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Pathophysiology of post-prandial hypotension in patients with progressive autonomic failure. IV. Cerebral blood flow during post-prandial hypotension
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Abstracts'/Journal of the Autonomic Nervous System 50 (1995) 359-384
from progressive autonomic failure, similar to that reported by Fichefet et al. (1965). (The Autonomic Nervous System, 30 (1993) 524-529)
Pathophysiology of Post-Prandiai Hypotension in Patients with Progressive Autonomic Failure. IV. Cerebral Blood Flow during Post-Prandial Hypotension Masaaki Hirayama, Akito Kume, Takashi Katoh *, Yasuo Koike, Yuko Takeuchi, Shigeo Takeuchi and Akira Takahashi
Department of Neurology, Nagoya University School of Medicine, Nagoya 466, * Department of Radiology, Nagoya University School of Medicine, Nagoya 466, Japan Patients with autonomic failure commonly complain of syncope, dizziness and general fatigue in the sitting position during a meal or afterwards. To analyze cerebral blood flow after eating, we performed hemodynamic investigations after oral glucose ingestion in four patients with autonomic failure and multiple system atrophy. Blood pressure and heart rate were measured with an automatic sphygmomanometer; cardiac output and blood flow in the lower limb with impedance plethysmograpby; cerebral blood flow with positron emission tomography with H2LSO. Oral intake of 75 g of glucose in 225 ml water produced significant and prolonged hypotension for 60 rain with a moderate increase in heart rate, cardiac output and lower limb blood flow. During a 30rain period after the ingestion of glucose, cerebral blood flow decreased in parallel with the fall in blood pressure, but it recovered starting at about 45 rain, at a time when blood pressure reached a stationary level. These results suggest that the rapid reactive regulation of cerebral blood flow, which is probably brought about neurogenically, is damaged in patients with autonomic failure. However, the slow reactive regulation of cerebral blood flow that is apparently controlled by chemical factors is not involved. The reactions of cerebral blood flow and lower limb blood flow to glucose ingestion may be different. (The Autonomic Nervous System, 30 (1993) 530-534)
Pathophysiology of Post-Prandial Hypotension in Patients with Progressive Autonomic Failure. V. Comparative Study of Hemodynamic Responses to Protein and Glucose I~adings Toshiaki Ieda, Masaaki Hirayama, Yasuo Koike, Yuko Takeuchi, Nobuo Sakurai, Yasuhiro Hasegawa*, Shigetaka Hakusui ** and Akira Takahashi
Department of Neurology, Nagoya University School of Medicine, Nagoya 466, * Department of Neurology, Nagoya National Hospital, Nagoya 460, • * Department of Neurology, Nagoya Daini Red Cross Hospital, Nagoya 466, Japan
In patients with post-prandial hypotension, food components have a strong influence on hemodynamic responses. We investigated the role of proteins and glucose as inductive agents of postprandial hypotension in 17 patients (13 with autonomic failure with multiple system atrophy, two with pure autonomic failure, and two with autonomic failure with Parkinson's disease). A 75 g glucose-loading test with 300 kcal (in 14 out of 17 cases; mean age: 62 + 11) and an isocaloric protein test (in 8 out of 17 cases; mean age: 63 _+ 10) were performed on each subject on different days. Blood pressure and heart rate were monitored with an automatic sphygmomanometer; cardiac output and lower limb blood flow were measured with impedance plethysmography; and portal blood flow with a transcutaneous Doppler ultrasound method. Blood pressure decreased significantly from the baseline with both protein (P < 0.05) and glucose (P < 0.01) loading. The response to protein was significantly milder than that to glucose at 45 min. Cardiac output increased significantly at 45 rain. Both protein and glucose loading increased portal vein blood flow, but glucose was significantly more effective than protein. Increases in lower limb blood flow were observed only after glucose loading. In conclusion, post-prandial hypotension after protein loading in patients with autonomic failure is relatively mild because of the increased cardiac output, a minimal increase in portal vein blood flow and a decrease in lower limb blood flow.
Abstracts'/Journal of the Autonomic Nervous System 50 (1995) 359-384
from progressive autonomic failure, similar to that reported by Fichefet et al. (1965). (The Autonomic Nervous System, 30 (1993) 524-529)
Pathophysiology of Post-Prandiai Hypotension in Patients with Progressive Autonomic Failure. IV. Cerebral Blood Flow during Post-Prandial Hypotension Masaaki Hirayama, Akito Kume, Takashi Katoh *, Yasuo Koike, Yuko Takeuchi, Shigeo Takeuchi and Akira Takahashi
Department of Neurology, Nagoya University School of Medicine, Nagoya 466, * Department of Radiology, Nagoya University School of Medicine, Nagoya 466, Japan Patients with autonomic failure commonly complain of syncope, dizziness and general fatigue in the sitting position during a meal or afterwards. To analyze cerebral blood flow after eating, we performed hemodynamic investigations after oral glucose ingestion in four patients with autonomic failure and multiple system atrophy. Blood pressure and heart rate were measured with an automatic sphygmomanometer; cardiac output and blood flow in the lower limb with impedance plethysmograpby; cerebral blood flow with positron emission tomography with H2LSO. Oral intake of 75 g of glucose in 225 ml water produced significant and prolonged hypotension for 60 rain with a moderate increase in heart rate, cardiac output and lower limb blood flow. During a 30rain period after the ingestion of glucose, cerebral blood flow decreased in parallel with the fall in blood pressure, but it recovered starting at about 45 rain, at a time when blood pressure reached a stationary level. These results suggest that the rapid reactive regulation of cerebral blood flow, which is probably brought about neurogenically, is damaged in patients with autonomic failure. However, the slow reactive regulation of cerebral blood flow that is apparently controlled by chemical factors is not involved. The reactions of cerebral blood flow and lower limb blood flow to glucose ingestion may be different. (The Autonomic Nervous System, 30 (1993) 530-534)
Pathophysiology of Post-Prandial Hypotension in Patients with Progressive Autonomic Failure. V. Comparative Study of Hemodynamic Responses to Protein and Glucose I~adings Toshiaki Ieda, Masaaki Hirayama, Yasuo Koike, Yuko Takeuchi, Nobuo Sakurai, Yasuhiro Hasegawa*, Shigetaka Hakusui ** and Akira Takahashi
Department of Neurology, Nagoya University School of Medicine, Nagoya 466, * Department of Neurology, Nagoya National Hospital, Nagoya 460, • * Department of Neurology, Nagoya Daini Red Cross Hospital, Nagoya 466, Japan
In patients with post-prandial hypotension, food components have a strong influence on hemodynamic responses. We investigated the role of proteins and glucose as inductive agents of postprandial hypotension in 17 patients (13 with autonomic failure with multiple system atrophy, two with pure autonomic failure, and two with autonomic failure with Parkinson's disease). A 75 g glucose-loading test with 300 kcal (in 14 out of 17 cases; mean age: 62 + 11) and an isocaloric protein test (in 8 out of 17 cases; mean age: 63 _+ 10) were performed on each subject on different days. Blood pressure and heart rate were monitored with an automatic sphygmomanometer; cardiac output and lower limb blood flow were measured with impedance plethysmography; and portal blood flow with a transcutaneous Doppler ultrasound method. Blood pressure decreased significantly from the baseline with both protein (P < 0.05) and glucose (P < 0.01) loading. The response to protein was significantly milder than that to glucose at 45 min. Cardiac output increased significantly at 45 rain. Both protein and glucose loading increased portal vein blood flow, but glucose was significantly more effective than protein. Increases in lower limb blood flow were observed only after glucose loading. In conclusion, post-prandial hypotension after protein loading in patients with autonomic failure is relatively mild because of the increased cardiac output, a minimal increase in portal vein blood flow and a decrease in lower limb blood flow.