Abstract
It is generally believed that ASA absorption is greater in the duodenum than stomach, similar to related salicylates (Rainsford, 1984). The objective of this experiment was to evaluate the GI location and kinetics of ASA uptake in rats. ASA or saline (control, n=6/group) was intragastrically administered to fasted rats at a dose of 100 mg ASA/kg and the gastric body, antrum, and proximal duodenum were collected, extracted in acetonitrile and ASA and salicylic acid (SA) concs were examined by HPLC. The ASA conc (µg ASA/g tissue) at 15, 30 and 60 min for: the gastric body was 278 ± 46, 78 ± 9 and 104 ± 34; antrum were 308 ± 54, 95 ± 12 and 0±0; and duodenum were 34.5 ± 10.8, 6.6 ± 1.9 and 7.9 ± 2.3 respectively. The SA concentration (µg SA/g tissue) at 15, 30 and 60 minutes for: gastric body were 524 ± 33, 434 ± 35 and 236 ± 48; antrum were 572 ± 31, 433 ± 37, and 240 ± 50; and duodenum were 1,052.0 ± 125, 630 ± 75.1 and 408 ± 103, respectively. Serum ASA conc peaked at 15 min at 3.4 ± 0.5 µg/ml falling to undetectable levels thereafter, whereas serum SA reached Cmax at 15 and 30 min at 178 ± 8 µg/ml and 152 ± 22, respectively. Conclusion Significantly greater amount of ASA (>8 times) is absorbed in the stomach of rats vs duodenum at 15 and 30 min (p<0.05). In contrast, SA absorption was not significantly different in the stomach and proximal duodenum at 15 or 30 minutes. Serum ASA peaked at 15 min falling thereafter, whereas SA remained elevated at values 40-50-fold higher for at least 30 min. Thus contrary to belief that aspirin is predominately absorbed in the duodenum due to its large surface area, this data provides evidence that aspirin is predominately absorbed in the stomach, where ASA-induced GI injury predominantly occurs. Supported by NIDDK T35DK007676-21A1.
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