ABSTRACTS
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Total Parenteral Nutrition, Intestinal Translocation, and Host Immune Function
Visceral Afferent Nerves Mediate Reactive Hyperemia of the Rabbit Esophageal Mucosa
Jian Shou, Jacqueline Lappin, Emery Minnard, John M. Daly Department of Surgery University of Pennsylvania Philadelphia, PA
B. J. Dunkin, L. McKie, D. Johnson, J. W. Harmon, B. L. Bass Surgical Service VA Medical Center George Washington University Washington, DC
Perioperative total parenteral nutrition (TPN) in surgical patients results in increased infectious complications compared with enteral nutrition support. The underlying mechanisms are unclear but do not appear due to energy deficiency. This study evaluated the effects of TPN on splenocyte and peritoneal macrophage (PM~) functions. Male Wistar rats (n = 26) underwent central vein cannulation and were randomized to receive isocaloric feeding of regular chow diet (RD) plus saline infusion or TPN for 7 days. Splenocytes and PMr were harvested to assess concanavalin A (con A) mitogenesis and superoxide production (-O2), Candida albicans phagocytosis (CAP), and nitric oxide (N:O) release after stimulation with LPS. Bacteria-positive mesenteric lymph nodes (MLN) were found in 77% (10 of 13) of TPN-fed rats compared with 17% (2 of 12) of RD-fed rats (p <0.01, Table I).
RD TPN
Con A (103 cpm)
-02 (nM/mg)
CAP (%)
N:O (nM/lO0 I~)
94--29 63 + 26*
37_+5 21 -+ 7*
58-+11 17 -+ 5t
4.5+-0.8 2.2 -+ 0.6 t
Mean _+SD; *p <0,05 vs. RD;tp <0.01 vs. RD.
In a second study, 15 rats received RD, TPN, and TPN with 10% of calories given by oral chow feeding (TPN + chow) for 7 days; splenocyte mitogenesis and PM4~ superoxide and CAP production were assessed
The esophageal mucosa is susceptible to erosive injury during gastroesophageal reflux. Reactive augmentation in mucosal blood flow (MBF) occurs in the esophagus and stomach during luminal exposure to potentially injurious agents, a phenomenon that may be a factor in mucosal protection. Since we have previously shown that visceral afferent nerves (VANs) are modulators of esophageal MBF, we hypothesized that VAN may mediate this reactive hyperemia. To test this hypothesis, we measured esophageal MBF in response to luminal challenge with a physiologic concentration of acid bile in three groups: (1) INTACT: intact VAN function (n = 8); (2) ABLATED: regional ablation of VAN function by topical treatment of cervical vagal trunks and celiac ganglia with 1% capsaicin in vehicle 14 days prior to perfusion (n -- 8); and (3) SHAM: treatment of vagal trunks and celiac ganglia with vehicle only, 14 days prior to perfusion (n -- 4). Perfusion of anesthetized rabbits was performed by cannulating the esophagus at the neck and EG junction. MBF was measured using 15-~g radioactive microspheres. After the measurement of baseline MBF, perfusion with 2 mM taurodeoxycholic acid, pH 2, was initiated. MBF was measured 2 and 10 minutes later. Hemodynamic parameters were similar among groups. Animals with intact VAN function (groups 1 and 3) showed a significant increase in MBF relative to baseline. This effect was short-lived, with return to baseline within 10 minutes.
(Table II).
RD TPN TPN + chow
% positive MLN
Con A ( x 103 cpm)
-02 (nM/mg)
CAP (%)
0 80* 40
109+_ 18 42 _+ 21" 70 + 27
36_+8 26 _+ 6* 35 _+ 8
63_+5 44 _+ * 61 _+ 14 t
Baseline 2 minutes 10 minutes
Intact
MBF* Ablated
Sham
43 + 8 70 + 9t 36 + 4
28 + 4 40 + 8 28 + 11
44 + 6 70 + 5t 22 + 9
*Mean • SEM (mL/min/lO0 g tissue), tp <0.05 vs, baseline.
Mean _+SD; *p < 0.05 vs. RD; tp < 0.05 vs. TPN.
TPN feeding resulted in significant impairment of PM4~ microbicidal and splenocyte proliferative functions, which may explain the increased infectious complications. The defective cellular functions that occur during TPN can be partially reversed by small amounts of oral feeding. Thus, even small amounts of enteral feeding may be beneficial in reducing TPN-related infection.
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Although a slight rise in MBF was observed in ablated animals, the response was blunted relative to intact animals and failed to reach statistical significance. These results support the hypothesis that VAN mediates the reactive hyperemia induced by potentially injurious physiologic luminal agents in the esophagus, a response that may contribute to the protection afforded by VAN.
THE AMERICAN JOURNAL OF SURGERY VOLUME 165 JUNE 1993