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[Anterior resection in rectal cancer: the role of lymphadenectomy. Comparison of 2 surgical experiences].

Of great interest today is the debate regarding the benefits and limitations of extended lymphadenectomy in rectal cancer, particularly with regard to patient survival. In the present report we review the experience of two different surgical departments: a total of 458 patients with rectal cancer were operated on in the 1st Surgical Department of S. Martino Hospital, Genoa, and in the 1st Surgical Department of Galliera Hospital, Genoa over the period from 1980 to 1989. Anterior rectal resection was performed in 137 rectal tumours at the S. Martino Hospital and in 146 at the Galliera Hospital. The mean follow-up was 48 months (range: 24-120 months). In the first group of patients, ligation at the origin of the mesenteric vessels (with subsequent peri-aortic lymphadenectomy) (D2-D3) was performed, while in the second group the mesenteric vessel ligation was done at the level of the origin of the left colic vessels (D1). There were no complementary therapies (radio or chemotherapy) either before or after surgery, because these were only introduced later. The data obtained from analysis of the long-term survival curves showed that there were no statistical differences between the two surgical experiences. The execution of extended lymphadenectomy would not appear to afford any additional benefit in terms of the survival of patients with rectal cancer. The well-matched starting conditions in the two groups allowed effective comparison between the two experiences and evaluation of the "pure" surgical aspect.

Adult↗

Cellular morphology in mesenteric resistance vessels from antihypertensive treated spontaneously hypertensive rats.

The effects on media smooth muscle cell size of long-term antihypertensive treatment with four different drugs were studied in isolated segments of mesenteric resistance arteries from spontaneously hypertensive rats (SHRs) using an unbiased stereological principle (the "disector"). Young SHRs were treated from age 4 weeks to 24 weeks with metoprolol (130 mg/kg/day), isradipine (42 mg/kg/day), captopril (60 mg/kg/day) or perindopril (1.5 mg/kg/day). At 24 weeks, when all drugs had lowered the blood pressure in SHRs compared to untreated controls (order of efficacy perindopril greater than captopril greater than isradipine greater than metoprolol), random arterial samples were taken from the mesenteric vascular bed close to the intestine and mounted on an isometric myograph, allowing standardized measurements of vascular dimensions. Although, taken together, the four treatments reduced blood pressure as well as the media:lumen ratio of the vessels and the number of cell layers, there was no significant effect of the treatments, taken together, on cell volume, cell number or on the ratio between interstitium and cells. However, cell volume correlated with blood pressure (P less than 0.05), suggesting that the most effective treatments (perindopril and captopril) had inhibited cell growth. It is, however, not clear whether the effect on cell volume was a specific effect of the drugs used, or whether it was only due to the blood pressure reduction.

Animals↗

[Vascular compression of the duodenum].

The acute vascular compression of the duodenum is a well-recognized clinical entity, characterized by recurrent vomiting, abdominal distention, weight loss, post prandial distress. The cause of compression is considered to be effect produced as a result of the angle formed by the superior mesenteric vessels and sometimes by one of its first two branches, and vertebrae and paravertebral muscles, when the angle between superior mesenteric vessels and the aorta it's lower than 18 degrees we can saw this syndrome. The duodenojejunostomy is the best treatment, as well as in our patient.

Adolescent↗

Contrast-enhanced three-dimensional magnetic resonance angiography of the mesenteric vasculature.

The diagnosis and treatment of mesenteric occlusive disease is important due to the high morbidity and mortality associated with ischemia of the bowel. This article describes the application of magnetic resonance angiography (MRA) as a minimally invasive tool for diagnosing mesenteric and portal vascular disease. The techniques for three-dimensional (3D) contrast-enhanced MRA and flow measurement of the mesenteric circulation are described. Excellent image quality is obtained using sagittal contrast-enhanced 3D MRA of the aorta and proximal mesenteric vessels. Delineation of the small distal mesenteric branch vessels is still limited due to the finite spatial resolution of MRA. The application of MRA techniques to the diagnosis of mesenteric ischemia, revascularization, transplantation, and portal hypertension are demonstrated. Finally, the merits of various acquisition techniques and future contrast agents are discussed. MR angiography using intravenously administered contrast agents provides the clinician with a powerful, minimally invasive method for diagnosing mesenteric vascular disease.

Contrast Media↗

Comparison of the pharmacological properties of EDHF-mediated vasorelaxation in guinea-pig cerebral and mesenteric resistance vessels.

In the presence of L-NNA (100 microM), indomethacin (10 microM) and ODQ (10 microM), acetylcholine induced a concentration-dependent vasorelaxation of guinea-pig mesenteric and middle cerebral arteries precontracted with cirazoline or histamine, but not with high K(+), indicating the contribution of an endothelium-derived hyperpolarizing factor (EDHF). In cerebral arteries, charybdotoxin (ChTX; 0.1 microM) completely inhibited the indomethacin, L-NNA and ODQ-insensitive relaxation; iberiotoxin (IbTX, 0.1 microM), 4-aminopyridine (4-AP, 1 mM), or barium (30 microM) significantly reduced the response; in the mesenteric artery, ChTX and IbTX also reduced this relaxation. Glibenclamide (10 microM) had no affect in either the mesenteric or cerebral artery. Neither clotrimazole (1 microM) nor 7-ethoxyresorufin (3 microM) affected EDHF-mediated relaxation in the mesenteric artery, but abolished or attenuated EDHF-mediated relaxations in the cerebral artery. AM404 (30 microM), a selective anandamide transport inhibitor, did not affect the vasorelaxation response to acetylcholine in the cerebral artery, but in the mesenteric artery potentiated the vasorelaxation response to acetylcholine in an IbTX, and apamin-sensitive, but SR 141816A-insensitive manner. Ouabain (100 microM) almost abolished EDHF-mediated relaxation in the mesenteric artery, but enhanced the relaxation in the cerebral artery whereas the addition of K(+) (5 - 20 mM) to precontracted guinea-pig cerebral or mesenteric artery induced further vasoconstriction. These data suggest that in the guinea-pig mesenteric and cerebral arteries different EDHFs mediate acetylcholine-induced relaxation, however, EDHF is unlikely to be mediated by K(+).

4-Aminopyridine↗

Intestinal ischaemia associated with carcinoid tumour: a case report with review of the pathogenesis.

A case of ischaemic ileal perforation associated with a macroscopically unapparent ileal carcinoid is described. The mesenteric vessels were non-pulsatile at operation but were anatomically patent when examined by the pathologist. The characteristic elastic perivascular sclerosis of mesenteric vessels, which probably caused a functional vascular obstruction, was only discovered after the histological sections were reviewed. The true incidence of this rare condition may be higher than previously suspected because the perivascular sclerosis can easily be overlooked. Awareness of the association between carcinoid tumour and mesenteric ischaemia may lead to early surgery and an improved outcome.

Aged↗

CT in the early detection of strangulation in intestinal obstruction.

The role of CT in evaluating the gastrointestinal tract has increased recently because CT demonstrates pathological conditions involving the bowels, mesenteric vessels, and peritoneal cavity well. In patients who have an intestinal obstruction, the observation of both bowel loop configuration and mesenteric vessels on CT is the key to identifying the site and cause of obstruction and determining the absence or presence of intestinal strangulation. Although many clinical and radiological findings reported in the literature are not seen in the early stages of intestinal strangulation, CT might assist in its early detection. This article reviews the clinical, pathophysiological, and radiological aspects of strangulating obstruction with emphasis on the role of CT in its early diagnosis.

Contrast Media↗

Anatomic segmentation of the intestinal immune response in nonhuman primates: differential distribution of B cells after oral and rectal immunizations to sites defined by their source of vascularization.

We show that the distribution of specific antibodies and antibody-secreting cells in the intestine after oral and rectal immunizations corresponds to the vascularization and lymph drainage patterns of the gut. Oral immunizations induce antibody responses along the parts of the intestine connected to the superior mesenteric vessels and lymph ducts, whereas rectal immunizations induce antibody responses along the parts of the intestine associated with the inferior mesenteric vessels and ducts.

Administration, Cutaneous↗

Sustained hypertension in Dahl rats. Negative correlation of agonist response to blood pressure.

The perfused mesenteric vasculature of Dahl salt-sensitive rats on a high salt diet for 5 days (prehypertensive or early hypertensive) is selectively supersensitive to norepinephrine. The present goal was to determine whether that supersensitivity was maintained as hypertension developed. Littermates of salt-sensitive and salt-resistant rats (Dahl Brookhaven strain) were followed on low or high salt for up to 6 weeks. Systolic blood pressure was elevated in the salt-sensitive, high salt rats after 3 or 6 weeks but not after 5 days of the diet. The perfused mesenteric vascular beds from salt-sensitive rats were supersensitive to norepinephrine and nerve stimulation but not to potassium chloride when the rats had been maintained for 5 days or 3 weeks on the high salt diet. However, responses to norepinephrine declined after 6 weeks of the high salt diet. To determine whether sustained high blood pressure has a negative effect on mesenteric vascular responses, we conducted additional experiments with perfused mesenteric vascular beds from salt-sensitive Brookhaven (high salt, 5 weeks) and Rapp (high salt, 6 weeks) animals. Both groups exhibited significant negative correlations between in vivo systolic pressure and maximal responses of mesenteric vessels to norepinephrine and potassium chloride. We suggest that sustained hypertension in Dahl rats has a negative effect on the contractility of the mesenteric arterial system that, by 5 to 6 weeks, masks the initial supersensitivity to norepinephrine. No effects of any diet on the dilating responses of the mesenteric vessels to acetylcholine were observed in any group.

Animals↗

Cellular mechanisms of diabetic vascular hypertrophy.

Mesenteric vascular hypertrophy occurs in experimental diabetes. The present study examines whether this medial hypertrophy originates via cellular hyperplasia or hypertrophy of smooth muscle cells or an increase in collagen content. Male Sprague-Dawley diabetic (streptozotocin, 50 mg/kg, i.v.) rats were compared with control rats after 3 weeks in order to study mesenteric and aortic smooth muscle cell size and degree of cellular polyploidy. Collagen content in the mesenteric vessels was examined via staining with Sirius red. Further groups of control and diabetic animals were studied after 7 and 14 days of diabetes to assess proliferation in the various layers of the vessel wall using incorporation of [3H]thymidine (0.5 mCi/kg, i.p.). Smooth muscle cell size was measured by a Coulter counter and polyploidy assessed using flow cytometry measurement of cellular DNA content. Diabetic smooth muscle cell size was reduced in both the aorta and the mesenteric vessels and polyploidy was increased in these cells. The collagen content of diabetic mesenteric media was proportionally increased. At day 7, diabetic mesenteric endothelial and adventitial layers showed increased [3H]thymidine labeling of cells and this was not observed in the media of these vessels. These findings indicate that increased endothelial and adventitial cell proliferation are early events in diabetes associated vascular hypertrophy. Furthermore, an increase in extracellular matrix within the media is an important feature of diabetes associated vascular hypertrophy.

Animals↗

Surgical treatment of pancreatic tumors invading the spleno-mesenteric-portal vessels. An Italian Multicenter Survey.

BACKGROUND/AIMS: The authors are interested in determining the diagnostic and surgical approach followed in different Italian institutions in the treatment of adenocarcinoma of the head of the pancreas, whenever the spleno-mesenteric-portal confluence is invaded. METHODOLOGY: A 10-item questionnaire was sent to 21 Italian Centers of Surgical Oncology and a total of 1185 patients treated with pancreaticoduodenectomy were collected from 15 centers. Among them, 164 spleno-mesenteric-portal vein (SMPV) resections were performed. RESULTS: In all collaborative centers, the diagnostic work-up is comparable with what is reported in the literature. An accurate pre- and intra-operative staging and a differential diagnosis between inflammatory and neoplastic involvement of the vessel walls is universally considered essential for its surgical and oncological implications. If vessel involvement is ruled out, 7 centers proceed to pancreasectomy anyway. Direct end-to-end vein reconstruction is used as the primary procedure, but interposition of PTFE and autologous vein grafting may be used. An overall 4.8% post-operative complications only have been reported. Mean perioperative mortality reported is 3.8% (0-11.5%) and morbidity is 22.8% (4.7-57%). Survival rate is 10 months overall. The mean actuarial 5-year survival is 12%. CONCLUSIONS: The attitude of the collaborative centers in cases of SMPV involvement varies, with a slight majority favoring a conservative behavior. Surgical resection extended to the vessels is still uncommon, even in centers mostly experienced in surgery of the pancreas. We believe that vascular resections can be safely performed in both of the different conditions: localized tumors locally invading the vessels and neoplasms with massive invasion of the peripancreatic structures. We share with others the opinion that, in experienced centers, extensive resections should have a role for palliation of carcinoma of the pancreas whenever they offer a better quality of life, although life expectancy may not be positively influenced.

Adenocarcinoma↗

Structure-activity study of chicken calcitonin gene-related peptide (CGRP) on vasorelaxation in rat mesenteric resistance vessels.

Structure-activity relationship of the chicken calcitonin gene-related peptide (cCGRP) was investigated and compared with human-alpha-CGRP (hCGRP) and rat CGRP (rCGRP) in the perfused mesenteric vascular beds of rats. In precontracted mesenteric vascular beds, cCGRP, hCGRP and rCGRP produced a concentration-dependent vasodilation. The vasodilator activities of cCGRP and rCGRP were equipotent and more potent than that of hCGRP. (Ala2,7)cCGRP and (Des-1-Ala)-alpha-deamino cCGRP were 100- and 10-fold less potent than cCGRP, respectively. However, cCGRP[1-36] reduced vasodilator activity. The cCGRP[8-37] produced a vasoconstriction. Both cCGRP[8-37] and hCGRP[8-37] caused parallel shifts of the concentration-response curves of rCGRP to the right, but both peptides did not affect the maximum response and vasodilator responses to isoproterenol, these peptides being equipotent antagonists (pA2 values: 7.6 and 7.4). In rat brain membrane preparations, cCGRP and its fragments and analogues, except for cCGRP[1-36], competed for specific binding sites with [125I]-hCGRP. These results suggest that cCGRP has a potent vasodilator activity for which the disulfide bridge at position 2 and 7 of cCGRP is an important site and that position 37 is necessary for the binding of the peptide to the receptor. Also, cCGRP[8-37] is a competitive CGRP-receptor antagonist.

Amino Acid Sequence↗