Toxic factors released from the intestine have been implicated in the pathophysiology of severe acute illness, including acute pancreatitis, trauma and hemorrhagic shock, and burns. Toxic factors in mesenteric lymph may induce an inflammatory systemic response while bypassing the portal circulation and liver. This paper reviews current knowledge of the anatomy, physiology and pathophysiology of mesenteric lymph and focuses on factors influencing its composition and flow, and potential therapeutic interventions. A search of the Ovid MEDLINE database up until the end of January 2006 yielded 1,761 relevant publications, the references of which were then searched manually to identify further related publications. A wide range of factors potentially affecting mesenteric lymph flow and composition were identified. Targeted interventions have been similarly broad, including medical therapy, nutritional support and surgery. Of the available surgical interventions, thoracic duct external drainage has been the most widely studied. This systematic review highlights significant gaps in our present understanding of the role of mesenteric lymph in health and disease. Further research is needed to identify factors responsible for the generation of biologically active mesenteric lymph, the role of agents modulating its flow and composition, the importance of intrinsic pump activity, the potential therapeutic role of lipophilic antioxidant agents, the comparative effects of low-fat enteral nutrition and standard enteral nutrition, and the therapeutic outcomes of thoracic duct ligation versus thoracic duct external drainage.

/pdf/mesenteric-lymph-the-bridge-to-future-management-of-critical-36n6aaw6nw.pdf

Mesenteric lymph: the bridge to future management of critical illness.

Hyperviscosity in the neonate

Objective— We investigated the effects of fluvastatin on hypoxia-induced (1 to 3 weeks, 10% O 2 ) pulmonary hypertension with focus on endothelial nitric oxide synthase (eNOS) activity. Methods and Results— Oral fluvastatin treatment (1 mg/kg daily) prevented the causing and progression of pulmonary hypertension as determined by the right ventricular pressure, right ventricular hypertrophy, and muscularization of pulmonary artery. We also revealed that fluvastatin treatments prevented the hypoxia-induced decrease in cGMP production in the rat lung and restored the endothelium-dependent relaxation in the pulmonary artery. We revealed that this beneficial effect was not dependent on the increase in eNOS mRNA or protein expression, but was dependent on the inhibition of the eNOS-tight coupling with caveolin-1, the eNOS dissociation from heat shock protein 90, and the decrease in eNOS Ser 1177 –phosphorylation induced by hypoxia. Furthermore, in a whole-mount immunostaining the hypoxia-induced eNOS protein condensation with caveolin-1 of pulmonary endothelial cells was restored by the fluvastatin-treatment. Conclusion— These results suggest that the fluvastatin exerts beneficial effects on chronic hypoxia-induced pulmonary hypertension by protecting against the eNOS activity at the post-transcriptional level.

Statin Protects Endothelial Nitric Oxide Synthase Activity in Hypoxia-Induced Pulmonary Hypertension

Gastrointestinal lymphatics in health and disease

We hypothesized that disrupted alveolarization and lung vascular growth caused by brief perinatal hypoxia would predispose infant rats to higher risk for developing pulmonary hypertension when reexposed to hypoxia. Pregnant rats were exposed to 11% inspired oxygen fraction (barometric pressure, 410 mmHg; inspired oxygen pressure, 76 mmHg) for 3 days before birth and were maintained in hypoxia for 3 days after birth. Control rats were born and raised in room air. At 2 wk of age, rats from both groups were exposed to hypoxia for 1 wk or kept in room air. We found that brief perinatal hypoxia resulted in a greater increase in right ventricular systolic pressure and higher ratio of right ventricle to left ventricle plus septum weights after reexposure to hypoxia after 2 wk of age. Moreover, perinatal hypoxic rats had decreased radial alveolar counts and reduced pulmonary artery density. We conclude that brief perinatal hypoxia increases the severity of pulmonary hypertension when rats are reexposed to hypoxia. We speculate that disrupted alveolarization and lung vascular growth following brief perinatal hypoxia may increase the risk for severe pulmonary hypertension with exposure to adverse stimuli later in life.

https://www.physiology.org/doi/pdf/10.1152/ajplung.2000.278.2.L356

Brief perinatal hypoxia increases severity of pulmonary hypertension after reexposure to hypoxia in infant rats.

Effect of blood viscosity on pulmonary vascular resistance

Lymphatic obstruction in the pathogenesis of intestinal mucosal atrophy.

Effect of chronic thoracic duct fistula on albumin kinetics in man.

Quick-gelling liquid Silastic was used to produce an obturator type, noninflammatory obstruction of the retroperitoneal and mesenteric lymphatics Comparisons between eight dogs with thoracic duct ligation were made with eight dogs receiving either retroperitoneal or mesenteric lymphatic obstruction After one year the dogs with the experimental lymphatic obstruction were found grossly to have focal lymphoid hyperplasia underlying atrophic mucosa in the small intestine There were no associated persistent changes in the serum protein levels, lymphocyte counts, or fecal fat levels Mesenteric lymphangiograms documented a high degree of lymphatic obstruction with collateral drainage The lymph nodes were depleted of lymphocytes in the paracortical areas It is suggested that intestinal lymphoid hyperplasia may result from an altered mucosal permeability to antigenic material in the intestinal lumen produced by the partial obstruction of the mesenteric lymphatics

Linea A. McNeel

Papers

Effect of blood viscosity on pulmonary vascular resistance

Lymphatic obstruction in the pathogenesis of intestinal mucosal atrophy.

Effect of chronic thoracic duct fistula on albumin kinetics in man.

Nodular lymphoid hyperplasia with experimental lymphatic obstruction.

Albumin kinetics in patients with chronic thoracic duct fistulas