The influence of food on postural hypotension in three groups with chronic autonomic failure--clinical and therapeutic implications.

Mathias, C. J.; Holly, Elizabeth A.; Armstrong, Edward John Lloyd; Shareef, Miqdhaadh; Bannister, R.

doi:10.1136/jnnp.54.8.726

Cited by 60 publications

(34 citation statements)

References 18 publications

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“…This may have therapeutic implications, as drugs which have selective constrictor effects on this vascular bed may have a greater therapeutic value in preventing postural hypotension in autonomic failure patients. The major neural defect in splanchnic control observed in our patients may explain why postural change after food ingestion considerably enhances symptoms of postural hypotension in some patients with autonomic failure (Mathias, Holly, Armstrong, Shareef & Bannister, 1991). We conclude that in normal man sympatho-neural activation by pressor stimuli which raise blood pressure, or head-up tilt which maintains blood pressure, causes active constriction of the superior mesenteric artery.…”

Section: Discussionmentioning

confidence: 70%

Abnormality of superior mesenteric artery blood flow responses in human sympathetic failure.

Chaudhuri

Thomaides

Mathias

1992

The Journal of Physiology

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SUMMARY1. Systemic and regional haemodynamic responses, including superior mesenteric artery blood flow, were measured during stimuli which increase sympatho-neural activity in age-matched normal subjects (controls) and in two groups of patients with sympathetic failure (pure autonomic failure and multiple system atrophy). The stimuli included the pressor tests (mental arithmetic, cutaneous cold and isometric exercise) and head-up tilt.2. In the controls, the blood pressure did not rise in some during mental arithmetic, but rose in all subjects during cutaneous cold and isometric exercise and was maintained during head-up tilt. In sympathetic failure patients, blood pressure was unchanged during each pressor test and fell during head-up tilt.3. In the controls, superior mesenteric artery blood flow did not fall significantly during mental arithmetic but fell (with a corresponding rise in calculated superior mesenteric artery vascular resistance), during cutaneous cold, isometric exercise and head-up tilt. In sympathetic failure patients, there were no changes in superior mesenteric artery blood flow and vascular resistance during the pressor tests and head-up tilt.4. There were no changes in cardiac index or forearm blood flow during each pressor test in both controls and patients. Cardiac index fell and forearm vascular resistance rose during head-up tilt in the controls only.5. In conclusion, active constriction of the superior mesenteric artery occurs in normal subjects during sympatho-neural activation induced by stimuli such as cutaneous cold, isometric exercise and head-up tilt. This does not occur in patients with sympathetic failure and probably contributes to postural hypotension, emphasizing the role of the splanchnic vascular bed in overall blood pressure control. This study confirms the necessity of integrity of sympathetic pathways in the neural control of the splanchnic vascular bed.

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Section: Discussionmentioning

confidence: 70%

Abnormality of superior mesenteric artery blood flow responses in human sympathetic failure.

Chaudhuri

Thomaides

Mathias

1992

The Journal of Physiology

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“…In MSA with a presumed central lesion, the capacity to increase sympathoneural activity probably was compromised to a lesser extent than PAF, with a peripheral lesion. This has been demonstrated in comparative studies in relation to other hypotensive stimuli such as food challenge [32] and exercise [33] that induce hypotension in the supine position; each of these stimuli causes a greater fall in blood pressure in PAF when compared to MSA. This suggests that subjects with MSA have a greater ability than PAF to activate residual adrenergic or alternative pressor pathways, or respond through neurohormonal mechanisms, so as to prevent a marked fall in blood pressure in response to hypotensive stimuli.…”

Section: S Responses To Head-up Tiltmentioning

confidence: 88%

Haemodynamic responses during head-up tilt and tilt reversal in two groups with chronic autonomic failure: pure autonomic failure and multiple system atrophy

Chandler¹

2002

Journal of Neurology

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Continuous haemodynamic responses to head-up tilt (HUT) and its reversal were studied in 21 subjects with sympathetic denervation due to primary chronic autonomic failure; 10 had pure autonomic failure (PAF; peripheral failure) and 11 had multiple system atrophy (MSA; central failure); 8 healthy subjects (controls) also were studied. Supine systolic, diastolic and mean arterial pressure (MAP) and total peripheral resistance (TPR) were highest in PAF. The MAP response to HUT and tilt reversal were different between groups. After HUT, MAP increased in controls (12+/-4 mmHg), but decreased in PAF and MSA (41+/-4 & 19+/-4 mmHg respectively); the fall in PAF was greater than in MSA. With tilt reversal, MAP returned promptly, but not entirely to pretilt levels in controls, with small (insignificant) overshoots in MSA and PAF. The TPR response to HUT and tilt reversal was different between groups. After HUT, TPR increased in controls (0.31+/-0.04 PRU), decreased in PAF (0.23+/-0.1 PRU) and was unchanged in MSA. With tilt reversal, TPR remained elevated (15 %) above baseline in the controls and rose in PAF (13 %) with no change in MSA. There were no differences in supine heart rate (HR), stroke volume (SV) or cardiac output (CO) between the three groups; HR, SV or CO responses to HUT or tilt reversal also did not differ between the groups. Thus, after HUT, MAP decreased, with greater hypotension induced in PAF than MSA. Since CO did not differ between groups, the decrease in TPR appears to account for the greater fall in BP in PAF than in MSA. The elevated TPR at rest pre-tilt and after tilt reversal probably contributed to supine hypertension in PAF. These haemodynamic observations may aid therapeutic strategies to reduce orthostatic hypotension and prevent supine hypertension.

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“…6 numbers in each subgroup in the initial series of studies reported above, no clear differences were observed between the two major subgroups with primary chronic autonomic failure. Recent studies indicate that postprandial hypotension is often greater in pure autonomic failure, 32 and this may be related to higher levels of insulin after an identical food challenge. 30 In some patients with the ShyDrager syndrome, we have observed minimal postural hypotension when assessed premeal, with a greater and often symptomatic postural fall postmeal.…”

Section: Figure 11 Graph Shows Effect Of Subcutaneous (S-c) Insulin mentioning

confidence: 99%

“…30 In some patients with the ShyDrager syndrome, we have observed minimal postural hypotension when assessed premeal, with a greater and often symptomatic postural fall postmeal. 32 This is of importance in relation to the assessment of postural hypotension and in evaluating responses to treatment.…”

Section: Figure 11 Graph Shows Effect Of Subcutaneous (S-c) Insulin mentioning

confidence: 99%

The influence of food on postural hypotension in three groups with chronic autonomic failure--clinical and therapeutic implications.

Cited by 60 publications

References 18 publications

Abnormality of superior mesenteric artery blood flow responses in human sympathetic failure.

Abnormality of superior mesenteric artery blood flow responses in human sympathetic failure.

Haemodynamic responses during head-up tilt and tilt reversal in two groups with chronic autonomic failure: pure autonomic failure and multiple system atrophy

Postprandial hypotension. Pathophysiological mechanisms and clinical implications in different disorders.

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