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At least 73 records · Page 4Linked to original sources
PubMed1999

Refractory proctosigmoiditis caused by myointimal hyperplasia of mesenteric veins: report of a case.

PURPOSE: Proctosigmoiditis occurring in young adults is usually idiopathic and usually responds to medical management. If the process progresses to pancolitis and is refractory to medical management, proctocolectomy may be required. Myointimal hyperplasia of mesenteric veins, though rare, may also cause proctosigmoiditis, but this entity, in contrast to the idiopathic variety, does not respond to medical management; surgical excision limited to the involved colonic segment is curative. Because the treatment of the two entities differs significantly, it is important to distinguish them diagnostically. The purpose of this case report is to increase awareness of myointimal hyperplasia of mesenteric veins and to emphasize the clinical features that distinguish it from idiopathic proctosigmoiditis. METHODS: We report the case of a twenty-two-year-old male with an inflammatory process involving the distal colon and rectum, initially thought to be idiopathic proctosigmoiditis. The inflammation did not respond to an extensive course of medical management, and the patient developed complications associated with both the disease process and his medical therapy. Surgical resection of the rectosigmoid was performed. RESULTS: Histologic examination of the resected colon revealed the underlying process to be colonic ischemia caused by myointimal hyperplasia of mesenteric veins not associated with idiopathic inflammatory bowel disease or systemic vasculitis. CONCLUSION: Proctosigmoiditis caused by myointimal hyperplasia of mesenteric veins and idiopathic proctosigmoiditis may present in a similar fashion. Although patients with myointimal hyperplasia of mesenteric veins do not respond to medical management, segmental resection is usually curative, and long-term drug therapy or even proctocolectomy can be avoided. Physicians should consider the possibility of myointimal hyperplasia of mesenteric veins when patients with apparent idiopathic proctosigmoiditis do not respond to medical therapy.

Adult↗
PubMed2005

PI3K and PKC contribute to membrane depolarization mediated by alpha2-adrenoceptors in the canine isolated mesenteric vein.

BACKGROUND: Norepinephrine (NE), a classic neurotransmitter in the sympathetic nervous system, induces vasoconstriction of canine isolated mesenteric vein that is accompanied by a sustained membrane depolarization. The mechanisms underlying the NE-elicited membrane depolarization remain undefined. In the present study we hypothesized that phosphatidylinositol 3-kinase (PI3K) and protein kinase C (PKC) are involved in the electrical field stimulation (EFS)-induced slow membrane depolarization (SMD) in canine isolated mesenteric vein. EFS (0.1-2 Hz, 0.1 ms, 15V, 10 s)-induced changes in the membrane potential were recorded with a conventional intracellular microelectrode technique and evaluated in the absence and presence of inhibitors of neuronal activity, alpha-adrenoceptors, membrane ion channels, PI3K, inositol 1,4,5-triphosphate (InsP3) receptors, and PKC. Activation of PI3Kgamma and PKCzeta in response to exogenous NE and clonidine in the absence and presence of receptor and kinase inhibitors were also determined. RESULTS: Contractile responses to NE and clonidine (0.05 - 10 microM) were significantly diminished in the presence of yohimbine (0.1 microM). Exogenous NE (0.1 microM) and clonidine (1 microM) elicited SMD. The resting membrane potential of canine mesenteric vein smooth muscle cells was -68.8 +/- 0.8 mV. EFS elicited a biphasic depolarization comprised of excitatory junction potentials and SMD that are purinergic and adrenergic in nature, respectively. The magnitude of the SMD in response to EFS at 0.5 Hz was 9.4 +/- 0.7 mV. This response was reduced by 65-98% by the fast Na+ channel inhibitor tetrodotoxin (1 microM), by the inhibitor of N-type Ca2+ channels omega-conotoxin GVIA (5 nM), the non-selective alpha-adrenoceptor blocker phentolamine (1 microM), the selective alpha2-adrenoceptor blocker yohimbine (0.1 microM), the ion channel inhibitors niflumic acid (NFA, 100 microM), 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB, 30 microM), 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS, 200 microM), and Gd3+ (30 microM), and the PI3K inhibitors wortmannin (100 nM) and LY-294002 (10 microM). The SMD remained unchanged in the presence of the L-type Ca2+ channel blocker nicardipine (1 microM) and the InsP3 receptor blockers 2-aminoethoxydiphenylborate (2APB, 50 microM) and xestospongin C (3 microM). The inhibitor of PKC chelerythrine (1 microM), but not calphostin C (10 microM), diminished the SMD. Exogenous NE and clonidine (1 microM each) activated both PI3Kgamma and PKCzeta, and the activation of these kinases was abolished by preincubation of tissue with the alpha2-adrenoceptor blocker yohimbine. CONCLUSION: Neuronally-released NE stimulates smooth muscle alpha2-adrenoceptors and activates PI3K and atypical PKC in the canine mesenteric vein. Events downstream of PKC lead to SMD and vasoconstriction. This represents a novel pathway for NE-induced membrane depolarization in a vascular smooth muscle preparation.

Adrenergic alpha-2 Receptor Antagonists↗
PubMed2000

Neuropeptide Y is a cotransmitter with norepinephrine in guinea pig inferior mesenteric vein.

Neuropeptide Y (NPY) is a cotransmitter with noradrenaline in guinea pig inferior mesenteric vein. Tyrosine hydroxylase-like immunoreactivity and NPY-like immunoreactivity were colocalized in a dense network of fibers within the adventitial layer of guinea-pig inferior mesenteric vein. Vasoconstrictor responses to electrical field stimulation (0.2-64 Hz, 0.1 ms, 12 V, for 10 s) appear to be mediated primarily by norepinephrine at 0.2 to 4 Hz and by NPY at 8 to 64 Hz. NPY Y1 receptors mediate the contractile responses to both endogenous and exogenous NPY. Norepinephrine and NPY are involved in neuromuscular transmission in guinea pig mesenteric vein suggesting that the sympathetic nervous system requires the coordinated action of norepinephrine and NPY to serve capacitance.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

[Direct assessment of mesenteric vein compliance in the rat during pregnancy].

This study was designed for two purposes. The first was to establish an in-vitro technique for the comparative study of isolated capacitance veins during pregnancy. Secondly, to test the hypothesis that pregnancy is associated with an increase in venous compliance and the unstressed volume of the veins. Capacitance-size mesenteric veins were mounted in a pressurized myograph system equipped with a video dimension analyzing system and a servo pressure control unit, which was modified for venous studies. After equilibration, the transmural pressure was changed from 2 to 10 mmHg in 2 mmHg increments every 15 minutes. The calculated change in volume over this pressure range consisted of both a change in vessel diameter and in axial length. The veins from the nonpregnant rats exhibited a greater change in axial length than those from the pregnant rats (21% vs. 14%). Unexpectedly, the compliance (change in volume/change in pressure) of the veins from the pregnant rats was significantly less (42%) than those from the nonpregnant rats. However, the basic component of the change in vascular capacitance, the unstressed volume, was significantly greater in the veins from the pregnant rats (100%). We conclude that pregnancy causes alterations in the wall of the capacitance veins, which results in an apparent increase in volume at the expense of wall compliance. Secondly, the pressurized myograph system is a valuable tool for studying the physiology of the capacitance veins during pregnancy under rigorously controlled conditions.

Animals↗
PubMedDate not supplied

Outcome from traumatic injury of the portal and superior mesenteric veins.

Traumatic injuries to the portal vein (PV) and superior mesenteric vein (SMV) are rare and carry a high mortality rate, and the best approach and method of repair is still subject to debate. The objective of the present study was to analyze risk factors for mortality in portal and superior mesenteric venous injuries. A retrospective analysis of 18 patients during a 5-year period was performed. Mechanism of injury, shock upon admission, Revised Trauma Score (RTS), Injury Severity Score (ISS), intraoperative fluid requirements, classification of venous injury severity, and associated injuries were analyzed as potential predictors of outcome. All patients were male, 9 were victims of gunshot wounds, and 11 were in shock at the time of admission. Eight patients sustained PV, and 12 sustained SMV injuries. The great majority of patients had more than 1 associated injury and 61% had an associated vascular injury. Mortality rate correlated with injury severity. Overall mortality rate was 72%. Nonsurvivors had higher ISS than survivors (24 +/-0.4 and 20 +/-1.7, respectively; p = 0.006). Uncontrollable intraoperative hemorrhage was the cause of death in 5 of 13 patients (38.4%). Six patients died during the postoperative period from complications of prolonged shock and multiple organ failure, and 2 died of sepsis. The physiologic status upon admission, the number of associated injuries, and the severity of the vascular injury are the most important factors related to mortality in PV and SMV injuries.

Abdominal Injuries↗
PubMed1990

Superior mesenteric vein inflow for liver transplantation when the portal vein is occluded.

An alternative solution to the problem of liver transplantation in the patient with an occluded portal vein is described. It uses a bridge graft of donor iliac vein from the superior mesenteric vein at the base of the colonic mesentery. The graft is tunnelled over the pancreas and under the stomach to the region of the liver hilum to provide portal inflow. This procedure was employed successfully in four patients, with patency for more than 2 years in the patient with the longest follow-up. By this approach it is routinely possible to perform a transplant procedure in a recipient with an occluded portal vein.

Adult↗
PubMed2005

Portal vein thrombosis after laparoscopic colectomy: thrombolytic therapy via the superior mesenteric vein.

Portal vein thrombosis is a rare but well-reported complication after laparoscopic surgery. We present a case of portomesenteric venous thrombosis that occurred 8 days after a laparoscopic-assisted right hemicolectomy. Systemic anticoagulation failed to improve symptoms. The early postoperative state precluded the use of transarterial thrombolytic therapy. Transjugular intrahepatic catheter-directed infusion of urokinase into the superior mesenteric vein resulted in clearance of thrombus and resolution of symptoms. The published data on laparoscopy-induced splanchnic venous thrombosis and transjugular intrahepatic intramesenteric thrombolysis are discussed.

Colectomy↗
PubMed1995

Nitric oxide-mediated neurogenic relaxation in monkey mesenteric veins.

The purpose of this investigation was to determine if neurally induced vasodilatation is mediated by nitric oxide (NO) in monkey mesenteric veins. Helical strips of the monkey mesenteric vein were exposed to the bathing media for isometric tension recording, and perivascular nerves were stimulated by nicotine. Nicotine produced a contraction, which was potentiated by treatment with NG-nitro-L-arginine, a NO synthase inhibitor, the effect being reversed by L-arginine. The nicotine-induced contraction was reversed to a relaxation by prazosin. The relaxation was abolished by the NO synthase inhibitor, and it was restored by L-arginine. D-Enantiomers were without effect. The response was not influenced by timolol and indomethacin, but was abolished by hexamethonium and oxyhemoglobin. There were perivascular nerve fibers containing NO synthase immunoreactivity in the monkey vein. Neurally induced venous relaxations appear to be mediated by NO from perivascular nerves, as seen in dog and monkey mesenteric arteries. It is concluded that monkey mesenteric veins are innervated by nitroxidergic and adrenergic nerves, which may balance the vascular tone.

Animals↗
PubMed1993

[Acute mesenteric vein thrombosis. A rare complication after splenectomy due to autoimmune hemolytic anemia in childhood].

Mesenteric vein thrombosis is a rare but severe complication in children requiring splenectomy. We report on a 5-year-old boy with an autoimmune hemolytic anemia who underwent splenectomy because of severe side effects from cortisone therapy. 10 months after splenectomy he presented with signs of a paralytic ileus. Laparotomy showed mesenteric vein thrombosis with hemorrhagic bowel infarction requiring resection of two thirds of the small intestine. An early recognition and thrombolytic or surgical treatment of mesenteric vein thrombosis may reduce the incidence of hemorrhagic infarction, peritonitis, and secondary complications in these patients.

Anemia, Hemolytic, Autoimmune↗
PubMed1988

Electrophysiology of neuromuscular transmission in guinea-pig mesenteric veins.

1. Neuromuscular transmission in the smooth muscle of mesenteric veins has been investigated by recording intracellular potential changes resulting from stimulation of the sympathetic nerves and comparing these potential changes with responses obtained by ionophoresis of noradrenaline. 2. Neural stimulation or exogenous noradrenaline acted similarly to cause two excitatory depolarizations, a slow response reported previously (Suzuki, 1981) and a separate fast depolarization. 3. The fast depolarization was distinct from the slow depolarizing response in that it had a different dependence on the level of stimulation, was readily desensitized and was more suppressed in low-chloride solution. 4. The fast but not the slow depolarization shared certain characteristics with constriction. The fast depolarization and constriction both increased with the intensity of stimulation; inactivation in both was dependent on the recovery interval between trains of stimuli and both were suppressed to a similar degree by antagonists to alpha-adrenoceptors. The fast depolarization was, however, not a prerequisite for constriction to occur. 5. The fast and slow depolarizations were activated after a long latency which had a high temperature coefficient consistent with the postulate that these responses are rate limited by intracellular biochemical reactions. 6. The fast depolarization was preferentially suppressed by prazosin, an antagonist to the alpha 1-adrenoceptor subtype. Suppression of the slow depolarization required relatively higher concentrations of antagonist, indicating that these responses were mediated by receptor interactions involving a different alpha-adrenoceptor subtype. 7. It is concluded that neuromuscular transmission in mesenteric veins occurs through activation of alpha-adrenoceptors. A number of responses result, including voltage-independent constriction and two distinct excitatory depolarizations which can lead to voltage-dependent constriction.

Action Potentials↗
PubMed1998

Endothelium-dependent potentiation of prostaglandin F2alpha-induced contractions by (+/-)-[6]-gingerol is inhibited by cyclooxygenase- but not lipoxygenase-inhibitors in mouse mesenteric veins.

The mechanism of potentiation of prostaglandin (PG) F2alpha-induced contraction of mouse mesenteric veins by (+/-)-[6-gingerol was investigated in vitro. (+/-)-[6]-Gingerol (0.3mM) potentiated the maximal contraction response elicited by PGF2alpha (0.28 mm) in the presence of intact vascular endothelium, but not in its absence (de-endothelialized preparations). The potentiating effect was completely inhibited by cyclooxygenase inhibitors (0.2 mm aspirin and 0.2 mm indomethacin) and partly by calcium antagonists (2 microM verapamil, 8 nM nitrendipine and 1 microM ryanodine), but not inhibited by nordihydroguaiaretic acid (NDGA), a lipoxygenase inhibitor and ONO-3708, a thromboxane (TX) A2 antagonist. The potentiation by (+/-)-[6]-gingerol is also observed in mesenteric veins of streptozotocin-diabetic mice where the enhancement of PGF2alpha-induced contraction is caused mainly by activation of lipoxygenase. The potentiation of PGF2alpha-induced contraction by (+/-)-[6]-gingerol may be caused by a cyclooxygenase-dependent release of vasoconstrictors, other than PGF2alpha and TXA2, or by inhibiting vasorelaxants released from endothelial cells of mouse mesenteric veins.

Animals↗
PubMed1998

Portal decompression using the inferior mesenteric vein.

We report five patients with variceal hemorrhage, in three cases secondary to diffuse thrombosis of the portal, superior mesenteric and splenic veins. Mesenteric angiography demonstrated patency of the inferior mesenteric vein (IMV) in each, and successful portal decompression by anastomosis of the IMV to the left renal vein (n = 4) or the inferior vena cava (n = 1) was accomplished. Bleeding was permanently controlled: four patients have survived from one to eight years post-operatively. Because shunt procedures utilizing the IMV are technically straightforward, subtotally decompress the portal system and avoid the right upper quadrant, they may be advantageous in certain clinical settings.

Adult↗
PubMed1996

Mucosal biopsy findings and venous abnormalities in idiopathic myointimal hyperplasia of the mesenteric veins.

Idiopathic myointimal hyperplasia of the mesenteric veins (IMHMV) is a rare cause of intestinal ischemia secondary to venous compromise. A patient with this condition who presented with crampy abdominal pain, diarrhea, and rectal bleeding initially attributed to inflammatory bowel disease had several colonoscopies and ultimately a sigmoid colectomy. The colonic mucosa in biopsies performed at initial presentation and subsequently and in the resection specimen contained numerous hyperplastic, thick-walled, hyalinized vessels in the lamina propria, which have not been described in this entity previously. Examination of the mucosa in 27 resection specimens of ischemic enterocolitis of various etiologies, in five resections of prolapsed rectum, and in seven colostomy specimens revealed no instance in which there were similar histologic abnormalities. When seen on biopsy, therefore, these features should lead to inclusion of IMHMV in the differential diagnosis. Furthermore, the characteristic lesions of the submucosal and extramural veins in IMHMV were compared with those of 14 examples, from several organs, of veins subjected to arterial pressure and 21 cases of venous hypertension. The marked similarity of the arterialized veins to the mural veins of IMHMV suggests a role for arteriovenous fistulization in the pathogenesis of IMHMV, and a mechanism by which this might occur is proposed.

Arteriovenous Malformations↗
PubMed1985

Superior mesenteric vein thrombosis: a case report.

Superior mesenteric vein thrombosis is an abdominal emergency that is rarely diagnosed early. Abdominal pain, vomiting, fever, and hematochezia are the characteristic presenting complaints. Tenderness, distension, and diminished intestinal sounds were the prominent abdominal physical findings in this case and were often associated with tachycardia and hypotension. This is a case that demonstrates all the nonspecifics, and one in which the patient survived beyond all others reported in the literature to date.

Humans↗
PubMed2001

Extensive mesenteric vein and portal vein thrombosis successfully treated by thrombolysis and anticoagulation.

Mesenteric vein thrombosis is generally difficult to diagnose and can be fatal. A case of extensive thrombosis of the mesenteric and portal veins was diagnosed early and successfully treated in a 26-year-old man with Down syndrome who was admitted to hospital because of abdominal pain, severe nausea and high fever. Ultrasonography revealed moderate ascites, and there was minimal flow in the portal vein (PV) on the Doppler examination. Computed tomography (CT) showed remarkable thickening of the walls of the small intestine and extensive thrombosis of the mesenteric, portal and splenic veins. Because neither intestinal infarction nor peritonitis was seen, combined thrombolysis and anticoagulation therapy without surgical treatment was chosen. Urokinase was administered intravenously and later through a catheter in the superior mesenteric artery. Heparin and antibiotics were given concomitantly. The patient's symptoms and clinical data improved gradually. After 10 days, CT revealed that collateral veins had developed and the thrombi in the distal portions of the mesenteric veins had dissolved, although the main trunk of the PV had not recanalized. The only risk factor of thrombosis that was detected was decreased protein S activity.

Adult↗