Autopsy data of 423 cases of primary tumor of the lung over a 36-year period were evaluated for the presence of gastrointestinal tract metastases. Fifty-eight cases (14%) were found and were analyzed for histologic nature of tumor, anatomic location, symptomatology and complications. The most common histologic type of lung tumor causing gastrointestinal tract metastasis was squamous cell (19 cases, 33%), followed by large cell (17 cases, 29%), and oat cell (11 cases, 19%). The esophagus was the most common site of involvement (33 cases). Fourteen of the 33 cases were involved by direct extension of the tumor. The middle third of the esophagus had metastases more commonly (16/33, 49%) than the other two sites. Most patients with gastrointestinal metastases had no symptoms. In those patients with symptoms, dysphagia was most common when the tumor involved the proximal gastrointestinal tract (esophagus, stomach), whereas, pain was most commonly seen with involvement of the distal gastrointestinal tract (small bowel, large bowel). Six of 20 patients (30%) with small bowel involvement experienced perforation and peritonitis as complications of metastatic involvement and two patients with large bowel metastasis had obstruction; a third had dehiscence of a previous anastomotic site. Gastrointestinal tract metastases from primary carcinoma of the lung are more common than previously thought and may be associated with serious clinical complications.

We have reported that short-term treatment of spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats with stannous chloride (SnCl 2 ), which selectively depletes renal cytochrome P4S0, restores blood pressure to normal in young but not in adult SHR, and is without effect on blood pressure of either young or adult WKY rats. We report in the present study that chronic treatment with SnCl 2 , begun at age 5 weeks, prevented the development of hypertension in SHR over a period of 15 weeks at which time they were killed. Suspension of SnCl 2 treatment after 8 weeks (i.e., at age 13 weeks) did not result in return of blood pressure to hypertensive levels in SHR. Age-matched WKY rats were not affected by tin treatment These findings provide additional evidence that administration of tin, which stimulates heme oxygenase, thereby producing depletion of cytochrome P450, restores blood pressure to normal levels in SHR. {Hypertension 1991;17:776-779) T he kidney, through its endocrine and excretory function, exerts a key role in the regulation of blood pressure. Prostaglandins and other arachidonic acid (AA) metabolites originating within the kidney participate in several mechanisms that can affect blood pressure by contributing to the regulation of extracellular fluid volume and renal hemodynamics. 1 ' 2 Of the variety of AA metabolites generated by the kidney, those arising from cytochrome P450-dependent monooxygenases also demonstrate the requisite biological activity to influence blood pressure. Several of these eicosanoids generated by a cytochrome P450 monooxygenase system operating intrarenally have been shown to affect vascular tone 3 ' 4 and to be capable of modulating Na + ,K + -ATPase activity. 56 To define possible relations between the renal cytochrome P450 system and regulation of blood pressure, we studied spontaneously hypertensive rats (SHR), the animal model most resembling human hypertension. In the SHR, renal Received September 21, 1990; accepted in revised form February 15, 1991. mechanisms are thought to play a decisive role in elevating blood pressure. 78 We have obtained evidence to support the hypothesis that eicosanoids generated by the renal cytochrome P450 system participate in the elevation of blood pressure. These renal metabolites are generated in increased amounts only by the young SHR, when compared with either the mature SHR or with age-matched normotensive Wistar-Kyoto (WKY) rats, during the developmental phase of hypertension from the fifth to the 13th week. 9 We have been able to restore blood pressure to normal levels in young 7-week-old SHR during the developmental stage of hypertension with short-term treatment with stannous chloride (SnCl 2 ). SnCl 2 induces heme oxygenase activity.10 Increased activity of heme oxygenase accelerates heme degradation, including that associated with cytochrome P450, thereby impairing the ability of the renal cytochrome P450 system to form eicosanoids 10 and, presumably, to metabolize other local and circulating hormones t...

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