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1. Rabbits in balance on a low sodium diet were given doses of sodium chloride either orally or intravenously. 2. Those receiving oral doses responded with a much greater natriuresis than those receiving intravenous ones. 3. This could be explained by the existence of a sodium input monitor somewhere in the gut or portal circulation.

1. Dietary sodium reduction in man is followed by rapid conservation of sodium by the kidneys. The rapidity of this response suggests that the gastrointestinal tract is involved in early recognition of changes in sodium intake or in mediation of the compensatory response. 2. In order to test the hypothesis, 100 mmol of sodium was given to normal volunteers in balance on a low-sodium diet (5 mmol/24 h): the dose was given either orally or intravenously. 3. Those who received their sodium orally excreted it more rapidly than those who received it intravenously and the difference was most marked in the first 8 h after the dose. 4. This finding is consistent with the presence of an input receptor for sodium in the gastrointestinal tract.

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An intravenous infusion of 40 mg of recombinant tissue-type plasminogen activator (t-t-PA) was given intravenously over 90 minutes to 123 patients with acute myocardial infarction (AMI) of less than 4 hours' duration. A coronary angiogram was recorded at the end of the infusion in 119 patients. Central assessment of the angiograms revealed a patent infarct-related artery in 78 patients (patency rate 66%, 95% confidence limits 57 to 74%). Patients with a patent infarct-related artery at the first angiogram were randomized in a double-blind manner to receive a subsequent B-hour infusion of either 30 mg of rt-PA or placebo. All patients had received an initial bolus of 5,000 IU of heparin and then 1,000Ill/hour until a second angiogram was recorded 6 to 24 hours after the start of the second perfusion. At central assessment of the second coronary angiogram the reocclusion rate was 2 of 36 patients who received II-PA at the second infusion and 3 of 37 patients not receiving this drug (or the 2 groups combined 7%, 95% confidence limits 2 to 15%). Three of 60 patients (5%, 95 % confidence limits 1 to 14 % ) with patent arteries on both previous angiograms had a later occlusion as judged on the angiogram recorded at hospital discharge.No difference in late reocclusion rates between the 2 treatment groups was observed.( Am J Cardiol 1987;60:231-237) A cute coronary thrombolysis with recombinant human tissue-type plasminogen activator (rt-PA] has been shown to be practicable and effective,*-5 but uncertainty persists about the most effective dosage schedule, both in terms of total dosage and distribution in timeeG To be clinically relevant, thrombolysis requires not only early recanalization, but also long-term maintenance of patency of the infarct-related artery. Different studies have shown widely varying rates of coronary reocclusion during the first hours or days after thrombolysis as documented by repeat angiography.7-2J The present trial was performed to determine the early and late predischarge reocclusion rates after patency of the infarct-related artery had been shown by coronary angiography in patients with acute myocardial infarction [AMI) treated with intravenous rt-PA. Because reocclusion was reported to occur within 1 hour after cessation of the rt-PA infusion6 an early repeat catheterization was planned at the end of the second infusion: 6 hours after start of the second infusion, the latest after 24 hours. A second aim was to assess whether a continued infusion with rt-PA over 6 hours could prevent early and late reocclusion and further reduce residual stenosis as measured by quantitative coronary angiography. The results of the quantitative angiography, performed with a computer-assisted cardiovascular angiography analysis system (CAAS], are reported separately.25 Methods Patients and management:Inclusion and exclusion criteria were the same as for the first 2 European 231