Tubular stomach or whole stomach for esophagectomy through cervico-thoraco-abdominal approach: a comparative clinical study on anastomotic leakage.

BACKGROUND: Esophagectomy through cervico-thoraco-abdominal approach is a useful surgical technique in treating patients with esophageal cancer. However, the cervical reconstruction is also known to have a high rate of anastomotic leakage, as well as anastomotic stricture, intrathoracic stomach syndrome, reflux esophagitis and other complications, thereby influencing postoperative recovery and quality of life. AIMS: The objective of this study was to investigate whether tubular stomach is superior to whole stomach in reducing anastomotic leakage for esophageal reconstruction through the cervico-thoraco-abdominal (3-field) approach. METHODS: A total of 850 patients undergoing the 3-field esophagectomy were retrospectively included in this study and divided into a tubular stomach reconstruction group (Group A, n=453) and a whole stomach reconstruction group (Group B, n=397). All patients underwent esophagectomy through right thorax, left cervical part, abdominal triple incisions and done in esophageal reconstruction by hand-sewn two-layer anastomosis. RESULTS: Results revealed that in comparison with whole stomach, esophageal reconstruction with tubular stomach had a lower incidence of anastomotic leakage (5.5 vs. 9.3%, P<0.05), less manifestation of intrathoracic syndrome (3.3 vs. 9.8%, P<0.001) and less occurence of reflux esophagitis (5.1 vs. 11.1%, P<0.01). However, for the incidence of anastomotic stricture, there was no significant difference between the two groups (9.3 vs. 9.8%). CONCLUSIONS: This observation study suggests that for esophageal cancer patients undergoing the 3-field esophagectomy tubular stomach is better than whole stomach for esophageal reconstruction as reflected by a reduced postoperative anastomotic leakage, intrathoracic syndrome and reflux esophagitis.

Substance P potentiates thermal hyperalgesia induced by intrathecal administration of D-serine in rats.

AIM: To investigate the functional interaction between substance P (SP) and D-serine, agonist for glycine regulatory site of N-methyl-D-aspartate (NMDA) receptor, in processing spinal nociception. METHODS: Behavior studies, by testing tail-flick latency (TFL) combined with intrathecal application of drugs, were conducted in lightly anesthetized rats. RESULTS: Decrease in TFL was observed 1.5 min after intrathecal injection of D-serine 1000 nmol. Following pretreatment with SP 0.05 nmol 6 min prior to injection of D-serine 10 nmol, D-serine-induced decrease in TFL was greatly enhanced. The potentiation was blocked by co-administration of 7-chlorokynurenic acid 1 pmol, the selective antagonist for glycine regulatory site of NMDA receptor, or H-7 10 micromol, the PKC non-selective inhibitor, with SP 0.05 nmol. CONCLUSION: SP potentiates the D-serine-induced thermal hyperalgesia. Glycine regulatory site of NMDA receptor and intracellular protein kinase system may participate in the interaction of SP and NMDA receptor in the spinal cord.

Neomycin blocks substance P-induced calcium entry in cultured rat spinal cord neurons.

Substance P (SP) plays an important role in sensitization of spinal cord neurons. In this study, we investigated SP-induced calcium activities in cultured rat spinal cord neurons with confocal laser scanning microscopy. Our results showed that SP increased [Ca(2+)](i) by calcium entry rather than release from intracellular calcium stores. Neomycin (100 microM), an antagonist of phosphatidylinositol 4,5-bisphosphate (PIP(2)), blocked SP-induced calcium entry. Ca(2+)-free medium induced capacitative entry, which was significantly potentiated by SP. As activation of SP receptor (NK-1) leads to production of inositol 1,4,5-trisphosphate (IP(3)) by PIP(2) turnover, the results indicates that SP-induced calcium entry and SP-potentiated capacitative calcium entry might be mediated or regulated by IP(3)/diacylglycerol (DG) pathway.

Detection of release of aspartate and glutamate in cat spinal dorsal horn following noxious stimulation of cutaneous and muscular afferent fibers using microdialysis.

To investigate the possible mechanisms underlying the difference of NMDA and non-NMDA receptors in spinal nociception originating in skin and muscle, release of aspartate (Asp) and glutamate (Glu) in the spinal dorsal horn was detected by stimulation of cutaneous and muscular nerves in cats using microdialysis technique. Asp and Glu were increased respectively by (323 +/- 55)% and (169 +/- 16)% following stimulation of cutaneous nerve, but by (150 +/- 16)% and (218 +/- 42)% respectively following stimulation of muscular nerve. Asp increase was approximately three times higher than that of Glu following cutaneous nerve-stimulation (P < 0.01), while Glu increase was approximately twice as high as that of Asp following muscular nerve-stimulation (P < 0.05). It is likely that nociceptive cutaneous and muscular inputs preferentially elicite release of Asp and Glu respectively, resulting in a functional differentiation of NMDA and non-NMDA receptor in the mediation of different nociceptive information.

Orphanin FQ/nociceptin modulates glutamate- and kainic acid-induced currents in acutely isolated rat spinal dorsal horn neurons.

The heptadecapeptide orphanin FQ (OFQ), also known as nociceptin (NOC), is a newly discovered endogenous ligand for the opioid-like G-protein coupled receptor, ORL1. In the present study, the effects of OFQ/NOC on glutamate (Glu), kainic acid (KA) and quisqualic acid (QA) induced currents were examined in isolated rat spinal dorsal horn neurons of young rats using whole-cell patch-clamp techniques. Glu, KA and QA elicited rapid inward currents in 90%, 69%, 83% of tested neurons. OFQ/NOC(0.03 approximately 300 nM) failed to induce any changes of membrane currents, but modulated Glu-, KA- and QA-elicited currents. OFQ/NOC inhibited and potentiated Glu-induced currents in 40.6% and 27.3% of examined cells (n=106) respectively. In about one third examined neurons, OFQ/NOC had no detectable effects on Glu responses. OFQ/NOC also inhibited and enhanced KA- and QA-induced currents (inhibition: KA, 67.1%, n=76; QA, 50%, n=36. Potentiation: KA, 23.7%, n=76; QA, 16.7%, n=36). In about 10% of tested cells, Glu-induced currents were potentiated after the application of OFQ/NOC, and lasted for 20 approximately 30 min. The inhibitory effects of OFQ/NOC on KA and QA responses were naloxone-insensitive. The C-terminal fragment OFQ(8-17) presented same effects on EAA-induced responses. Taken together, OFQ/NOC primarily inhibited Glu-, KA- and QA-induced currents in isolated rat spinal dorsal horn neurons via non-opioid mechanism, which might contribute to nociceptive transmission in the spinal level.

[Comparison of NMDA and non-NMDA receptor antagonists-induced inhibition in hindpaw withdrawal response to noxious thermal stimulation].

In our previous electrophysiological study, it was shown that NMDA receptors are predominantely involved in the transmission of nociceptive cutaneous afferents, whereas non-NMDA receptors are mainly concerned with the transmission of nociceptive muscular afferents. In the present investigation, the effects of NMDA and non-NMDA receptor antagonists were tested in rat hindpaw withdrawal response to noxious thermal stimulation. Intrathecal application of non-NMDA receptor antagonist 1 nmol/L DNQX (6,7-dinitroquinoxaline-2,3(1H, 4H)-dione) had no effect on paw withdrawal latencies (PWL), but NMDA receptor antagonist 1 nmol/L APV [(+/-) 2-amino-5-phosphonovalerate)] significantly prolonged PWL (P < 0.05). Both APV and DNQX at 10 nmol/L significantly increased PWL with the former agent being more potent. The results further support that both NMDA and non-NMDA receptors are involved in the transmission of spinal nociception, with the former being more preferentially involved in the transmission of nociceptive information from the skin.