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PubMed1989

The effect of anesthetics on lymphatic contractility.

Spontaneous contractions and those elicited by electrical stimulation were studied in isolated segments of bovine mesenteric lymphatic vessels. The effects of three general anesthetics, pentobarbitone, halothane, and ether, on these spontaneous and evoked contractions were studied. Pentobarbitone and halothane inhibited spontaneous contractions in a dose-dependent fashion. In doses of 10(-4) M or greater both drugs completely abolished spontaneous contractility but when contractions were elicited by electrical stimulation pentobarbitone inhibited them in a dose-dependent manner whereas halothane did not. In contrast to the above results ether in doses as high as 10(-2) M had little effect on lymphatic contractility. It is concluded that, in doses similar to plasma levels found during general anaesthesia, halothane and pentobarbitone significantly depressed lymphatic contractility while ether did not.

Anesthetics↗
PubMed2006

Lengthening of small bowel mesentery: stepladder incision technique.

The surgical option of choice in most patients with mucosal ulcerative colitis or familial adenomatous polyposis is restorative proctocolectomy with ileal pouch anal anastomosis. The tension-free anastomosis is one of the most critical steps but may be technically difficult or impossible in some patients because of shortened small bowel mesentery. Various techniques have been described to increase the length of small bowel mesentery. These techniques usually involve selective division of mesenteric blood vessels and meticulous dissection. We describe a new technique of stepladder transverse, transmesenteric incisions in the avascular windows of small bowel mesentery. This provides additional small bowel length without compromising blood supply to the pouch and a simple and safe method of increasing the length of small bowel mesentery. To date, no complications have been reported using this technique.

Colonic Diseases↗
PubMed2006

Opposing viscerovisceral effects of surgically induced endometriosis and a control abdominal surgery on the rat bladder.

OBJECTIVE: To determine, in rats, how surgically induced endometriosis and a control surgery (partial hysterectomy; sutures in abdomen) affects micturition thresholds and bladder vascular permeability. DESIGN: Two animal studies, each performed in three groups of urethane-anesthetized rats in proestrus. SETTING: Academic facility. ANIMAL(S): Seventy-three female, regularly cycling Sprague-Dawley rats studied in proestrus. INTERVENTION(S): Surgical induction of endometriosis (ENDO), surgical control (shamENDO), intact control (NoSURG), and bladder inflammation via intravesicular turpentine in all three groups. MAIN OUTCOME MEASURE(S): [1] Micturition thresholds (MTs; volume voiding thresholds), as measured by repetitive transurethral cystometry before and after bladder inflammation and [2] bladder inflammation, as assessed by extravasation of Evans Blue dye. RESULT(S): In the uninflamed bladder, MTs were significantly lower and dye extravasation significantly higher in ENDO rats than in shamENDO and NoSURG rats. Bladder inflammation increased dye extravasation in all groups and reduced MTs in the NoSURG and ENDO rats, but not in the shamENDO rats. CONCLUSION(S): Endometriosis reduces MTs and produces signs of inflammation in the healthy bladder. Surprisingly, the control surgical procedure (partial hysterectomy; sutures on mesenteric blood vessels) protects bladder reflexes from the influence of bladder inflammation, a condition that is named silent bladder inflammation. Such cross-system inducing and masking effects have important clinical relevance.

Abdomen↗
PubMed2006

Interaction between liposomes and RBC in microvessels in vivo.

Liposomes are phospholipid vesicles that can serve as carriers of biologically active agents in vitro and in vivo. Here, we describe the movement of liposomes suspended with blood flowing in capillaries. Liposomes were coated with a polymer to extend their lifespan in rat mesenteric blood vessels and detected by fluorescent staining. Liposome activity was observed by intravital microscopy using a high-speed camera system at 5 and 60 min after liposome administration. Liposome velocity was determined using two-dimensional cross-correlation, and blood flow was measured by high-resolution PIV (particle image velocimetry). The results showed that the motion of polymer-coated liposome followed the phase averaged velocity distribution of heartbeats while flowing with red blood cells in microvessels. Liposome particles tend to move toward the near blood vessel wall in the low velocity of blood flow.

Animals↗
PubMed2006

Nitric oxide inhibits neutrophil migration by a mechanism dependent on ICAM-1: role of soluble guanylate cyclase.

In the present study, we addressed the role of intercellular adhesion molecule type 1 (ICAM-1/CD54) in neutrophil migration to inflammatory site and whether the inhibitory effect of nitric oxide (NO) upon the neutrophil rolling, adhesion and migration involves down-modulation of ICAM-1 expression through a cyclic GMP (cGMP) dependent mechanism. It was observed that neutrophil migration induced by intraperitoneal administration of endotoxin (LPS), carrageenan (Cg) or N-formyl peptide (fMLP) in ICAM-1 deficient (ICAM-1-/-) is similar to that observed in wild type (WT) mice. The treatment of mice with NO synthase (NOS) inhibitors, NG-nitro-l-arginine, aminoguanidine or with a soluble guanylate cyclase (sGC) inhibitor, ODQ enhanced LPS- or Cg-induced neutrophil migration, rolling and adhesion on venular endothelium. These parameters induced by LPS were also enhanced by 1400 W, a specific iNOS inhibitor, treatment. On the other hand, the treatment of the mice with S-nitroso-N-acetylpenicillamine (SNAP), an NO donor, reduced these parameters induced by LPS or Cg by a mechanism sensitive to ODQ pretreatment. The NOS inhibitors did not enhance LPS-, Cg- or fMLP-induced migration and adhesion in ICAM-1-/- mice. Moreover, genetic (iNOS-/- mice) or pharmacological inhibition of NOS or of sGC enhanced LPS-induced ICAM-1 expression on mesenteric microcirculation vessels of WT mice. By contrast, SNAP reduced the ICAM-1 expression by a mechanism dependent on cGMP. In conclusion, the results suggest that although during inflammation, ICAM-1 does not contribute to neutrophil migration, it is necessary for the down-modulatory effect of inflammation-released NO on the adhesion and transmigration of neutrophils. Moreover, these NO effects are mediated via cGMP.

Animals↗
PubMed1998

Extrinsic denervation increases myenteric nitric oxide synthase-containing neurons and inhibitory neuromuscular transmission in guinea pig.

Enteric nerves can function normally without connections with the central nervous system. A contributing component of the functional autonomy exhibited by enteric nerves is their plasticity. In the present study, the number of nitric oxide synthase-immunoreactive (NOS-ir) myenteric neurons and inhibitory neuromuscular transmission were studied in extrinsically denervated ileal segments. Segments of ileum were extrinsically denervated by crushing the mesenteric blood vessels supplying a loop of ileum in anesthetized guinea pigs. Some unoperated animals were treated with capsaicin or 6-hydroxydopamine (6-OHDA) to disrupt primary afferent and sympathetic nerves, respectively. NOS-ir was localized using indirect immunofluorescence. Nerve-mediated relaxations of longitudinal muscle were studied in vitro using standard methods. At 7 weeks after extrinsic denervation there was a 93% increase in the number of NOS-ir myenteric neurons. The number of neurons containing detectable vasoactive intestinal peptide-ir neurons was not changed after extrinsic denervation. Neurogenic relaxations caused by 10, 20 and 50 Hz transmural stimulation were larger in extrinsically-denervated tissues compared to control tissues. The NOS antagonist, nitro-L-arginine (300 microM) inhibited neurogenic relaxations in control and extrinsically-denervated tissues. Capsaicin- but not 6-OHDA-treatment mimicked the effects of extrinsic denervation on NOS-ir and neurogenic relaxations of the longitudinal muscle. Active or passive properties of the longitudinal muscle were unaffected by extrinsic denervation. These data indicate that extrinsic denervation is associated with an increase in the number of myenteric neurons expressing detectable NOS-ir and potentiation of inhibitory transmission to longitudinal muscle. This effect is due to loss of extrinsic sensory nerves.

Animals↗
PubMed2001

Role of the angiotensin AT2 receptor in blood pressure regulation and therapeutic implications.

The angiotensin (ANG) Type 2 (AT2) receptor is one of two major ANG II receptors that have been identified, cloned, and sequenced. Most of the biologic actions of ANG II are thought to be mediated by the AT1 receptor, but evidence is beginning to emerge that the AT2 receptor has a significant role in the regulation of blood pressure. In the adult rat, the AT2 receptor is expressed, albeit in low concentrations in kidney, mesenteric blood vessels, and heart. Most of the evidence suggests that the AT2 receptor stimulates a vasodilator signaling cascade that includes bradykinin, nitric oxide, and guanosine cyclic 3',5'-monophosphate. At lease some of the beneficial actions of AT1 receptor blockade are mediated by the AT2 receptor through this pathway. Several recent studies suggest that AT2 receptors may mediate vasodilation and hypotension. The AT2 receptor represents a potential therapeutic target for agonist action and a candidate molecule in the pathophysiology of hypertension.

Animals↗
PubMedDate not supplied

Multiple nodular metastases in mesenteric panniculitis by uterine papillary serous adenocarcinoma (UPSC): CT appearance of a case.

Intra-abdominal panniculitis is a thickening of the mesentery of the small/large intestine due to infiltration of lipid-laden macrophages associated with a variable amount of fibrosis. This condition is rarely associated with malignant neoplasms. We report the computed tomography (CT) findings of a patient treated for uterine papillary serous adenocarcinoma (UPSC). She had mesenteric panniculitis where metastatic tumor nodules implanted. This was the only intraperitoneal recurrence. To our knowledge, no such finding has been reported in the gynecologic and radiologic literature to date. On CT images, the differential diagnosis is with cystic dilatations of mesenteric lymph vessels.

Aged↗
PubMed1997

Evidence that the substance P-induced enhancement of pacemaking in lymphatics of the guinea-pig mesentery occurs through endothelial release of thromboxane A2.

1. In vitro studies were performed to examine the mechanisms underlying substance P-induced enhancement of constriction rate in guinea-pig mesenteric lymphatic vessels. 2. Substance P caused an endothelium-dependent increase in lymphatic constriction frequency which was first significant at a concentration of 1 nM (115 +/- 3% of control, n = 11) with 1 microM, the highest concentration tested, increasing the rate to 153 +/- 4% of control (n = 9). 3. Repetitive 5 min applications of substance P (1 microM) caused tachyphylaxis with tissue responsiveness tending to decrease (by an average of 23%) and significantly decreasing (by 72%) for application at intervals of 30 and 10 min, respectively. 4. The competitive antagonist of tachykinin receptors, spantide (5 microM) and the specific NK1 receptor antagonist, WIN51708 (10 microM) both prevented the enhancement of constriction rate induced by 1 microM substance P. 5. Endothelial cells loaded with the Ca2+ sensing fluophore, fluo 3/AM did not display a detectable change in [Ca2+]i upon application of 1 microM substance P. 6. Inhibition of nitric oxide synthase by NG nitro-L-arginine (L-NOARG; 100 microM) had no significant effect on the response induced by 1 microM substance P. 7. The enhancement of constriction rate induced by 1 microM substance P was prevented by the cyclooxygenase inhibitor, indomethacin (3 microM), the thromboxane A2 synthase inhibitor, imidazole (50 microM), and the thromboxane A2 receptor antagonist, SQ29548 (0.3 microM). 8. The stable analogue of thromboxane A2, U46619 (0.1 microM) significantly increased the constriction rate of lymphangions with or without endothelium, an effect which was prevented by SQ29548 (0.3 microM). 9. Treatment with pertussis toxin (PTx; 100 ng ml-1) completely abolished the response to 1 microM substance P without inhibiting either the perfusion-induced constriction or the U46619-induced enhancement of constriction rate. 10. Application of the phospholipase A2 inhibitor, antiflammin-1 (1 nM) prevented the enhancement of lymphatic pumping induced by substance P (1 microM), without inhibiting the response to either U46619 (0.1 microM) or acetylcholine (10 microM). 11. The data support the hypothesis that the substance P-induced increase in pumping rate is mediated via the endothelium through NK1 receptors coupled by a PTx sensitive G-protein to phospholipase A2 and resulting in generation of the arachidonic acid metabolite, thromboxane A2 this serving as the diffusible activator.

Androstanes↗
PubMed1999

Evidence that the ATP-induced increase in vasomotion of guinea-pig mesenteric lymphatics involves an endothelium-dependent release of thromboxane A2.

1. Experiments were made to investigate mechanisms by which adenosine 5'-trisphosphate (ATP) enhanced vasomotion in mesenteric lymphatic vessels isolated from young guinea-pigs. 2. ATP (10-8 - 10-3 M) caused a concentration-dependent increase of perfusion-induced vasomotion with the endothelium mediating a fundamental role at low ATP concentrations (10-8 - 10-6 M). 3. The response to 10-6 M ATP showed tachyphylaxis when applied at intervals of 10 min but not at intervals of 20 or 30 min. 4. Suramin (10-4 M) or reactive blue 2 (3x10-5 M) but not PPADS (3x10-5 M) abolished the excitatory response to 10-6 M ATP confirming an involvement of P2 purinoceptors. 5. The excitatory response to 10-6 M ATP was abolished by treatment with either pertussis toxin (100 ng ml-1), antiflammin-1 (10-9 M), indomethacin (3x10-6 M) or SQ29548 (3x10-7 M), inhibitors of specific G proteins, phospholipase A2, cyclo-oxygenase and thromboxane A2 receptors respectively. 6. ATP simultaneously induced a suramin-sensitive inhibitory response, which was normally masked by the excitatory response. ATP-induced inhibition was mediated by endothelium-derived nitric oxide (EDNO) as the response was abolished by NG-nitro-L-arginine (L-NOARG; 10-4 M), an inhibitor of nitric oxide synthase. 7. We conclude that ATP modulates lymphatic vasomotion by endothelium-dependent and endothelium-independent mechanisms. One of these is a dominant excitation caused through endothelial P2 purinoceptors which because of an involvement of a pertussis toxin sensitive G-protein may be of the P2Y receptor subtype. Their stimulation increases synthesis of phospholipase A2 and production of thromboxane A2, an arachidonic acid metabolite which acts as an endothelium-derived excitatory factor.

Adenosine Triphosphate↗
PubMed2002

ATP-induced endothelium-independent enhancement of lymphatic vasomotion in guinea-pig mesentery involves P2X and P2Y receptors.

1. The present study has investigated mechanisms underlying ATP-induced endothelium-independent enhancement of vasomotion in guinea-pig mesenteric lymphatic vessels. 2. Lymphatic vasomotion, vessel tone and smooth muscle [Ca(2+)](i) showed similar ATP concentration-response curves. 3. ATP, at 0.1 mM, caused a biphasic increase in tonic [Ca(2+)](i) and superimposed vasomotion-associated Ca(2+) transients. All ATP-induced [Ca(2+)](i) changes were abolished by incubating the smooth muscle with suramin (0.1 mM). 4. alpha,beta-MeATP (0.1 mM) and UTP (0.1 mM) caused similar changes in [Ca(2+)](i) but the responses to these agonists were smaller than to ATP. 5. The actions of alpha,beta-MeATP (0.1 mM) were inhibited by suramin (0.1 mM) and PPADS (30 micro M) but not by reactive blue 2 (30 micro M). 6. In the presence of alpha,beta-MeATP (0.1 mM), the increases in tonic [Ca(2+)](i) and vasomotion-associated Ca(2+) transients induced by ATP (0.1 mM) were inhibited by U73122 (5 micro M), CPA (20 micro M) and heparin, whereas U73343 (5 micro M) and pre-treatment with PTx (100 ng ml(-1)) had no significant effects. 7. Depletion of the intracellular stores with CPA (20 micro M) caused an increase in [Ca(2+)](i), which was not blocked by desensitization of P(2X) receptors with alpha,beta-MeATP. 8. The data indicate that ATP, at relatively high concentrations increases lymphatic smooth muscle [Ca(2+)](i) and vasomotion through activation of P(2X1) and P(2Y2) purinoceptors present on lymphatic smooth muscle. The increase in [Ca(2+)](i) is likely to result from Ca(2+) release from inositol-1,4,5-trisphosphate-sensitive stores as well as Ca(2+) influx through store-operated channels and P(2X)-gated channels.

Adenosine Triphosphate↗
PubMed1997

Redgut in sheep: a disease with a twist.

Redgut is a condition of sheep characterised by sudden death. Post-mortem findings are reddened small and large intestines, which are usually displaced. Sheep are predisposed to the condition by a combination of circumstances, including a small rumenoreticulum because of the nature of the feed (usually highly digestible forage), and increased large intestinal size and function. To accommodate this, and because there is not a large rumenoreticulum to stabilise the gut position, the intestinal mass moves to an unstable position in the peritoneal cavity. Some unknown event precipitates a further change in intestinal position, resulting in accidental torsion of the intestinal mass, with resultant obstruction of the mesenteric blood vessels and death from shock. The condition can be prevented by careful attention to feeding regimes that prevent development of the predisposing feature of small forestomachs and an oversized large intestine, resulting in a displaced intestinal mass. This is achieved by intermittent grazing of dangerous pastures.

Journal Article↗
PubMed1990

Stimulation of endothelin mRNA and secretion in rat vascular smooth muscle cells: a novel autocrine function.

Endothelin (ET), a peptide originally isolated from the supernatants of cultured endothelial cells, exerts a wide variety of biological effects in different tissues. Endothelial-cell-synthesized ET-1 has been proposed to act in a paracrine manner on adjacent smooth muscle cells (SMC) in vivo, with effects that include both vascular reactivity (vasodilation/vasoconstriction) and mitogenesis. This study, by the use of immunocytochemically characterized SMC (rVSMC) isolated from the aortas of spontaneously hypertensive rats, has investigated a possible autocrine role for ET in regulation of the vasculature. Although quiescent cultures of rVSMC apparently did not constitutively express prepro ET-1mRNA, ET-specific transcripts could be induced by a variety of growth factors (transforming growth factor beta [TGF-beta]; platelet-derived growth factor-AA homodimer [PDGF-A chain]) and vasoactive hormones (angiotensin II [Ang II], arginine-vasopressin, and ET-1 itself). The kinetics for prepro ET-1mRNA induction in rVSMC were characteristically rapid in onset and transient. Down-regulation of protein kinase C by 48 h pretreatment of rVSMC with phorbol ester markedly reduced the subsequent ability of rVSMC to express ET-1 transcripts and secrete ET-1 peptide in response to Ang II. Inducible prepro ET-1mRNA expression was accompanied by a cycloheximide-inhibitable release of ET-1 peptide into the medium of rVSMC. ET-1 peptide was determined by both radioreceptor- and radioimmunoassay. Stimulated rVSMC accumulated ET-1 (approximately 200 pg.10(6) cells-1 x 4 h-1) at levels that attained biological relevance (approximately 10(-10) M). Sep-pak C18 extracts of medium from stimulated rVSMC elicited contraction of isolated endothelium-denuded rat mesenteric resistance vessels, and this response was characteristically protracted and difficult to "wash out." Synthetic (porcine) ET-1 promoted the expression of transcripts for PDGF-A chain, TGF-beta, and thrombospondin in quiescent rVSMC. Such effects of ET-1 on gene expression may be relevant to the mitogenic potential of ET-1 on VSMC. Our findings imply a role for ET-1 in the control of vascular function via both paracrine and autocrine regulatory mechanisms. The expression of prepro ET-1mRNA and peptide biosynthesis by rVSMC may have both short-term (e.g., vasoconstriction) and long-term (e.g., structural remodeling) consequences. A sustained loop of autocrine stimulation by ET-1 in SMC could contribute toward the pathogenesis of vasospasm and/or atherosclerosis.

Animals↗
PubMed1999

Microvascular "supercharged" cervical colon: minimizing ischemia in esophageal reconstruction.

Traditional colonic reconstruction of the esophagus is performed by cervical transposition of an isolated segment of colon with the vascular supply derived from one of the mesenteric colic vessels. The transposed cervical portion of the colon is farthest from the vascular supply and is at risk of ischemic injury. Despite notable risk of ischemic complications to the colonic neoesophagus, reports advocating a "supercharged" microvascular augmentation of the vascular supply to the cervical portion of the colon remain few in number. Herein, the ischemic complications associated with traditional transposition of the colon for esophageal reconstruction are reviewed, and avoidance by microvascular "supercharging" of the cervical colon is advocated under particular circumstances. The authors present a case of colonic interposition for esophageal replacement requiring a cervical microvascular anastomosis for survival of the transferred colon.

Adult↗
PubMed2005

Patent ductus arteriosus, indomethacin and necrotizing enterocolitis in very low birth weight infants: a population-based study.

BACKGROUND: Patent ductus arteriosus is a risk factor for the development of necrotizing enterocolitis. The use of indomethacin to treat patent ductus arteriosus in preterm infants may either decrease the incidence of necrotizing enterocolitis by stabilizing or closing the ductus arteriosus or increase its incidence by a direct constricting effect on mesenteric blood vessels. The authors sought to evaluate the interrelationship between patent ductus arteriosus, treatment with indomethacin and the risk of necrotizing enterocolitis in very low birth weight infants. METHOD: The Israel National database includes prospectively collected data on 99% of all very low birth weight infants in Israel. The study population comprised 6146 infants of 24-34 weeks' gestation born between 1995 and 2000. The effect of patent ductus arteriosus on necrotizing enterocolitis was assessed using multiple regression analysis. RESULTS: Necrotizing enterocolitis occurred in 5.5% (n = 343) of all infants, in 9.4% of infants with patent ductus arteriosus and in 8.9% of infants who received indomethacin. The occurrence of necrotizing enterocolitis was independently associated with the presence of patent ductus arteriosus among infants not treated with indomethacin (odds ratio, 1.85) and those who received indomethacin therapy (odds ratio, 1.53). Indomethacin therapy in absence of patent ductus arteriosus was not associated with an increased risk of necrotizing enterocolitis (odds ratio, 0.72). CONCLUSIONS: Patent ductus arteriosus is an independent risk factor for the development of necrotizing enterocolitis in very low birth weight infants. Therapy with indomethacin did not have a significant effect on the risk for necrotizing enterocolitis.

Cardiovascular Agents↗
PubMed1989

The mechanism of action of endothelin-1 as compared with other agonists in vascular smooth muscle.

The effects of endothelin-1 (ET-1) on tension and membrane potential in rat isolated mesenteric resistance vessels (MRVs) and on 45Ca influx, 45Ca efflux, inositol-1,4,5-triphosphate (IP3) production, and cytoplasmic Ca2+ concentration ([Ca2+]1) in cultured aortic smooth muscle cells were compared with those of other agonists. ET-1 induced contractions of the MRVs, which were slow in onset, but reached a similar maximum amplitude (at 10 nM ET-1) as that seen with norepinephrine (NE, 10 microM) or [arg8]vasopressin (AVP, 0.1 microM). The EC50 for ET-1 was 1.3 +/- 0.1 nM. Removal of extracellular Ca2+ reduced ET-1-induced contractions to 11 +/- 3% of those in Ca2+-containing medium. With NE, the same procedure reduced contractions to 47 +/- 7% of those in Ca2+-containing medium, while with AVP, the reduction was similar in magnitude to that induced by ET-1 (11 +/- 5% of those in Ca2+-containing medium). Relaxation of ET-1-induced and NE-induced contractions by diltiazem was not complete (maximal at 58 +/- 6% with 10 microM diltiazem after 6 nM ET-1, and at 70 +/- 3% after 0.1 microM NE), in contrast to that of 80 mM K+-induced contractions, which were potently (IC50 = 0.2 microM) and completely reversed (100% relaxation at 10 microM diltiazem). ET-1 (6 nM) caused a small but significant depolarization of the MRVs (approximately 7 mV), the magnitude of which was only about one-third of that induced by equieffective contractile concentrations of NE and AVP. The voltage-sensitive Ca2+ channel agonist Bay K 8644 (1 microM), in contrast to ET-1, NE, and AVP, produced a small contraction (30 +/- 2% of the maximum response to NE), but no further depolarization when added in the presence of 15 mM K+ (which elicited approximately 12 mV depolarization but no contraction).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1998

A new and simple technique of total hepatic ischemia in the mouse.

BACKGROUND: A model of total hepatic ischemia is currently not available in mice. Models described in rats using portosystemic shunts to achieve total ischemia have been notoriously difficult. In mice, the problem is compounded further when using this type of technique because of the small size of the animal. A new technique is described combining partial hepatectomy with clamping of the remnant liver. METHODS: A partial (30%) hepatectomy is performed with resection of the caudate, right lateral, and quadrate lobes, and papillary process. Vascular microclamps are placed across the pedicles of the median and left lateral lobe at the level of the hilum to achieve total ischemia. Spontaneous portocaval shunts through caudate branches and collateral vessels prevent mesenteric congestion. Animals were studied for survival. RESULTS: The procedure consistently took less than 30 min (25+/-2 min), and no bleeding of the resected tissue was observed. Evidence for total hepatic ischemia and spontaneous shunts was demonstrated by the use of an intraportal dye. All animals survived 60 min of ischemia, whereas all died after 90 min of ischemia. CONCLUSION: This is a technically simple and rapid procedure to perform. In the current environment of multiple knockout mice and bioreagents that are available, a model of this type is essential.

Animals↗