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Multimedia article. Laparoscopic restorative proctocolectomy for ulcerative colitis.

BACKGROUND: With increasing experience, laparoscopic techniques have been applied even to extended colorectal operations as restorative proctocolectomy for ulcerative colitis and familial adenomatous polyposis. METHODS: A 36-year-old woman with a 7-year history of ulcerative colitis was transferred for elective surgery 6 weeks after an episode of toxic megacolon treated conservatively. The procedure was performed in modified lithotomy position using six trocars. After initial medial transection of the three main vascular pedicles of the ileocolic and middle colic vessels and the inferior mesenteric artery and vein, the colon was dissected free laterally, from the sigmoid orally toward the ileum. Special consideration was necessary for dissection of the omentum. The rectum was mobilized down to the pelvic floor in two steps, starting at the level of the promontory and the upper rectal stalks. It was transected at the level of the dentate line. Through a Pfannenstiel incision, the bowel was extracted. After transection of the ileum and removal of the specimen, a J-pouch was created. The anastomosis was completed laparoscopically using a double-stapling technique. Finally, a diverting loop ileostomy was created. RESULTS: A total of 13 patients underwent surgery. The medium age of these patients was 25.5 years (range, 19-57 years). There was no conversion to an open procedure. The median length of hospital stay was 11.5 days (range, 7-107 days). Four patients experienced major complications, including one case each of pouch failure after arterial occlusion, pouch-vaginal fistula, infected hematoma, and intraabdominal abscess formation. There was no postoperative mortality. CONCLUSIONS: For restorative proctocolectomy, laparoscopic techniques proved to be safe and feasible. With further experience, they may have the potential to become an appealing alternative to open surgery.

Adult↗

Laparoscopic total colectomy for slow-transit constipation.

INTRODUCTION: Total colectomy is the preferred surgical option in proven slow-transit constipation. With advances in technology and instrumentation, laparoscopic total colectomy has become feasible. METHODS: After a mechanical bowel preparation, the patient is placed in a modified lithotomy position and pneumoperitoneum is established. Using a subumbilical 12-mm trocar the camera is inserted. Two further 12-mm and 5-mm trocars, each, are used for access to the peritoneal cavity. In an approach from medial to lateral, ileocolic, middle colic vessels and the inferior mesenteric artery are divided. Medial mobilization is completed before the sigmoid is freed up laterally. The lateral mobilization continues orally to the descending, transverse, and ascending colon with the omentum being separated from the transverse colon completely. The mesorectum is divided using the harmonic scalpel, and the upper rectum is transected with either one or two passes of the endoscopic linear cutting stapler. The colon is exteriorized through a 5-cm Pfannenstiel incision. The terminal ileum is transected extracorporeally. After pneumoperitoneum has been reestablished, the ileorectal anastomosis is performed laparoscopically using a double-stapling technique. RESULTS: The video reports about a 56-year-old lady who had been suffering from chronic constipation since childhood and had become dependent on laxatives. A dolichocolon had been found in barium enema. A prolonged colonic passage was proven in an x-ray transit study. There were no intraoperative or postoperative complications. After surgery, first bowel movements occurred on the second day and the patient was discharged from the hospital on the sixth postoperative day. CONCLUSIONS: Laparoscopic total colectomy is a safe, feasible operation for slow transit constipation. With fast recovery and short length of stay it may become an attractive surgical approach.

Anastomosis, Surgical↗

Somatostatin is present in a subpopulation of noradrenergic nerve fibres supplying the intestine.

Somatostatin and dopamine beta-hydroxylase have been localized in the coeliaco-mesenteric ganglia, in mesenteric nerves and in the wall of the guinea-pig small intestine. Nerve lesions were used to determine the sources of the nerves. Nerve cell bodies in the coeliaco-mesenteric ganglia with immunoreactivity for both somatostatin and dopamine beta-hydroxylase project to the intestine via the mesenteric nerves. Most of their terminals are in the submucous ganglia, where they make up the full complement of noradrenergic terminals, and in the mucosa where other noradrenergic terminals, not containing somatostatin immunoreactivity, are also present. The small number of noradrenergic fibres present in the tertiary component of the myenteric plexus and in the circular muscle all show immunoreactivity for somatostatin. The noradrenergic fibres supplying the mesenteric and intestinal blood vessels and those ramifying in the myenteric ganglia do not contain somatostatin. The numerous somatostatin-immunoreactive nerves in the enteric plexuses that do not contain dopamine beta-hydroxylase come from enteric nerve cell bodies. These results, considered in the context of other published work, indicate that post-ganglionic sympathetic noradrenergic neurons are chemically coded according to the target tissue they supply and suggest that neurons that were hitherto thought to be neurochemically equivalent, but which serve different functions, are in fact chemically distinct.

Adrenergic Fibers↗

Preventing contrast-induced nephropathy with fenoldopam.

Fenoldopam is an interesting orphan drug that is a variant of dopamine. It differs significantly from dopamine in that it is a specific agonist for the type I (DA-1) receptor. The DA-1 receptors are particularly prominent in the renal vasculature, renal tubules, mesenteric vasculature, and peripheral vessels. The DA-1 receptor stimulation vasodilates renal and peripheral vessels, causing a decrease in blood pressure and an increase in renal blood flow (RBF). Stimulation of the DA-1 receptors in the tubules causes an increase in sodium excretion, which gives rise to an increase in urine volume on the basis of a sodium natriuresis. Animal testing with fenoldopam has indicated that it is 6 times more potent than dopamine in its ability to decrease renal vascular resistance and increase RBF; this suggests that it could be a much more selective and potent renal protective agent against any toxin or stimulus that causes renal dysfunction by reducing RBF or increasing renal ischemia. The clinical activity of fenoldopam, which is administered intravenously, begins almost immediately and is clearly noticeable after 5 minutes. The drug has no rebound effect, and its use can be stopped at any time. The protocol for the use of fenoldopam as a renal protective agent (performed at the University of Minnesota) involves starting an intravenous fenoldopam infusion 2 hours before the procedure at a rate of 0.1 microg/kg/min and increasing the dose in increments of 0.1 microg/kg/min every 20 minutes, until a rate of 0.5 microg/kg/min is reached or the systolic blood pressure falls more than 40 mm Hg (or below 110 mm Hg). Any infusion level at or above 0.1 microg/kg/min is considered acceptable because the response in individual patients varies so widely. The fenoldopam infusion is maintained at the maximum rate throughout the procedure and for up to 4 hours after the end of the contrast administration. At the University of Minnesota, we have had anecdotal experience using the drug in 29 patients. The drug was used for patients who were thought to be at the highest risk for contrast-induced nephropathy, ie, patients who have both diabetes and pre-existing renal failure. In this small group of patients in whom hydration and other variables were not controlled, there was a startling lack of contrast-induced creatinine increase at any point during the 24 to 48 hours after the administration of contrast in all but 1 patient. Our experience suggests that fenoldopam may be of distinct benefit to high-risk patients who need intravascular contrast, especially those who may receive a large contrast dose, such as patients undergoing peripheral or coronary angiography and intervention and/or computed tomography. Although it is impossible on the basis of simple anecdotal case reports to determine whether or not the drug was the primary reason that such a marked protective effect was seen, the results are promising enough to indicate that a careful, prospective, randomized trial of fenoldopam versus hydration is warranted.

Animals↗

Interaction between sympathetic nervous system and adrenal medulla in the control of cardiovascular changes in hypertension.

The role of the sympathetic nervous system and adrenal medulla in the development of cardiovascular changes and hypertension was studied in spontaneously hypertensive rats (SHRs), and the results compared with age-matched normotensive Wistar-Kyoto (WKY) rats. Sympathectomy was initiated in newborn rats through daily injection with antiserum to nerve growth factor for 1 week, followed by daily injection with guanethidine for 3 weeks. Removal of the adrenal medulla was carried out in 4-week-old rats after the last guanethidine injection. Such a combination treatment was effective in permanently preventing the development of hypertension in the SHRs, and the blood pressure was maintained at the level of WKY rats. The heart rate of the SHRs and WKY rats was not affected by such treatment. Hypertrophy of the heart and of the vessel wall in the mesenteric arteries was also prevented by such treatment. We conclude that in the SHR, the sympathetic nervous system and the adrenal medulla are essential for the development of cardiovascular changes and hypertension.

Adrenal Medulla↗

Extraluminal gastrointestinal stromal tumour in the second portion of the duodenum.

The preoperative diagnosis of extraluminal gastrointestinal stromal tumours in the duodenum is difficult to establish due to their rare occurrence and the lack of pathognomonic signs. This report describes the case of a 61-year-old woman who suffered from an immunohistologically confirmed gastrointestinal stromal tumour in the second portion of the duodenum. Preoperative, abdominal, multislice computed tomography showed an extraluminal but intramural tumour located between the head of the pancreas and the duodenum. Rapid postprocessing analysis by three-dimensional, volume-rendered images revealed a strong arterial blood supply and an early draining vessel into the superior mesenteric vein during the portal-venous phase. The combination of endoscopic ultrasonography and non-invasive multislice computed tomography provided an early suggestion of gastrointestinal stromal tumour.

Duodenal Neoplasms↗

Vasodilator actions of TRK-100, a new prostaglandin I2 analogue.

TRK-100, a stable analogue of prostaglandin I2 (PGI2), relaxed isolated arteries of the dog precontracted with PGF2 alpha or K+; the relaxation was in the order of mesenteric and renal greater than coronary and femoral greater than basilar and middle cerebral arteries. The relaxation by TRK-100 was not affected by treatment with atropine, propranolol, cimetidine, aminophylline, and indomethacin, but was suppressed by diphloretin phosphate, a prostaglandin antagonist. Treatment with TRK-100 attenuated the contraction induced by PGF2 alpha and Ca2+ in mesenteric and basilar arteries previously exposed to Ca2+-free medium, but did not significantly alter the contractile response to Ca2+ in the arteries exposed to Ca2+-free medium and depolarized by excess K+. TRK-100 and nitroglycerin relaxed isolated mesenteric arteries to a similar extent; however, when continuously infused into mesenteric arteries in anaesthetized dogs, TRK-100 produced greater vasodilatation than nitroglycerin. It is concluded that TRK-100 relaxes dog mesenteric and renal arteries more than cerebral arteries; the relaxation appears to derive from interference with the release of Ca2+ from intracellular stores and with the transmembrane Ca2+ influx through a receptor-operated channel. TRK-100 may vasodilate large and small mesenteric arteries and resistance vessels to a similar extent, whereas nitroglycerin preferentially dilates the large artery.

Animals↗

Flow dynamics in the human aorta.

The aorta is the major blood vessel transporting blood pumped by the left ventricle to the systemic circulation. The tricuspid aortic value at the root of the aorta provides a centralized flow with nearly uniform velocity profile into the ascending aorta. The aorta consisting of the ascending limb, the aortic arch, and the descending segment is a vessel of complex geometry including curvature in multiple planes, branches and bifurcation as well as taper. The understanding of the development of blood flow in this distensible vessel has been the subject of several theoretical as well as experimental investigations. Flow development in the aorta and in the branch vessels has been of interest in delineating the role of wall shear stresses on the etiology of atherosclerosis. In this paper, a review of the current status on our understanding of the complex flow dynamics in the aorta is presented. With the advent of transesophageal echocardiography and magnetic resonance velocity mapping, further evidence of the presence of secondary flows even in the descending aorta has been reported. The importance of the effect of secondary flow in the descending aorta on the perfusion of distal blood vessels (such as superior mesenteric and renal arterial branches) as well as in the iliac bifurcation is also included in the discussion.

Aorta↗

A comparison of the acute pathology induced by 3-phenylamino-1,2-propanediol (PAP) and its mono-oleoyl ester in rodents with the toxic oil syndrome in man.

Phenylamino-1,2 propanediol (PAP) and its mono-oleoyl ester have been identified in samples of the cooking oil thought to be responsible for the Toxic Oil Syndrome (TOS) which occurred in Spain in 1981. The acute toxicity of PAP and its mono-oleoyl ester have been examined in rats and mice, after daily administration for periods of up to 14 days to determine whether these compounds could produce any of the pathologies of TOS. Even at the highest dose, the 1-mono-oleoyl ester of 3-phenylamino-1,2 propanediol did not cause any toxicity in rats or mice when given intraperitoneally. 3-Phenylamino-1,2 propanediol, however, was toxic when administered to rats by this route. After 6-10 consecutive daily doses of PAP, at the highest dose administered (350 mg kg-1), all of the rats became unwell. Postmortem examination showed that the major pathology present was massive pulmonary thromboembolism. Further investigations of the toxicity of PAP after intravenous administration showed that it was not directly vasotoxic. The pulmonary thromboembolism seen with intraperitoneally administered PAP was due to the toxic effect of PAP on the mesenteric tissue and blood vessels, causing thrombosis which subsequently embolised the blood vessels in the lung. Intra-gastric administration of PAP caused no toxicity in rats. Comparatively, the pathology seen after intraperitoneal administration of PAP was not thought to be representative of the pathology of the toxic oil syndrome in man.

Animals↗

The role of extracellular cations in the development of myogenic contraction in isolated rat small arteries.

The purpose of this study was to determine the roles of extracellular cations (Na+, Ca2+ and K+), membrane K+ channels and Na+/K+ ATPase in the development of myogenic contraction (transmural pressure-induced contraction) in isolated rat skeletal muscle and mesenteric small arteries. The vessels were pressurized under no-flow conditions in a tissue bath. Lumen diameter was measured with a videomicroscopic system. Myogenic contraction was evoked by increasing the lumen pressure from 40 to 100 mmHg. The vessels demonstrated myogenic contraction in low-Na+ (Na+ 1.18 mmol/L) physiological salt solution (PSS), and this was abolished by removing Ca2+ or by applying nifedipine or nisoldipine (10 mumol/L). Neither tetraethylammonium (TEA, 1 mmol/L), Ba2+ (10 mumol/L) nor glibenclamide (1 mumol/L) affected the magnitude of the myogenic contraction. K(+)-free PSS and ouabain (0.1 mmol/L) partially depressed myogenic contraction. In conclusion, myogenic contraction was triggered by a cellular process that requires extracellular Ca2+, but not Na+ or K+. This triggering process is not affected by TEA, Ba2+ or glibenclamide.

Animals↗

Passage of particles through the wall of the gastrointestinal tract.

In the normal process of digestion, not only substances in solution are absorbed. Solid, undissolved particles in macrocorpuscular form, are "kneaded" into the mucosa during their passage through the digestive tract. These particles in the micrometer size range pass between the epithelial cells into the subepithelial layer. From here they are transmitted both by the lymph vessels and by the mesenteric veins into the circulation, where they remain for a considerable time. This phenomenon, termed persorption, was investigated in detail.

Absorption↗

Technical aspects of intestinal transplantation in the rat.

The microsurgical technique for rat intestinal transplantation used in our laboratory is described. A 25-cm segment of jejunum is harvested from the donor on a pedicle of superior mesenteric artery (SMA) and superior mesenteric vein (SMV). These vessels are then anastomosed end-to-side with 10-0 nylon to the infrarenal aorta and inferior vena cava of the recipient. The bowel ends are placed in isoperistaltic continuity with the host intestine. The procedure was performed in 423 animals with an 86 percent success rate and has been used to investigate all aspects of small bowel transplantation. The technique is described in detail with schematic drawings and intraoperative photographs, with the goal of making the procedure more understandable and accessible to other investigators wishing to study vascularized intestinal transplantation in the rat.

Anastomosis, Surgical↗

Hypercoagulable states.

PURPOSE: To describe the major pathophysiologic mechanisms underlying inherited and secondary hypercoagulable states and to evaluate the frequency, natural history, diagnosis, and management of the various clinical disorders. DATA SOURCES AND STUDY SELECTION: Relevant clinical literature obtained from bibliographies in hematology textbooks and from computerized indexes was reviewed. A hypothesis was formed based on this literature review and on recent developments from a number of experimental studies. DATA SYNTHESIS: Hypercoagulable states include various inherited as well as acquired clinical disorders characterized by an increased risk for thromboembolism. Primary hypercoagulable states include relatively rare inherited conditions that lead to disordered endothelial cell thromboregulation. These conditions include decreased thrombomodulin-dependent activation of activated protein C, impaired heparin binding of antithrombin III, or down-regulation of membrane-associated plasmin generation. The major, inherited, inhibitor disease states include antithrombin III deficiency, protein C deficiency, and protein S deficiency and should be considered in patients who have recurrent, familial, or juvenile deep-vein thrombosis or occlusion in an unusual location such as a mesenteric, brachial, or cerebral vessel. Secondary hypercoagulable states may be seen in many heterogeneous disorders. In many of these conditions, endothelial activation by cytokines leads to loss of normal vessel-wall anticoagulant surface functions with conversion to a proinflammatory thrombogenic phenotype. Important clinical syndromes associated with substantial thromboembolic events include the antiphospholipid syndrome, heparin-induced thrombopathy, the myeloproliferative syndromes, and cancer. CONCLUSIONS: Physiologic thromboregulation occurs at the vessel-wall surface. Quantitative and qualitative deficiencies of normal, steady-state endothelial anticoagulant activities are associated with primary hypercoagulable states. Activated endothelial cell surfaces express a thrombogenic phenotype and contribute to secondary or acquired hypercoagulability.

Blood Coagulation Disorders↗