the time tracing from the point at which it was cut by the sloping line. The [Lewis, 1924] 13,20,25,30,32,35,38,40,, and 450 C. 0…”

Section: Methodsmentioning

confidence: 99%

The effect of temperature on blood flow and deep temperature in the human forearm

Barcroft¹,

Edholm²

1943

The Journal of Physiology

298

117

View full text Add to dashboard Cite

“…was measured along the time tracing from the point at which it was cut by the sloping line. The [Lewis, 1924] 13,20,25,30,32,35,38,40,, and 450 C. 0…”

Section: Methodsmentioning

confidence: 99%

The effect of temperature on blood flow and deep temperature in the human forearm

Barcroft¹,

Edholm²

1943

The Journal of Physiology

298

117

View full text Add to dashboard Cite

“…Some studies have suggested that the vasodilatation seen in neurally mediated syncope results from a withdrawal of sympathetic tone (14)(15)(16). Consistent with this view, there is evidence of reduced cardiac and renal norepinephrine (NorEpi) 1 spillover in patients who fainted during cardiac catheterization (17).…”

Section: Introductionmentioning

confidence: 99%

Sympathetic and baroreceptor reflex function in neurally mediated syncope evoked by tilt.

et al. 1997

View full text Add to dashboard Cite

The pathophysiology of neurally mediated syncope is poorly understood. It has been widely assumed that excessive sympathetic activation in a setting of left ventricular hypovolemia stimulates ventricular afferents that trigger hypotension and bradycardia. We tested this hypothesis by determining if excessive sympathetic activation precedes development of neurally mediated syncope, and if this correlates with alterations in baroreflex function. We studied the changes in intraarterial blood pressure (BP), heart rate (HR), central venous pressure (CVP), muscle sympathetic nerve activity (MSNA), and plasma catecholamines evoked by upright tilt in recurrent neurally mediated syncope patients (SYN, 5 Ϯ 1 episodes/mo, n ϭ 14), age-and sex-matched controls (CON, n ϭ 23), and in healthy subjects who consistently experienced syncope during tilt (FS ϩ , n ϭ 20). Baroreflex responses were evaluated from changes in HR, BP, and MSNA that were obtained after infusions of phenylephrine and sodium nitroprusside. Compared to CON, patients with SYN had blunted increases in MSNA at low tilt levels, followed by a progressive decrease and ultimately complete disappearance of MSNA with syncope. SYN patients also had attenuation of norepinephrine increases and lower baroreflex slope sensitivity, both during tilt and after pharmacologic testing. FS ϩ subjects had the largest decrease in CVP with tilt and had significant increases in MSNA and heart rate baroreflex slopes. These data challenge the view that excessive generalized sympathetic activation is the precursor of the hemodynamic abnormality underlying recurrent neurally mediated syncope. ( J. Clin. Invest. 1997. 99:2736-2744.)

show abstract

“…However, with a severe haemorrhage a second pattern of response becomes evidentnamely a bradycardia and a vasodilatation, leading to a fall in blood pressure and syncope (Barcroft, Edholm, McMichael & Sharpey-Schafer, 1944). This depressor response may be the result of a reflex arising from the heart (Evans, Ludbrook & Potocnik, 1989) due to an activation of cardiac C fibre afferents carried in the vagus (Oberg & Thoren, 1972).…”

Section: Introductionmentioning

confidence: 99%

Attenuation of the Acute Cardiovascular Responses to Haemorrhage by Tissue Injury in the Conscious Rat

1989

View full text Add to dashboard Cite

SUMMARYA moderate haemorrhage of 0-75 + 0-09 ml (100 g body weight)-1 (I 111 + 1-3 % of estimated blood volume) in the conscious rat produces a tachycardia, possibly mediated by the baroreflex, which serves to maintain mean arterial blood pressure. A severe haemorrhage of 120 + 006 ml (100 g)-1 (> 195 + 1[5 % of estimated blood volume) produces a bradycardia and mnarked hypotension. The bradycardia is reflex in nature and is due to an increased vagal efferent activity to the heart. This bradycardia is markedly attenuated in animals treated neonatally with capsaicin to render them deficient in C fibres, suggesting that peripheral C fibres (possibly cardiac C fibre afferents, Oberg & Thoren, 1972) are of importance in the bradycardic response to a severe haemorrhage. Concomitant tissue injury produced by bilateral hindlimb ischaemia in a group of animals with normal C fibre afferents markedly attenuates or abolishes the bradycardia and reduces the fall in mean arterial blood pressure produced by severe haemorrhage, although the tachycardia seen with smaller haemorrhages is affected to a much lesser degree. It is concluded that tissue injury can modify the cardiovascular response to a severe haemorrhage, possibly by interacting with the reflex effects of stimulating cardiac C fibre afferents.

show abstract

Posthæmorrhagic Fainting

Cited by 262 publications

References 9 publications

The effect of temperature on blood flow and deep temperature in the human forearm

The effect of temperature on blood flow and deep temperature in the human forearm

Sympathetic and baroreceptor reflex function in neurally mediated syncope evoked by tilt.

Attenuation of the Acute Cardiovascular Responses to Haemorrhage by Tissue Injury in the Conscious Rat

Contact Info

Product

Resources

About