The effects of propranolol on blood flow through gastroesophageal collaterals and on systemic and hepatic hemodynamics were investigated in 23 cirrhotic patients with portal hypertension. Gastroesophageal collateral blood flow was evaluated by the measurement of azygos venous blood flow by continuous thermal dilution. Azygos venous blood flow was markedly increased in these patients (544 +/- 48 ml per min, as compared with 132 +/- 18 ml per min in subjects without portal hypertension (p less than 0.001). Propranolol at doses achieving effective beta-blockage (83 +/- 5 mg) (mean +/- S.E.M.) markedly reduced azygos venous blood flow (to 354 +/- 34 ml per min, p less than 0.001). Reduction of azygos venous blood flow (-34.2 +/- 3.6%) was significantly greater (p less than 0.01) than reductions in cardiac output (-22.6 +/- 1.9%), hepatic venous pressure gradient (-11.5 +/- 2.4%) and hepatic blood flow (-13.4 +/- 7.4%). The hemodynamic effects of propranolol were not related to plasma norepinephrine levels. Reduction of gastroesophageal collateral blood flow may be the mechanism by which oral propranolol therapy reduces the risk of repeated episodes of variceal bleeding in cirrhotic patients with portal hypertension.
The pentaplex panel of mononucleotide repeats performs better than the NCI panel for the detection of mismatch repair-deficient tumors. Simultaneous assessment of the instability of BAT26 and NR24 is as effective as use of the pentaplex panel for diagnosing mismatch repair deficiency.
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