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At least 523 records · Page 29Linked to original sources
PubMed1998

Involvement of calcitonin gene-related peptide (CGRP) receptors in insulin-induced vasodilatation in mesenteric resistance blood vessels of rats.

1. The vascular effect of insulin in the mesenteric resistance blood vessel and the role of calcitonin generelated peptide (CGRP)-receptor in insulin-induced vascular responsiveness were investigated in rats. 2. The mesenteric vascular beds isolated from Wistar rats were perfused with Krebs solution, and perfusion pressure was measured with a pressure transducer. In preparations contracted by perfusion with Krebs solution containing methoxamine in the presence of guanethidine, the perfusion of insulin (from 0.1 to 3000 nM) caused a concentration-dependent decrease in perfusion pressure due to vasodilatation. The pD2 value and maximum relaxation (%) were 6.94+/-0.22 and 43.9+/-5.2, respectively. 3. This vasodilator response to insulin was unaffected by 100 nM propranolol (beta-adrenoceptor antagonist) plus 100 nM atropine (muscarinic cholinoceptor antagonist), 100 microM L-NG-nitroarginine (nitric oxide synthase inhibitor), 1 microM ouabain (Na+-K+ ATPase inhibitor), or 1 microM glibenclamide (ATP sensitive K+-channel inhibitor). 4. In preparations without endothelium, perfusion of insulin produced a marked vasodilatation. The pD2 value and maximum relaxation (%) were 7.62+/-0.21 and 81.0+/-4.6, respectively, significantly greater than in preparations with intact endothelium. 5. The vasodilator responses to insulin in the preparations without endothelium were significantly inhibited by CGRP[8 37], a CGRP receptor antagonist, whereas pretreatment with capsaisin, a toxin for CGRP-containing nerves, did not affect insulin-induced vasodilatation. 6. These results suggest that insulin induces non-adrenergic, non-cholinergic and endothelium-independent vasodilatation, which is partially mediated by CGRP receptors.

Animals↗
PubMed2004

Critical intestinal ischaemia in a patient with patent mesenteric vasculature.

We present a case of a 62-year-old man with known coeliac disease who was admitted for investigation of abdominal pain and weight loss. He underwent multiple biochemical, haematological, radiological and endoscopic investigations (which were all normal) and also had a normal laparoscopy. Abdominal computerized tomography angiography, however, suggested significant mesenteric stenosis. Mesenteric angiography confirmed superior mesenteric artery stenosis and reproduced the patient's abdominal pain when the catheter crossed the lesion. Balloon angioplasty successfully dilated the stenosis, and since then the patient has gained 19 kg in weight (returning his body mass index from 17 to 23) and has been symptom free. Symptomatic single vessel mesenteric ischaemia (other than coeliac artery stenosis in median arcuate syndrome) is not previously well described. The symptom reproduction on catheterization highlights how useful angiography can be in diagnosis of disease significance. Symptom resolution after angioplasty demonstrated clearly how even single vessel disease can cause significant compromise to the mesenteric circulation.

Abdominal Pain↗
PubMed1998

Attenuation of diabetes-associated mesenteric vascular hypertrophy with perindopril: morphological and molecular biological studies.

Vascular disease is now the major cause of morbidity and mortality in the diabetic population. Our group explored the vascular changes associated with experimental diabetes and examined whether these changes can be ameliorated by angiotensin-converting enzyme (ACE) inhibition. The ACE inhibitor perindopril (PE) was administered to streptozotocin-induced diabetic rats for 24 weeks. At death, mesenteric vessels were perfused in vivo followed by assessment of the vascular architecture by quantitative histomorphometry. In a subgroup of animals, RNA was extracted from the mesenteric vasculature for assessment of gene expression of the prosclerotic cytokine, transforming growth factor beta 1 (TGFbeta1), and the matrix protein, type IV collagen. Diabetes was associated with smooth muscle hypertrophy and extracellular matrix (ECM) accumulation. ECM accumulation, particularly collagen deposition, was observed in the medial and adventitial layers. ACE inhibition prevented mesenteric vascular hypertrophy after 24 weeks of diabetes. In addition, overexpression of TGFbeta1 in the vessels of diabetic animals was prevented by PE treatment. Similarly, type IV collagen mRNA levels were increased in diabetic vessels, and this overexpression was also prevented by PE therapy. In summary, ACE inhibition attenuates many of the vascular changes observed in experimental diabetes and may have important clinical implications as a vasoprotective agent in human diabetes.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2001

Aortic side branch embolization before endovascular aneurysm repair: incidence of type II endoleak.

PURPOSE: To assess the feasibility of embolization of aortic side branches and its impact on the incidence of type II endoleak after endovascular aneurysm repair. MATERIALS AND METHODS: Endovascular aneurysm repair was performed in 74 patients. Aortic side branch vessels were evaluated on the preoperative angiogram and computed tomography (CT) and, where embolization of lumbar and inferior mesenteric vessels was considered technically possible, this was attempted prior to endovascular repair. Follow-up CT was used to assess the presence of type II endoleak. RESULTS: Seventy-two patients were followed up for longer than 1 month. Embolization was attempted in 25 cases, successfully in 10, with partial success in 11, and failure in four. Twenty patients with successful or partly successful preoperative embolization were discharged and followed-up. Four (20%) had demonstrable type II endoleak during follow-up, with two of these persisting at latest follow-up. Of 43 patients without previous embolization, there were 10 (23.3%) type II endoleaks during the follow-up period, four of these persisting. In cases with type II endoleak, mean sac diameter change was -0.5 mm in the cases with previous embolization and +3.1 mm without. The mean period to onset of type II endoleak was 6.9 months without, and 15.3 months with, previous embolization. CONCLUSION: Although the cohort size is below a level that would confer significance, the trend of these findings is such as to suggest a lack of influence of aortic side branch embolization on the incidence of type II endoleak during the follow-up period.

Angiography↗
PubMed1998

[Acute disorders of intestinal perfusion; a nonrigid abdomen may still be acute].

Three patients, a man aged 50 years and two women aged 46 and 45 years, with abdominal pains and an undistended abdomen, were found to have acute mesenteric ischaemia. The causes were: unknown, a thrombus in the descending aorta and severe atherosclerosis, respectively. In the male patient, only 30 cm of vital small intestine ultimately remained; in one woman embolectomy sufficed, in the other, resection of a limited portion of the jejunal tract. All three patients fully recovered. Acute mesenteric ischaemia is a potentially lethal disease. Diagnosis in the first reversible phase makes full recovery of the intestine possible. This may be difficult since the clinical signs and symptoms are not specific in this phase and invasive diagnostic procedures (angiography) are required for accurate diagnosis. By making an angiogram of the mesenteric vessels in each patient with severe abdominal pain, no signs of peritonitis and leukocytosis, without another diagnosis, reversible mesenteric ischaemia can be diagnosed and a vascular surgical reconstruction can be planned.

Abdomen, Acute↗
PubMed1976

[Etiology of shock lung: case report (author's transl)].

In a woman, 29, two times resection and anastomosis of the small intestine because of extended infarction was performed. Following peritonitis and septic shock a progressive respiratory insufficiency developed and patient died 48 hours later despite intensive ventilatory treatment. Autopsy findings were manifold vascular damage (aorta) and thromboembolisms in mesenteric vessels and iliac veins too. Patient received oral contraceptives over several years, changed the preparation previously and contraceptive therapy was continued with another one. Thromboembolic complications may understood as undesirable side effects of the contraceptives. By microscopy of lung thrombosis in capillaries was seen and in small arteries too, as embolism carried by the blood stream. In pathogenesis of shock lung macrothrombosis as an aetiologic factor is to be discussed.

Adult↗
PubMed1997

Transaortic mesenteric endarterectomy.

Although a number of methods for mesenteric artery reconstruction have been suggested, we believe that patients with atherosclerotic stenosis and occlusion of mesenteric vessels presenting with either acute or chronic visceral ischemia are best managed by either antegrade aortomesenteric bypass or transaortic mesenteric endarterectomy. Antegrade bypass is the most versatile technique and is therefore best adapted to extensive mesenteric disease. Transaortic mesenteric endarterectomy lends itself well to simultaneous renal artery endarterectomy when clinically significant osteal atherosclerosis is present at both sites. With any method of reconstruction, the technical adequacy of repair should be defined intraoperatively. In this regard, intraoperative duplex sonography provides both anatomic and hemodynamic data necessary to ensure technical success and late patency.

Arterial Occlusive Diseases↗
PubMed2000

Effects of aldose reductase inhibition on responses of the corpus cavernosum and mesenteric vascular bed of diabetic rats.

We examined the effects of 2 months of streptozotocin-induced diabetes mellitus in rats on relaxation and contraction of corpus cavernosum and the mesenteric vascular bed in vitro. A further diabetic group was treated from diabetes induction with 10 mg/kg/day of the aldose reductase inhibitor, WAY121509. For corpus cavernosum, maximal acetylcholine-induced relaxation was 35.5% reduced (p < 0.001) by diabetes, and this deficit was completely prevented by WAY121509 treatment. Neither diabetes nor treatment affected contractile responses to field stimulation of noradrenergic nerves; however, nonadrenergic noncholinergic nerve relaxation responses were 32.9% decreased by diabetes and WAY 121509 attenuated this by 84% (p < 0.001). For the mesenteric vascular bed, diabetes depressed maximal endothelium-dependent vasodilation to acetylcholine by 25.2% (p < 0.001), and this was partially (50.6%; p < 0.01) prevented by WAY121509. Nitric oxide synthase blockade revealed endothelium-derived hyperpolarising factor-mediated vasodilation to acetylcholine that was 73.5% (p < 0.001) depressed by diabetes; WAY121509 provided partial (43.4%; p < 0.001) protection. Neither diabetes nor treatment affected endothelium-independent vasorelaxation to the nitric oxide donor, sodium nitroprusside, in corpus cavernosum or mesenteric vessels. Thus the data show protective effects of WAY121509 on nitric oxide-mediated cavernosal vasorelaxation responses and on mesenteric endothelium-derived hyperpolarising factor responses. Together these findings could account for the beneficial effects of aldose reductase inhibition on diabetic complications in experimental models.

Aldehyde Reductase↗
PubMed2005

Disturbance of hepatic and intestinal microcirculation in experimental liver cirrhosis.

AIM: To analyze hepatic, mesenteric and mucosal microcirculation and leukocyte-endothelium interaction (LEI) in a rat model with liver cirrhosis. METHODS: Hepatic cirrhosis was induced in Wistar rats by gavage with carbon tetrachloride, and intravital videomicroscopy was performed in liver, mesentery and small intestine mucosa. Special emphasis is given on microcirculatory and morphometric changes during cirrhotic portal hypertension. RESULTS: LEI was influenced significantly in the cirrhotic liver but not in the gut. Blood flow measurement showed significant differences among liver, main mesenteric vessels and the mucosa. The results of our study indicate that liver cirrhosis leads to alterations in hepatic and mesenteric blood flow but not in mucosal blood flow. CONCLUSION: The enhanced inflammatory response in hepatic microvessels may be caused by a decrease of antithrombin III levels and could be responsible for disturbances of organ pathology.

Animals↗
PubMed1981

[Functional assessment of the hepatic arterial blood flow by pharmacoradiography (author's transl)].

By means of celiacography it was possible to demonstrate that parenteral medication with parathormone creates a selective dilatation of the liver vessels in man, provided that they are dilatable. This hemodynamic hormone effect could not be traced in the other mesenteric vessels. The increase of portal hypertension resulting from cirrhosis leads to a loss of the dilating ability of liver vessels. This regressive reaction is well demonstrated on the parathormon-celiaco-gram. Thus a functional assessment of the hepatic blood flow is possible. The extent of the dilatability of the liver artery seems to be of great importance for the prognosis and indication of the porto-systemic shunt-operation. Moreover we could show that an increase in the liver perfusion demonstrates pathologic liver processes in a better way.

Celiac Artery↗
PubMed2004

Signaling of angiotensin II-induced vascular protein synthesis in conduit and resistance arteries in vivo.

BACKGROUND: From in vitro studies, it has become clear that several signaling cascades are involved in angiotensin II-induced cellular hypertrophy. The aim of the present study was to determine some of the signaling pathways mediating angiotensin II (Ang II)-induced protein synthesis in vivo in large and small arteries. METHODS: Newly synthesized proteins were labeled during 4 hours with tritiated leucine in conscious control animals, or animals infused for 24 hours with angiotensin II (400 ng/kg/min). Hemodynamic parameters were measure simultaneously. Pharmacological agents affecting signaling cascades were injected 5 hours before the end of Ang II infusion. RESULTS: Angiotensin II nearly doubled the protein synthesis rate in the aorta and small mesenteric arteries, without affecting arterial pressure. The AT1 receptor antagonist Irbesartan antagonized the actions of Ang II. The Ang II-induced protein synthesis was associated with increased extracellular signal-regulated kinases (ERK)1/2 phosphorylation in aortic, but not in mesenteric vessels. Systemic administration of PD98059, an inhibitor of the ERK-1/2 pathway, produced a significant reduction of protein synthesis rate in the aorta, and only a modest decrease in mesenteric arteries. Rapamycin, which influences protein synthesis by alternative signaling, had a significant effect in both vessel types. Rapamycin and PD98059 did not alter basal protein synthesis and had minimal effects on arterial pressure. CONCLUSION: ERK1/2 and rapamycin-sensitive pathways are involved in pressure-independent angiotensin II-induced vascular protein synthesis in vivo. However, their relative contribution may vary depending on the nature of the artery under investigation.

Angiotensin II↗
PubMed1995

Shock-associated right colon ischemia and necrosis.

Ischemic complications associated with hemorrhagic shock after blunt or penetrating trauma can result in acute renal, pulmonary, or hepatic failure. Less well described is the association between hemorrhagic shock and ischemic necrosis of the right colon, with only 14 cases reported in the literature. Herein, we report three previously healthy young trauma victims with shock-associated right colon necrosis. Each patient suffered a period of hypotension after injury. Diagnosis and operation took place within 2 days of initial injury in all three cases. In each patient, a right colectomy and primary anastomosis was performed without complication. Pathologic examination of the resected specimens showed ischemic necrosis, but no evidence of vascular thrombosis or embolic occlusion of the mesenteric vessels. The etiology of this type of ischemic colitis is not clear, but seems to represent a form of nonocclusive mesenteric ischemia. Knowledge of this disease process will lead to early recognition, prompt treatment, and a satisfactory outcome.

Adolescent↗
PubMed1989

Pheochromocytoma and ischemic enterocolitis.

In the nine year period, 1978-1987, two patients with pheochromocytoma presented to Sacred Heart Hospital, Yankton, South Dakota. Both cases were complicated pre-operatively by ischemic enterocolitis--a rarely reported, usually fatal complication of pheochromocytoma. It is thought that catecholamine-induced vasoconstriction of the mesenteric vessels resulted in the wide-spread hemorrhagic necrosis of the gut. Both patients survived not only the initial ischemic mesenteric insult, but also excision of the tumor.

Adrenal Gland Neoplasms↗
PubMed1980

Polyarteritis overlap syndrome with extensive bowel infarction.

An elderly female with laboratory evidence of rheumatoid arthritis presented with malnutrition, elevated erythrocyte sedimentation rate, peripheral eosinophilia with eosinophilic infiltration of the pleura, uterus, skin and muscle without granuloma formation. She developed a necrotizing vasculitis of the mesenteric vessels without granuloma and died. This case illustrates that polyarteritis nodosa, even of the overlap type, may produce severe widespread mesenteric vasculitis.

Female↗
PubMed1985

Cellular changes in mesenteric arteries and veins after acute perfusions of angiotensin II and vasoactive amines.

Cross-sections of rat mesenteric vessels were examined histologically after short-term perfusions of angiotensin II (AII), norepinephrine (NE), 5-hydroxytryptamine (5-HT), and histamine. Mesenteric veins (300-400 micron) and muscular venules (50-100 micron) exhibited dose-dependent constrictor responses to AII, but not to NE. Arterioles of comparable size (50-100 micron) did not constrict at low doses of AII or NE, but responded when higher pressor concentrations of each agonist were perfused. At equipressor doses, constriction of mesenteric arterioles was greater following NE when compared with AII. Short perfusions of 5-HT resulted in mild venoconstriction, while histamine induced dilation of the muscular venules. Ultrastructurally, vascular damage in response to AII was minimal and confined to the formation of small vacuoles in the endothelial cytoplasm. Endothelial integrity was preserved and no autonomous endothelial contraction was observed. Vacuolation induced by NE was far more extensive and particularly evident in arteries and arterioles.

Amines↗
PubMed2002

[Reaction of regional abdominal blood flow in peritonitis to vasoactive medication based on data of selective angiography and rheography].

With the help of selective arteriography of the mesenteric vessels and rheography it was found that patients with peritonitis are characterized by a reduction of blood flow in the superior mesenteric artery as a result of a spasm of the artery and its branches in the small intestine wall. This reaction is functional and can be eliminated or attenuated by purposeful measures, the most effective of them being prolonged peridural anesthesia (PPA) and droperidol injections. Thus the both methods of correction of the peritonitis dynamics (PPA and droperidol) can block up the transition of the reactive stage of peritonitis to toxic. The use of regional rheography is thought to be more expedient in medical practice than selective angiography for the assessment of the character of mesenteric blood flow in operated peritonitis patients as a more accessible and safe method for multiple performances.

Adjuvants, Anesthesia↗
PubMed1981

Intestinal infarction associated with mesenteric vascular thrombotic disease in the horse.

Intestinal infarction associated with cranial mesenteric artery thrombosis, without strangulation obstruction of the intestine, was studied in 18 horses. Findings normally of value in evaluating horses with acute abdominal pain (heart rate, rectal palpation findings, gastric reflux) or classification of the degree of pain were not helpful in diagnosing the problem. Similarly, packed cell volume, plasma total protein, circulating white blood cell count, peritoneal white blood cell count, and peritoneal fluid total protein were not of value in predicting severity of the intestinal damage, location of infarction, or patient survival. In one half of the cases, peritoneal fluid color was of aid in distinguishing intestinal infarction from strangulation. Findings on gross dissection and limited histologic examination did not support the premise that thromboembolism was the major mechanism for production of infarction. In most of the horses, a thrombus or embolus was not found in the peripheral mesenteric vessels.

Animals↗