Pathophysiology of postprandial hypotension in patients with progressive autonomic failure. Difference of cerebral blood flow during post-prandial hypotension between pure autonomic failure and multiple system atrophy

Pathophysiology of postprandial hypotension in patients with progressive autonomic failure. Difference of cerebral blood flow during post-prandial hypotension between pure autonomic failure and multiple system atrophy

130 Abstracts Department of Neurology, Nagoya National Hospital, Nagoya 460, *Department of Neurology, Nagoya Daini Red Cross Hospital, Nagoya 466, ...

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130

Abstracts

Department of Neurology, Nagoya National Hospital, Nagoya 460, *Department of Neurology, Nagoya Daini Red Cross Hospital, Nagoya 466, **Department of Neurology, Nagoya University School of Medicine, Nagoya 466, ***Japan Mutual Aid Association of Public School Teachers, Tokai Chuo Hospital, Gifu 504, Japan To assess the role of vasoactive intestinal substances such as peptides (neurotensin, somatostatin) and serotonin in post-prandial hypotension, we conducted a study on 11 patients with multiple system atrophy or Parkinson's disease and we compared the effect of oral glucose ingestion (75 g) with that of intravenous glucose infusion (25 g). Blood pressure significantly decreased after oral glucose loading, but not after intravenous glucose loading. Plasma concentrations of neurotensin and somatostatin rose significantly after oral glucose loading, but not after intravenous glucose loading. In contrast, no significant changes were found in pulse rate, plasma serotonin, norepinephrine, vasopressin, osmolality or hematocrit in the two groups. Although the increase in blood glucose level was higher with intravenous than with oral glucose loading, there was no significant difference in insulin increment between the two groups. These findings indicate that the hypotensive effect of glucose in patients with autonomic failure appears only after its oral ingestion, and that post-prandial hypotension is partly the result of glucose-dependent secretion of neurotensin.

(The Autonomic Nervous System, 31 (1994) 448-454)

Pathophysiology of Postprandial Hypotension in Patients with Progressive Autonomic Failure. Difference of Cerebral Blood Flow During Post-prandial Hypotension Between Pure Autonomic Failure and Multiple System Atrophy Masaaki Hirayama, Yasuo Koike, Akito Kume, Toshiaki Ieda, Takashi Katoh *, Kengo Itoh *, Mitsuru Ikeda ** and Akira Takahashi

Department of Neurology, Nagoya University School of Medicine, Nagoya 466, * Department of Radiology, Nagoya University School of Medicine, Nagoya 466, ** Department of Medical Information and Medical Record, Nagoya University Hospital, Nagoya 466, Japan Generally, patients suffering from pure autonomic failure (PAF) and multiple system atrophy (MSA) have severe autonomic failure. Patients with MSA commonly complain of syncope, dizziness and general fatigue in the sitting position during or after eating, and sudden death after eating is not rare. The prognosis is apparently favourable in patients with PAF, while the majority of patients with MSA die within about 5 years after onset. In order to

compare the pathophysiological difference in the autoregulation of cerebral blood flow between the two groups, we performed hemodynamic investigations during post-prandial hypotension (PPH) in five patients with MSA and three patients with PAF. Blood pressure and heart rate were measured with an automatic sphygmomanometer; cardiac output and leg blood flow with impedance plethysmography; and cerebral blood flow with positron emission tomography (PET) using H2~50. Blood pressure fell for 60 min in PPH. In the two groups of patients, the change in systemic blood pressure after a meal was not different, there was no increase in heart rate or cardiac output, and leg blood flow was elevated. In patients with MSA, cerebral blood flow fell within 30 min after eating, but then recovered, while the fall in blood pressure remained stationary. In patients with PAF, the cerebral blood flow was unchanged, while blood pressure fell as in MSA patients. In conclusion, autoregulation of cerebral blood flow may be impaired in MSA patients due to autonomic dysfunction, but not in PAF patients in which both baroreflex input and the central regulation system function normally.

(The Autonomic Nervous System, 31 (1994) 455-461)

The Effect of Aging on Blood Pressure Elevation in Response to Muscle Sympathetic Nerve Activity Yoshiki Sugiyama, Hisashi Okada, Takemasa Watanabe, Toshiyoshi Matsukawa, Satoshi Iwase and Tadaaki Mano

Research Institute of Environmental Medicine, Division of Higher Nervous Control, Department of Autonomic and Behavioral Neurosciences, Nagoya University, Nagoya 464-01, Japan The aim of this study was to clarify the effect of aging on blood pressure elevation in response to muscle sympathetic nerve activity (MSNA). We observed changes in heart rate, blood pressure wave by Finapress ~ and MSNA by microneurography during deep respiration at a frequency of 6 cycles per min for 200 s. All the variables showed short-term fluctuation over a period of 10 s. A cosine function with a cycle duration of 10 s was fitted to the observed data using the least square method. The latency from MSNA to diastolic blood pressure and the increasing rate of diastolic blood pressure to MSNA were calculated. The latency in the aged group was 7.0 + 0.4 s, significantly longer than in the young group (5.4 + 0.4 s). The reactivity in the aged group was 11.3 ___ 1.3 m m H g / V per s, significantly lower than in the young group (32.7 ___8.7 m m H g / V per s). These results suggest that the delayed and weaker response of the vessels to MSNA may contribute to the deterioration of regulatory functions of the cardiovascular system in the elderly.

(The Autonomic Nervous System, 31 (1994) 462-467)