Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “MESENTERIC VESSELS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,477 records · Page 82Linked to original sources
PubMed1991

Microlymphography of spontaneous lymph vessel anastomosis in small bowel transplantation in the rat.

Following small bowel transplantation, new lymph vessel anastomoses form spontaneously. Surgical anastomoses of the lymphatic vessels are unnecessary. The formation occurs in three stages. To the second postoperative day, lymph stays within the lymphatic vessels of the transplant. Following the fourth postoperative day, lymph flows within preexistent adventitial lymphatic vessels along the transplanted mesenteric artery to the arterial anastomosis at the aorta and stops there. From the sixth postoperative day on, lymph crosses the arterial anastomosis for the first time and flows along the recipient's aorta. To the eighth postoperative day a new lymph anastomosis is formed between the adventitia of the aorta and the neighbouring major lymphatic vessels. In the experiments presented here, these are represented by the vasa lymphatica testicularia sinistra of the recipient. Thus, the new anastomosis between lymphatic vessels is complete on the eight postoperative day. These new vessels gradually dilate with time.

Animals↗
PubMed1996

Openings in frog microvascular endothelium induced by high intravascular pressures.

1. We have investigated the effects of microvascular pressures, high enough to rupture the vessel wall, upon the ultrastructure and permeability of mesenteric capillaries in pithed frogs. 2. The vessels were perfused via micropipettes with Ringer solutions containing bovine serum albumin (1 mg ml-1) and a few human red cells. After a perfused section of vessel had been closed downstream, pressure (applied via the micropipette) was raised in a series of steps of 10 mmHg, each lasting approximately 10 s, until the vessel ruptured. Fluid filtration through the vessel wall prior to rupture was estimated from the movements of the red cells. 3. Seven vessels were fixed in glutaraldehyde immediately after rupture and prepared for electron microscopy. The electron micrographs revealed openings in the vessel walls and thirty-six of these gaps were completely defined in runs of serial sections made on four of the vessels. Twenty-nine of these gaps passed through the endothelial cells (transcellular) and seven were intercellular. 4. The pressure at which a vessel ruptured, Pb, was measured in twenty-nine vessels and had a mean +/- S.E.M. value of 79.6 +/- 5.0 cmH2O. In ten of these vessels, which had a mean +/- S.E.M. Pb of 84.2 +/- 6.5 cmH2O, microvascular pressure was lowered immediately after the initial rupture and the vessel perfused at a pressure of 20 cmH2O. Pb was then remeasured and found to be 69.9 +/- 8.4 cmH2O, which was not significantly different from its initial value. 5. Hydraulic permeability (Lp) was measured in six vessels over the range of 15-30 cmH2O before and 10 min after the vessel wall ruptured at high pressure. Mean values were 5.5 x 10(-7) and 4.0 x 10(-7) cms-1 cmH2O-1 and were not significantly different. 6. At pressures equal to and 10 mmHg below Pb, small short-lived increases in filtration rate were observed. It is suggested that these may correspond to the increased permeability to fluid and macromolecules observed at high microvascular pressures in intact capillary beds.

Animals↗
PubMed2005

Enhanced vascular responses to adrenomedullin in mice overexpressing receptor-activity-modifying protein 2.

Adrenomedullin (AM) levels are elevated in cardiovascular disease, but little is known of the role of specific receptor components. AM acts via the calcitonin receptor-like receptor (CLR) interacting with a receptor-activity-modifying protein (RAMP). The AM1 receptor is composed of CLR and RAMP2, and the calcitonin gene-related peptide (CGRP) receptor of CLR and RAMP1, as determined by molecular and cell-based analysis. This study examines the relevance of RAMP2 in vivo. Transgenic (TG) mice that overexpress RAMP2 in smooth muscle were generated. The role of RAMP2 in the regulation of blood pressure and in vascular function was investigated. Basal blood pressure, acute angiotensin II-raised blood pressure, and cardiovascular properties were similar in wild-type (WT) and TG mice. However, the hypotensive effect of IV AM, unlike CGRP, was enhanced in TG mice (P<0.05), whereas a negative inotropic action was excluded by left-ventricular pressure-volume analysis. In aorta relaxation studies, TG vessels responded in a more sensitive manner to AM (EC50, 8.0+/-1.5 nmol/L) than WT (EC50, 17.9+/-3.6 nmol/L). These responses were attenuated by the AM receptor antagonist, AM(22-52), such that residual responses were identical in all mice. Remaining relaxations were further inhibited by CGRP receptor antagonists, although neither affected AM responses when given alone. Mesenteric and cutaneous resistance vessels were also more sensitive to AM in TG than WT mice. Thus RAMP2 plays a key role in the sensitivity and potency of AM-induced hypotensive responses via the AM1 receptor, providing evidence that this receptor is a selective target for novel therapeutic approaches.

Adrenomedullin↗
PubMed2005

Cells expressing the stem cell factor receptor, c-kit, contribute to neoangiogenesis in diabetes.

While neoangiogenesis in diabetes is of greatest clinical significance in the retina, the pathological formation of new blood vesselsalso develops in other vascular beds in diabetes, including the mesentery of the streptozotocin-induced diabetic rat. However, the contribution of bone marrow-derived cells to this process of vasculogenesis is unknown. In this study, male Sprague-Dawley rats were randomised to receive either streptozotocin or vehicle, and their mesenteric vasculature was examined after three weeks. Origins from bone marrow and endothelial cell differentiation were identified by immunolabelling for the stem cell factor receptor, c-kit and von Willebrand factor (vWF), respectively. Expression for the angiogenic chemokine, stromal derived factor-1 (SDF-1) was assessed by quantitative real-time polymerase chain reaction (PCR). At three weeks, rats with diabetes had a dramatic (190-fold) increase in lectin-labelled blood vessel profiles in the mesenteric bed (p < 0.0001) in association with a five-fold increase in SDF-1 mRNA (p < 0.01). Immunohistochemical studies identified abundant large, ovoid, lumen-forming, c-kit+ cells in the mesentery of diabetic, but not control, rats. Many of these c-kit+ cells also showed positive immunolabelling for vWF, consistent with endothelial differentiation. In conclusion, cells of bone marrow origin contribute to new vessel formation in the diabetic mesentery. This phenomenon may also apply to the neovascularisation that develops at clinically important sites such as in the retina.

Animals↗
PubMed1988

Role of alpha-adrenoceptors in constrictor responses of rat, guinea-pig and rabbit small arteries to neural activation.

1. We have investigated the adrenoceptors mediating the force and electrical responses of rat mesenteric small arteries (i.d. 100-300 microns). Some mechanical experiments were also performed using guinea-pig and rabbit mesenteric small arteries. 2. Vessels were mounted on an isometric myograph and stimulated either with short (3 s) trains of electric field stimuli (ca. 0.2 ms pulse width) at 25 Hz (nerve stimulation) or with 10 microM-exogenous noradrenaline. 3. Nerve stimulation caused a force response equal to ca. 40% of the response to exogenous noradrenaline and, in the rat vessels, excitatory junction potentials (EJPs), which normally summated to give a depolarization of ca. 10 mV (although action potentials were sometimes seen). 4. Almost complete and reversible inhibition of the force responses of all vessels to both exogenous noradrenaline and to nerve stimulation was obtained using prazosin (0.1 microM) or phentolamine (1 microM). 5. Irreversible blockade of alpha 2-receptors enhanced the force response of all vessels to nerve stimulation by ca. 50%, but did not affect the force response of rat and guinea-pig vessels to exogenous noradrenaline. In the rabbit vessels this force response was abolished by alpha 2-blockade. 6. Following alpha 2-blockade, in the rat vessels the alpha-antagonists prazosin (0.1 microM), phentolamine (0.1 microM), phenoxybenzamine (0.01 microM) and benextramine (10 microM) all totally abolished the force response to exogenous noradrenaline, and inhibited the response to nerve stimulation by at least 80%. Similar effects of phentolamine were seen in the guinea-pig and, for the response to nerve stimulation, in the rabbit vessels. 7. In the rat vessels, alpha-adrenoceptor antagonists did not affect the EJPs, but did inhibit the small depolarization which resulted from several seconds of nerve stimulation. The ATP analogue alpha, beta-methylene-ATP (3 microM) abolished the EJPs, but only slightly reduced the force responses. 8. The results suggest that the force response to nerve stimulation of the rat mesenteric small arteries is mediated primarily through alpha-adrenoceptors, but also to a small degree through non-alpha-adrenoceptors, possibly ATP receptors.

Action Potentials↗
PubMed1998

Effect of vasopressin antagonism on structure and mechanics of small arteries and vascular expression of endothelin-1 in deoxycorticosterone acetate salt hypertensive rats.

The structural and mechanical properties of small arteries are altered in rat models of hypertension. The precise role of humoral factors in these changes has not been determined. In deoxycorticosterone acetate (DOCA) salt hypertension, endothelin-1 (ET-1) peptide content and gene expression are enhanced in mesenteric resistance arteries. These vessels also present augmented vasoconstrictor responsiveness to vasopressin versus control uninephrectomized rats. To determine whether an interaction exists between vasopressin and ET-1 in the pathogenesis of small-artery structural alterations in DOCA-salt rats, we examined the effect of chronic V1 vasopressin receptor antagonism (OPC-21268, 30 mg/kg BID) on the structure and mechanical properties of mesenteric resistance arteries using a pressure myograph and the effect on preproendothelin-1 (preproET-1) gene expression, determined by Northern blot analysis of preproET-1 mRNA. Tail-cuff systolic pressures were elevated in DOCA-salt (200+/-11 mm Hg) versus uninephrectomized rats (109+/-4 mm Hg) and decreased slightly but significantly by OPC-21268 to 187+/-7 mm Hg (P<0.01). Treatment with DOCA-salt increased vascular media-lumen ratios and media cross-sectional areas and reduced both stress and incremental elastic modulus for a given pressure. However, there was no change in distensibility or incremental elastic modulus versus media stress. OPC-21268 partially attenuated the vascular growth in DOCA-salt rats. PreproET-1 mRNA was increased 2-fold in mesenteric arteries of DOCA-salt rats versus uninephrectomized rats, an effect abrogated by OPC-21268. Thus, DOCA-salt hypertension is associated with altered morphology of the small-arterial wall, without altering stiffness of the arterial wall components. OPC-21268 regressed in part these changes, suggesting the involvement of vasopressin. The concomitant attenuation of enhanced ET-1 expression by OPC-21268 suggests that ET-1 may be involved in mediating in part the vascular effects of vasopressin in DOCA-salt hypertensive rats.

Animals↗
PubMed1992

CT arterial portography: causes of technical failure and variable liver enhancement.

OBJECTIVE: We studied the causes of technical failure and enhancement variability encountered during CT arterial portography. MATERIALS AND METHODS: CT arterial portograms and digital arteriograms were obtained via the superior mesenteric artery before partial liver resection in 43 patients with malignant tumors. These studies were reviewed for causes of technical failure and variable enhancement. RESULTS: Eleven (26%) of 43 procedures were technical failures. Causes of failure included aortic injection after catheter dislodgement (four), dense hyperenhancement associated with laminar flow in the portal vein produced by rapid venous return from a selective injection into a proximal branch vessel of the superior mesenteric artery (two), premature scanning beginning at the iliac crest (two), reflux into a replaced right hepatic artery (one), hepatic arterial enhancement via the pancreaticoduodenal arcade (one), and portal hypertension (one). Of the 32 remaining studies, 28 showed areas of parenchymal hypoenhancement or hyperenhancement. Causes of variable enhancement included impaired portal vein perfusion from mass effect of the tumor, laminar flow in the portal vein, and focal fatty infiltration. CONCLUSION: Technical failures and enhancement variability are common in CT arterial portography. Factors leading to technical failure include catheter choice and position, portal hypertension, and operator error.

Carcinoma, Hepatocellular↗
PubMed1988

Effects of sophoramine, an alkaloid from Sophora alopecuroides on isolated dog blood vessels.

In helical strips of dog mesenteric, coronary and cerebral arteries and mesenteric veins contracted with prostaglandin F2 alpha, sophoramine (10(-4) and 10(-3) M) produced a concentration-related relaxation, which was not influenced by treatment with indomethacin, atropine, aminophylline, propranolol, metoprolol, cimetidine, ouabain and methylene blue, and also not by removal of endothelium. Relaxations induced by sophoramine did not differ in strips of proximal and distal coronary arteries. Contractile responses to transmural stimulation in mesenteric arteries and veins were potentiated by treatment with sophoramine (10(-4) M). Treatment with cocaine, indomethacin, propranolol and saralasin did not alter the potentiating effect of sophoramine, whereas yohimbine, an alpha 2 adrenoceptor antagonist, attenuated it. Sophoramine did not significantly affect the contractile response to norepinephrine in mesenteric arteries and veins and the response to phenylephrine and clonidine in mesenteric veins. Sophoramine appears to non-specifically dilate dog arteries and veins and to facilitate the release of transmitter norepinephrine from adrenergic nerves via a mechanism of action on the prejunctional site sensitive to yohimbine.

Adrenergic Fibers↗
PubMed1977

The generation of prostacyclin by arteries and by the coronary vascular bed is reduced in experimental atherosclerosis in rabbits.

Experimental atherosclerosis in rabbits was associated with a suppression of prostacyclin generation from exogenous arachidonic acid by the coronary vascular bed. The spontaneous formation of prostacyclin by incubated rings of mesenteric artery was also diminished. These results suggest that in atherosclerosis an impaired activity of the endothelial prostacyclin synthexizing system contributes to the intra-arterial formation of thrombi.

Animals↗
PubMed1980

[Microcirculatory changes in the mesentery and skeletal muscle of the rat in relation to systemic arterial pressure during stimulation of the hypothalamic nuclei].

In acute experiments on anesthetized rats, hypothalamus sites were stimulated through bipolar electrodes. Vasomotor reactions and blood flow in mesenteric and spinotrapezius muscle vessels were studied and recorded by intravital microscopy and microphotography. Systemic blood pressure (BP) was measured in the carotid artery via a catheter. The results indicate that electric stimulation of different hypothalamus sites induces pressor, depressor or biphasic BP reactions that are related to the site stimulated. Microcirculatory changes were monotonous. Regardless of BP reaction in the microcirculatory network of the mesentery, the transient acceleration, slowdown and stoppage of the blood flow were observed in mesenteric microvessels (10--70 micrometer) without changes in their diameter. Pronounced constriction of the diameter of small arteries (90--250 micrometer) were also recorded in the mesentery. During BP pressor reaction the dilatation of microvessels (5--40 micrometer) of the skeletal muscle and an increase in their blood content were noted.

Animals↗
PubMed1996

Effects of exercise training on responses of peripheral and visceral arteries in swine.

Blood flow to skeletal muscle during exercise is greater in the trained state. We hypothesized that intrinsic vasomotor reactivity of arteries to active muscle during training bouts would be altered to favor a relative vasodilation after training. To test this hypothesis, miniature swine were pen confined (Sed; n = 30) or treadmill trained for 5 days/wk over 16-20 wk (Trn; n = 32). Efficacy of training was indicated by myocardial hypertrophy (4.84 +/- 0.11 and 5.81 +/- 0.12 g/kg body wt for Sed and Trn, respectively, P < 0.0005), training bradycardia at several submaximal running speeds of a maximal exercise test, increased running time to exhaustion (26 +/- 1 and 35 +/- 1 min for Sed and Trn, respectively, P < 0.0005), and increased oxidative capacities of several locomotory skeletal muscles. Segments of femoral, brachial, mesenteric, renal, and hepatic arteries were isolated from Sed and Trn swine. Isometric contractile and relaxation properties of vascular rings cut from these segments were determined in vitro. Contractile responses to KCl and norepinephrine (NE) were determined, as were relaxation responses to sodium nitroprusside and adenosine, agents acting directly on vascular smooth muscle, and the endothelium-dependent agents bradykinin and the calcium ionophore A-23187. Responses to vasocontractile and vasorelaxation agents were not different between Sed and Trn swine for vessels serving active muscles (i.e., femoral, brachial). On the other hand, renal arterial rings from Trn swine exhibited lesser contractile responses than those from Sed swine across a range of NE concentrations (P < 0.05) and approximately 25% less maximal contractile response to NE (32.7 +/- 2.6 and 24.2 +/- 2.1 g for Sed and Trn, respectively, P < 0.01). Responses of other vessels serving viscera (i.e., mesenteric, hepatic) were unchanged with training. These data indicate that vasomotor reactivity of porcine conduit-type arteries generally does not change with exercise training. An exception is the lesser contractile response to NE in renal artery, which could permit better preservation of renal blood flow during acute exercise in trained animals.

Animals↗
PubMed2003

Contribution of Na+ -Ca2+ exchanger to pinacidil-induced relaxation in the rat mesenteric artery.

1 Pinacidil relaxes blood vessels through opening the K(ATP) channels with a resultant membrane hyperpolarization and inhibition of Ca(2+) influx. The aim of this study was to examine the mechanisms thereby pinacidil induces K(+) channel-independent relaxation in isolated endothelium-denuded rat mesenteric artery. 2 Pinacidil-induced relaxation was inhibited by glibenclamide (1-10 micro M) in phenylephrine-preconstricted rings, but was unaffected by glibenclamide after inhibition of K(+) channels and VGCCs. Pinacidil-induced K(+) channel-independent relaxation remained unchanged after treatment with cyclopiazonic acid (10 micro M), thapsigargin (1 micro M), ouabain (100 micro M), propranolol (10 micro M), Rp-cAMPS triethylamine (30 micro M), L-NNA (100 micro M), or ODQ (10 micro M). 3 Pinacidil induced more relaxant effect in the presence of nifedipine than in the presence of 60 mM K(+) plus nifedipine. Pretreatment with Na(+)-Ca(2+) exchanger inhibitors, nickel (30-300 micro M) or benzamil (20 micro M) attenuated pinacidil-induced relaxation in normal or in nifedipine-containing solution. Pinacidil (1 micro M) produced less relaxant effect with decreasing extracellular Na(+) concentration. Na(+)-free condition abolished the inhibitory effect of benzamil. Both nickel and benzamil inhibited pinacidil-induced relaxation in the presence of glibenclamide (10 micro M). Nickel (300 micro M) did not affect the relaxant response to sodium nitroprusside. 4 Pinacidil relaxed the rings preconstricted by active phorbol and U46619 with similar potency. 5 The present results indicate that stimulation of the forward mode Na(+)-Ca(2+) exchange pathway is in part responsible for pinacidil-induced K(+) channel-independent vasorelaxation. Pinacidil also induces K(+) channel-dependent but VGCCs-independent relaxation. The PKC-mediated cellular pathway may be a target site for pinacidil only in higher concentrations.

Animals↗
PubMed2003

Early endothelial dysfunction following renal mass reduction in rats.

BACKGROUND: Endothelial dysfunction has been previously described in severely hypertensive rats with renal mass reduction (RMR) receiving large dietary Na loads. Because hypertension and Na loading reduce endothelium-dependent vasodilation, the effect of renal failure per se is unclear. METHODS: Responses to acetylcholine in noradrenaline-contracted isolated perfused mesenteric arteries were studied. Vessels were obtained from RMR rats kept on a normal diet, 3 and 10 days after surgery, and the results were compared with those from sham-operated rats (SN). The role of three putative mediators of endothelium-dependent vasodilation was assessed using: L-NAME (10(-4) mol L(-1)); indomethacin (INDO, 10(-5) mol L(-1)); and a mixture of charybdotoxin and apamin (C/A, both 10(-7) mol L(-1)), inhibitors of Ca-activated K-channels to mediate the effects of endothelium-derived hyperpolarizing factor (EDHF). RESULTS: Response to acetylcholine but not that to nitroprusside (endothelium-independent) was decreased in RMR. L-NAME reduced further acetylcholine relaxations in SN but not in RMR. By contrary, INDO decreased acetylcholine vasodilation in RMR but had no effect in SN. C/A had similar effects in the SN and RMR rats. The levels of 6-keto prostaglandin F1alpha were elevated in the urine of the RMR rats and were perfusate from the RMR vessels. CONCLUSION: Endothelial dysfunction occurs early after RMR, even when systolic blood pressure is only minimally elevated and Na intake is normal. This alteration may be because of decreased availability of nitric oxide, partially compensated by increased prostacyclin production.

6-Ketoprostaglandin F1 alpha↗
PubMedDate not supplied

[Dunbar's syndrome: clinical reality or physiopathologic hypothesis?].

The authors report the cases of two patients presenting a symptomatic intestinal angina caused by median arcuate ligament compression. Arteriography demonstrates severe coeliac artery stenosis in both of them and a retrograde filling of the coeliac axis from the superior mesenteric artery branch collateral vessels. The patients became asymptomatic after surgical release of the celiac trunk by section of the median arcuate ligament of the diaphragm. At 2 and 3 years follow-up, both patients report no further abdominal pain. Dunbar's syndrome is still a questionable subject; how can be a narrowing or an occlusion of the celiac artery semeiotically and clinically important? Some have proposed an ischemic base to explain the abdominal pain: the compression of the celiac trunk could be responsible of a celiac steal which results in shunting of blood from the superior mesenteric artery to the celiac distribution through the collateral system. There are very strong proofs that partial or even complete obstruction of the celiac artery should not lead to visceral ischemia such as: the rich collateral anastomosis of the celiac axis, the surgical ligation of the celiac axis performed without untoward consequences, the finding of asymptomatic celiac stenosis in the 49% of an arteriographic study, impossibility to formulate a consistent and rational for the surgical results. Shearing this view, few authors would prove that a stenotic type of the celiac artery is only a normal anatomic variant, refuting the existence of this syndrome.

Adolescent↗
PubMed1991

Effect of hydralazine on the mesenteric vasculature of hypertensive rats.

To test whether structural alterations observed in the mesenteric vasculature of Wistar-Kyoto spontaneously hypertensive rats (SHR) were dependent on the presence of hypertension, male SHR and Wistar-Kyoto normotensive (WKY) rats were treated in utero and postnatally with hydralazine up to 28 weeks of age. Treated SHR, WKY, and untreated WKY rats had comparable blood pressures that were less than those of untreated SHR. Treatment altered the dimensions of the superior mesenteric, intermediate-sized, and small arteries of the mesenteric vasculature. In the case of the superior mesenteric artery and intermediate vessels, hydralazine treatment increased the lumen and medial cross-sectional areas of the arteries in WKY rats and slightly decreased both parameters in SHR. Within the small arteries, treatment significantly increased the lumen size in SHR but not WKY rats and had no significant effect on the media of the vessels. Despite the above alterations, the media-to-lumen cross-sectional area ratios remained significantly elevated in SHR over WKY rats in both the treated and control groups of animals within all classes of arteries. The results indicate that there is an inherent increase in the quantity of media surrounding the arteries of SHR when compared with WKY rats that cannot be abolished by normalizing the blood pressure in utero and postnatally with hydralazine treatment. In SHR, such changes persist not only in arteries that exhibit an increase in the media-to-lumen ratio before hypertension but also in the superior mesenteric artery in which an increase in the ratio occurs after hypertension development.

Animals↗
PubMed1985

Intestinal Buerger's disease.

We describe a 50-year-old man who, at 26 years of age, underwent a hemicolectomy on the right side of the abdomen due to infarction of the right colon. At 35 years of age, a stenotic, ischemic segment of distal jejunum was resected. Later he had had intermittent claudication, migratory thrombophlebitis, and recurrent cerebral infarctions. The mesenteric and mural blood vessels of both resected specimens of bowel showed an occlusive process with organized and recent thrombi and marked transmural inflammation. The internal elastic lamina and media in the arteries were preserved and there was no evidence of atheroma or calcification. The histologic findings were consistent with thromboangiitis obliterans. We suggest that the same mechanism may be responsible for intestinal peripheral and cerebrovascular involvement.

Colon↗
PubMedDate not supplied

Differences in IgM synthesis to gut bacterial peptidoglycan polysaccharide after burn injury and gut ischemia.

Both burn injury and intestinal ischemia have been proven to induce bacterial translocation from the gut. It is still unknown, however, whether the bacteria induces immune response in these different models. To assess this, we measured in vitro IgM synthesis to peptidoglycan polysaccharide (PGPS), a ubiquitous gut bacterial antigen, after burn injury or gut ischemia-reperfusion in a mouse model. Eighty-five BALB/c mice were divided into four groups. Gut ischemia was produced by placing a vessel loop around the superior mesenteric artery at celiotomy (group Isc; n = 31). After 45 minutes, the abdomen was reopened, and the vessel loop removed. All animals had visible gut ischemia. Control mice (group Isc-C; n = 15) underwent two sham operations. Burn injury was 25% body surface area full-thickness to the dorsum (group B; n = 27). Another control group (B-C; n = 12) was also used. Animals were euthanized 24 hours after recirculation or 5 days after the burn injury. All spleens were removed, and cell suspensions prepared. Cells were cultured in 2.5 micrograms/ml lipopolysaccharide for 5 days, and anti-PGPS IgM level in the supernatant was measured by an enzyme-linked immunosorbent assay. Intestinal ischemia produced a significant rise in in vitro anti-PGPS IgM synthesis per 10(5) lymphocytes, which is the principal immunoglobulin response to infection. However, anti-PGPS IgM in mice after burn injury was significantly decreased. This decreased IgM synthesis after burn injury compared to gut ischemia may represent continued immune impairment from the burn wound, and may account for organ dysfunction related to bacterial translocation after burn injury.

Animals↗