Background: The doubling times of liver metastases were calculated in order to clarify their usefulness in predicting the presence of residual cancer in the abdominal cavity in patients who had undergone curative resection of primary colorectal cancer. Patients and Methods: Tumor doubling times were calculated retrospectively in 22 patients by serial measurement of the size of their liver metastases. Results: Patients with a tumor doubling time of less than 92.4 days had a significantly poorer prognosis than those with a doubling time more than or equal to 92.4 days (p < 0.05). Local recurrence or peritoneal dissemination was significantly more likely to occur when the tumor doubling time was less than 92.4 days than when it was more than or equal to 92.4 days (p < 0.01). Conclusion: The doubling time of hepatic metastases in patients with colorectal carcinoma may be a useful prognostic indicator, with patients who have a shorter tumor doubling time carrying a greater risk of residual primary cancer in the abdominal cavity.
The effect of metoclopramide, a dopamine blocker, on arginine vasopressin (AVP) secretion was investigated in normal males. After a bolus injection of metoclopramide (10 mg), all subjects (n = 7) demonstrated an increase of 80.3% (from 0.71 +/- 0.12 (Mean +/- S.E.) to 1.28 +/- 0.24 pg/ml, P less than 0.005) in plasma AVP at 15 min. In controls (n = 7) plasma AVP levels did not change after saline injection (2 ml). Because plasma osmolality and blood pressure did not change, the elevation of plasma AVP levels induced by treatment with metoclopramide may be due to its central effect as a dopamine inhibitor. Although plasma AVP levels increased again at 90 and 120 min after a bolus injection of metoclopramide, accompanying falls in blood pressure (4-5%) make the interpretation concerning the contribution of dopamine to AVP secretion in a late phase uncertain. In summary, plasma AVP levels were shown to be significantly increased by a metoclopramide bolus, suggesting that AVP secretion is under tonic inhibition by dopamine.
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