渗透敏感机制与饮水所致增压反应有关

来源 :世界核心医学期刊文摘(神经病学分册) | 被引量 : 0次 | 上传用户:gf930
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Background: Water drinking elicits a sympathetically mediated pressor response in multiple-system atrophy patients through an unknown mechanism. We reasoned that gastrointestinal distention, hyposomotic stimulation, or both contribute to the water-induced pressor response. Methods: We compared the response to normal saline and water on blood pressure in 10 patients with probable multiple-system atrophy. Patients featured moderate to severe autonomic dysfunction. EKG and finger arterial blood pressure were recorded continuously, and 500 mL normal saline and distilled water were each given in a single-blinded fashion. Fluids were applied through a previously inserted nasogastric tube within a 5-minute period. Results: Blood pressure began to increase within 10 minutes after water administration and reached a maximum after 20 minutes. Blood pressure did not change after saline administration. The blood pressure change after 20 minutes was 8 ±9/2 ±5 mmHg with water and -1 ±11/-1 ±7 mmHg with normal saline administration (p = 0.02 between interventions). Heart rate did not change with either intervention. Conclusion: Ingestion of water elicits a greater pressor response than the ingestion of normal saline. Thus, gastric distention is probably not the crucial mechanisms for the water-induced pressor response. Instead, the response may be mediated through osmosensitive afferent structures in the gastrointestinal tract, portal vein, and liver. Background: Water drinking elicits a sympathetically mediated pressor response in multiple-system atrophy patients through an unknown mechanism. We reasoned that gastrointestinal distention, hyposomotic stimulation, or both contribute to the water-induced pressor response. Methods: We compared the response to normal saline and water on blood pressure in 10 patients with probable multiple-system atrophy. Patients with moderate to severe autonomic dysfunction. EKG and finger arterial blood pressure were recorded continuously, and 500 mL normal saline and distilled water were each given in a single-blinded fashion Fluids were applied through the previously inserted nasogastric tube within a 5-minute period. Results: Blood pressure began to increase within 10 minutes after water administration and reached a maximum after 20 minutes. Blood pressure did not change after saline administration. The blood pressure change after 20 minutes was 8 ± 9/2 ± 5 mmHg with water and -1 ± 11 / -1 ± 7 mmH Conclusion: Ingestion of water elicits a greater pressor response than the ingestion of normal saline. Thus, gastric distention is probably not the crucial mechanisms for the water-induced pressor response. Instead, the response may be mediated through osmosensitive afferent structures in the gastrointestinal tract, portal vein, and liver.
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