The effects of loop excision of the transformation zone on cervical length: implications for pregnancy.

OBJECTIVE: This study was undertaken to determine whether previously described significant and quantitative cervical shortening caused by loop excision of the transformation zone persists after 3 months of healing. STUDY DESIGN: A prospective study was designed in which 20 patients were enrolled. Each underwent transvaginal ultrasonography for determination of cervical length before the loop excision of the transformation zone and >/=3 months after the loop excision of the transformation zone. Simple regression analysis and the Student paired t test was performed to determine whether the length of the cervix had changed significantly between the measurements. RESULTS: The mean cervical lengths as measured by transvaginal ultrasonography before and after loop excision of the transformation zone were 3.1 +/- 0.8 cm and 3.1 +/- 0.7 cm, respectively. The correlation between ultrasonographic measurements before and after loop excision of the transformation zone was r = 0.88 (P <.0001). A paired t test resulted in a P value of 1.0000, which indicates that the ultrasonographic measurement after loop excision of the transformation zone was not different from the ultrasonographic measurement before loop excision of the transformation zone. The mean difference between measurements was 0.0 +/- 0.4 cm. CONCLUSION: After adequate healing time after loop excision of the transformation zone, the length of the cervix, as measured by transvaginal ultrasonography, does not appear to remain shortened.

Annexin II inhibition of G protein-regulated inositol trisphosphate formation in rat aortic smooth muscle.

Vasoconstrictor hormones contribute to the pathogenesis of hypertension through intracellular signals that stimulate vascular smooth muscle (VSMC) contraction and/or growth. We previously showed that the glucocorticoid dexamethasone (DEX) inhibited angiotensin II-stimulated inositol trisphosphate (IP3) formation in VSMC, but the mechanism of inhibition is not known. Because glucocorticoids stimulate the expression of annexins and annexin II potently binds phosphoinositides, the role of DEX and annexin II in VSMC G protein-coupled phosphoinositide hydrolysis was investigated. DEX incubation blunted increases in guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S)-stimulated IP3 generation and angiotensin II-induced intracellular Ca2+ mobilization but stimulated elevations in VSMC annexin II content. VSMC incubation with exogenous purified annexin II resulted in concentration-dependent decreases in GTP gamma S-stimulated IP3 formation. In DEX-treated cells, exogenous annexin II did not further diminish GTP gamma S-stimulated IP3 formation, suggesting that endogenous annexin II may be a mediator of DEX-induced inhibition of G protein-coupled IP3 generation. These data represent the first direct evidence of G protein-dependent phosphoinositide hydrolysis regulation by glucocorticoids or annexins. We speculate that annexin II may play a role in the pathogenesis of hypertension through stimulation of VSMC growth.