Lymphoreticular cells in invasive carcinoma of the uterine cervix: an immunohistological study.

In the present study the immunohistology of the cellular stromal reaction of invasive squamous cell carcinoma of the cervix is investigated. Tumor tissue from 10 patients with invasive squamous cell carcinoma of the uterine cervix (stages Ib-IIb, according to FIGO) was immunostained by the alkaline phosphatase-anti-alkaline phosphatase (APAAP) method. The monoclonal antibodies OKT3, OKT4, OKT8, TO15, Ki-M1, and Ki-M6 were applied. The cells in the stroma and the tumor foci were evaluated separately. In all cases, the overwhelming majority of lymphoreticular cells were found in the stroma and the tumor-cell complexes contained relatively low numbers of these cells. While B-lymphocytes were present only in low numbers or were virtually absent from the lymphoreticular infiltrates, cells of the mononuclear-phagocyte system were found to be another prominent constituent of the tumor's cellular stromal reaction.     

Sodium nitroprusside potentiates the depressor response to the phosphodiesterase inhibitor zaprinast in rats

To determine if the presence of an activator of guanylate cyclase alters the depressor response to a selective inhibitor of low Km cyclic GMP (cGMP) phosphodiesterase (PDE), zaprinast (3-30 mg/kg) was given i.v. to conscious, spontaneously hypertensive rats during a steady state of i.v. infusion of sodium nitroprusside (15 micrograms/kg per min). Sodium nitroprusside significantly increased the magnitude of the depressor response to zaprinast. In contrast, fenoldopam (20 micrograms/kg per min), an activator of adenylate cyclase, did not affect the depressor response to zaprinast. Zaprinast (10 mg/kg) significantly decreased mean arterial pressure (MAP) in rats given an infusion of sodium nitroprusside, an activator of soluble guanylate cyclase, at doses of 15 and 25 micrograms/kg per min but not at a dose of 5 micrograms/kg per min. However, in rats given atrial natriuretic peptide (ANP; 0.5, 1 and 2 micrograms/kg per min), an activator of particulate guanylate cyclase, zaprinast (10 mg/kg) did not affect MAP. In contrast to the potentiation of the depressor response to zaprinast, sodium nitroprusside (15 micrograms/kg per min) significantly attenuated the reductions in MAP produced by CI-930, a selective inhibitor of low Km cAMP PDE. It is concluded that sodium nitroprusside, but not ANP or fenoldopam, potentiates the depressor response to zaprinast. Furthermore, the potentiation of the depressor response to zaprinast is dependent upon the dose of sodium nitroprusside and is selective for zaprinast; the depressor response to CI-930 is attenuated by sodium nitroprusside.