GONADOTROPIN-RELEASING-HORMONE AGONIST THERAPY REDUCES POSTOPERATIVE ADHESION FORMATION AND REFORMATION AFTER ADHESIOLYSIS IN RAT MODELS FOR ADHESION FORMATION AND ENDOMETRIOSIS
Ja. Wright et Kl. Sharpetimms, GONADOTROPIN-RELEASING-HORMONE AGONIST THERAPY REDUCES POSTOPERATIVE ADHESION FORMATION AND REFORMATION AFTER ADHESIOLYSIS IN RAT MODELS FOR ADHESION FORMATION AND ENDOMETRIOSIS, Fertility and sterility, 63(5), 1995, pp. 1094-1100
Objectives: To evaluate the effectiveness of GnRH agonist (GnRH-a) the
rapy on adhesion formation and reformation in established rat models f
or surgically induced adhesion formation and endometriosis. Design: Be
fore surgery, female Sprague-Dawley rats were injected with GnRH-a or
control diluent. Six days later, rats were assigned to one of four sur
gical groups: [1] endometriosis, [2] endometriosis sham, [3] adhesion
model, or [4] adhesion sham. Three weeks after surgery, a second-look
laparotomy was performed, adhesions were scored (0 = no adhesions to 3
= severe adhesions) and mechanically disrupted, and rats received a s
econd GnRH-a or diluent injection either analogous to their initial in
jection or in a crossover design. Three weeks after the second injecti
on, rats were killed and adhesion reformation was scored. Data were ev
aluated using nonparametric tests including Mann-Whitney, Kruskal-Wall
is, and Friedman's tests comparing GnRH-a treatments with diluent cont
rols. Results: Preoperative GnRH-a therapy reduced adhesion scores in
rats with surgically induced endometriosis (mean +/- SEM; GnRH-a 1.1 /- 0.2 versus diluent 2.2 +/- 0.2) and adhesions (GnRH-a 0.3 +/- 0.1 v
ersus diluent 0.6 +/- 0.1). Pretreatment GnRH-a therapy did not affect
adhesion scores in the endometriosis sham procedure. Combined preoper
ative and postoperative GnRHa therapy (GnRH-a-GnRH-a) but not postoper
ative GnRH-a therapy alone (diluent-GnRH-a) reduced adhesion reformati
on after adhesiolysis in the endometriosis model (GnRH-a-GnRH-a 1.1 +/
- 0.3, diluent-GnRH-a 1.6 +/- 0.7), the endometriosis sham (GnRH-a-GnR
H-a 0.7 +/- 0.2, diluent-GnRHa 1.8 +/- 0.1), and the adhesion model (G
nRH-a-GnRH-a 0.3 +/- 0.2, diluent-GnRHa 1.0 +/- 0.5). No adhesions wer
e observed in the adhesion sham group. Conclusions: Gonadotropin-relea
sing hormone agonist therapy was successful in reducing adhesion forma
tion and reformation. These studies suggest that GnRH-a therapy for ad
hesion prevention in women should be explored.