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BACKGROUND: Management of malignant renal tumors involving the inferior vena cava (IVC) depends on tumor extension within the cava. METHODS: Of 295 patients treated for renal cancer, propagation of tumor mass through the renal vein to IVC was seen in 22 (7%) patients. Cephalad extension of the tumor was suprarenal: infrahepatic in 12, retrohepatic in 6, and within the right atrium in 4 patients. All patients had radical nephrectomy, cavotomy, and complete resection of tumors except I with diffuse peritoneal metastasis. RESULTS: Twenty-one patients had curative resections. No operative deaths and no instances of pulmonary embolism or exsanguination occurred. Seventeen patients were alive at 2 years and 12 at 5 years, resulting in 77% and 55% survival rates, respectively. CONCLUSIONS: An aggressive approach for vena cava involvement from malignant renal neoplasms resulted in prevention of tumor embolus, minimization of blood loss, and maintenance of venous return to the heart. Am J Surg. 1998; 176:137-139. [C] 1998 by Excerpta Medica, Inc.

Thoracic trauma Trauma Equipment* Nondrug Cervical collar (semirigid, such as Philadelphia) or sandbags with tape immobilization of head Cervicothoracic orthosis Endotracheal tube Flexible bronchoscope Foley catheter IV catheters (large-bore) Nasogastric [...]

The effects of hypoxia-reoxygenation on internal mammary (IMA) and radial (RA) arteries used for coronary artery bypass grafting (CABG) were examined to identify mechanisms regulating contractile function and differences that could contribute to vasospasm. Isolated endothelium-intact IMA and RA rings precontracted with KCl (30 mM) rapidly dilated to hypoxia (95% N(2)/5% CO(2)) with a greater relaxation in RA than IMA. Inhibitors of cyclooxygenase (10 microM indomethacin) and the thromboxane A(2) (TxA)(2) receptor [1 microM [1S-[1alpha,2alpha(Z),3alpha,4alpha]]-7-[3-[2-(phenylamino)carbonyl]hydrazine]methyl]-7-oxabicyclo[2.2.1]hept-2-yl]-5-heptenoic acid (SQ-29548)] potentiated the relaxation to hypoxia in IMA, but not RA, a response associated with increases in TxA(2). Relaxation of IMA and RA to hypoxia appears to involve a calcium-reuptake mechanism inhibited by cyclopiazonic acid (0.2 mM), and it was not attenuated by a blocker of potassium channels (10 mM TEA). The recovery of force generation of IMA, but not RA, upon reoxygenation after 30 min of hypoxia was significantly reduced in the initial phase of reoxygenation by indomethacin and SQ-29548 and by endothelin receptor blocker BQ-123 [cyclo(l-Leu-d-Trp-d-Asp-l-Pro-d-Val)]. Thus, hypoxia relaxes IMA and RA by a prostaglandin-independent mechanism potentially involving enhanced intracellular calcium reuptake. The prostaglandin-mediated alterations of responses to hypoxia-reoxygenation seen in IMA, but not in RA, may predispose IMA to vasospasm-related complications of CABG.