Gallbladder (GB) bile Ca2+ concentrations are increased prior to
gallstone formation and may serve as a nidus for cholesterol crystallization.
This phenomenon may be due to passive concentration of lumenal Ca2+
by H2O absorption or active Ca2+ secretion by the GB
wall. We have shown that stimulation of epithelial Na+ transport in
vitro leads to increased Ca2+ secretion. The mechanisms responsible
for increased GB bile Ca2+ concentrations are unknown. Recent
studies have identified the Na+/Ca2+ exchanger (NCX) as
a rapid Ca2+ transport mechanism in cardiac myocytes. We hypothesize
that the Na+/Ca2+ exchanger is also expressed by the GB
and may play an important role in Ca2+ secretion. Total RNA was
isolated from prairie dog and rabbit GB tissues and reverse transcribed into
cDNA using the Perkin Elmer protocol. Template cDNA was then amplified by PCR
using primers constructed from the conserved transmembrane domains of human
cardiac NCX-1. The amplified PCR product was electrophoresed on 2% agarose gel
and stained with ethidium bromide. {figure not available}
Both prairie dog (lane A) and rabbit (lane B) gallbladders demonstrated
expression of a single band at approximately 684bp as predicted from the known
sequence of NCX. This is the first reported isolation of NCX in the GI tract and
specifically in the gallbladder. Its presence across species suggests a
conserved role for Na+/Ca2+ exchange in Ca2+
homeostasis by the gallbladder. Future studies are directed to the contribution
of NCX to Ca2+ secretion during gallstone formation.
Methods: Patients scheduled for an elective antireflux surgery at one
institution were randomly assigned to one of two groups. Group I had a standard
laparoscopic Nissen with a large esophageal bougie (56 Fr). Group II had
exactally the same repair with no bougie. Patients with giant paraesophogeal
hernias, Collis lengthening procedures or partial fundoplications (done for
motility disorders) were excluded from this analysis. Complications related to
bougie use were recorded. Dysphagia was assessed according to a frequency and
severety score preop, immediately postop (< 4 weeks) and for long term (>4
weeks). Results were tabulated and subjected to a student - T test for
statistical validity.
Results: Between 3/96 and 12/96 88 laparoscopic antireflux surgeries were
randomized to the study. 38 met the criteria of simple, uncomplicated Nissen
fundoplications and were analyzed for this study. Data was collected in a
blinded fasion. There were 20 patiens in the no stent group and 18 in the
stented group. The incidence of bougie injuries in group I was 5%(I pharyngeal
laceration). Preoperative dysphagia was present in 40% of group I and 67% of
group II. Early postop dysphagia was noted in 84% of group I and 62% of group
II. Late dysphagia was described in 47% and 36% respectedly for group I and II.
No patients in either group have recieved intervention for their dysphagia. The
mean dysphagia score for group I for the three time frames was 3.4, 10.5, 1.9
respectively. For group II the scores were 7.1, 4.2, 1.9. These differences were
significant for the early postop group (p=.03) but not for the preop score
(p=.13) or for the late post op period (p=.93).
Conclusion: We present the first randomized prospective study that attempts
to validate the use of esophageal stenting in Nissen fundoplication and show
that there is, infact, a higher incidence of transient dysphagia in patients
when a bougie is not used. On the other hand, long term dysphagia rates were not
different. The avoidence of early dysphagia must be balanced against an
incidence of bougie related injuries (5%) during the laparoscopic procedure.
Based on these results we feel that the routine use of an esophageal stent
during a laparoscopic fundoplication is not indicated.
