A new electric sphygmomanometer.
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Biomedical subjects
Publications and source records attributed to G Gomez.
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The purpose of this study was to characterize the effect of peptide YY (PYY) on acid-stimulated pancreatic bicarbonate secretion and to determine whether PYY affects the release of secretin in response to intraduodenal infusion of acid. Six dogs were prepared with gastric and pancreatic cannulas. In study 1, graded doses of hydrochloric acid (HCl) (3, 6, 12, and 24 mEq/h) were given intraduodenally alone or in combination with intravenous PYY (400 pmol/kg.h). In study II, and ED50 of intraduodenal HCl (6 mEq/h) was given alone or in combination with graded doses of PYY (12.5, 25, 50, 100, 200, and 400 pmol/kg.h, i.v.). Bicarbonate output was significantly inhibited during PYY infusion at 200 and 400 pmol/kg.h, but plasma secretin levels were unchanged. The calculated maximal response for bicarbonate secretion (5.1 +/- 1.3 mEq/15 min) was significantly reduced by PYY (2.1 +/- 0.7 mEq/15 min). We concluded that PYY can inhibit acid-stimulated pancreatic bicarbonate secretion without affecting the release of secretin. The mechanism of the inhibitory effect of PYY on acid-stimulated pancreatic bicarbonate secretion is compatible with a noncompetitive type of inhibition.
Release of neurotensin from the small intestine in response to administration of fat directly into the duodenum and ileum was examined in conscious dogs. The present results show that: (1) intraduodenal administration of fat causes a diphasic release of neurotensin which is mediated, at least in part, by cholinergic mechanisms, and (2) both a fatty acid (sodium oleate) and a triglyceride, when infused directly into an isolated ileal loop, stimulate a significant release of neurotensin. Our findings indicate that release of neurotensin is triggered by mechanisms originating in the proximal small intestine and by a direct contact of nutrients with the ileal mucosa.
BACKGROUND: Percutaneous transluminal treatment of a thrombotic vein graft yields poor results. We have previously reported our experience with transluminal percutaneous coronary ultrasound thrombolysis (CUT) in the setting of acute myocardial infarction (AMI). This report describes the first experience with ultrasound thrombolysis in thrombus-rich lesions in saphenous vein grafts (SVGs), most of which were occluded. METHODS AND RESULTS: The patients (n=20) were mostly male (85%), aged 64+/-4 years old. The presenting symptom was AMI in 2 patients (10%) and unstable angina in the rest. Fifteen patients (75%) had totally occluded SVGs. The median age of clots was 6 days (range, 0 to 100 days). The ultrasound thrombolysis device has a 1.6-mm-long tip and fits into a 7F guiding catheter over a 0.014-in guidewire in a "rapid-exchange" system. CUT (41 kHz, 18 W, </=6 minutes) led to device success in 14 (70%) of the patients and residual stenosis of 65+/-28%. Procedural success was obtained in 13 (65%) of the patients, with a final residual stenosis of 5+/-8%. There was a low rate of device-related adverse events: 1 patient (5%) had a non-Q-wave myocardial infarction, and distal embolization was noted in 1 patient (5%). Adjunct PTCA or stenting was used in all patients. There were no serious adverse events during hospitalization. CONCLUSIONS: Ultrasound thrombolysis in thrombus-rich lesions in SVGs offers a very promising therapeutic option.
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