Ultrastructural Changes in the Canine Ileal Mucosal Cell After Mesenteric Arterial Occlusion: A Sequential Study
TL;DR: The mitochondria were somewhat swollen, however, lysosomes, rough endoplasmic reticulum, and nuclei were normal, and the lyssomes still appeared normal.
Abstract: Laparotomy was performed on seven healthy male mongrel dogs. The control sample of ileal mucosa was taken and a clamp applied to the superior mesenteric artery. Sections of ileal mucosa were obtained after clamping for electron microscopic study. By ten minutes after clamping, there was an accumulation of fluid infranuclearly with bulging of plasma and basement membranes. The mitochondria were somewhat swollen, however, lysosomes, rough endoplasmic reticulum, and nuclei were normal. Thirty minutes after clamping, the terminal web was clear with loss of protein normally present. Mitochondria were swollen with destruction of cristae, the rough endoplasmic reticula were dilated, and the outer membrane of the nucleus was separated. The lysosomes still appeared normal. Most striking was the large size of the intercellular spaces infranuclearly with fracturing of the intercellular membrane and lifting of the cell.
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TL;DR: Results of field and laboratory studies show that pre-exercise ingestion of foods rich in dietary fibre, fat and protein, as well as strongly hypertonic drinks, may cause upper GI symptoms such as stomach ache, vomiting and reflux or heartburn, but there is no evidence that the ingestion of nonhypertonic drink during exercise induces GI distress and diarrhoea.
Abstract: Digestion is a process which takes place in resting conditions Exercise is characterised by a shift in blood flow away from the gastrointestinal (GI) tract towards the active muscle and the lungs Changes in nervous activity, in circulating hormones, peptides and metabolic end products lead to changes in GI motility, blood flow, absorption and secretion In exhausting endurance events, 30 to 50% of participants may suffer from 1 or more GI symptoms, which have often been interpreted as being a result of maldigestion, malabsorption, changes in small intestinal transit, and improper food and fluid intake Results of field and laboratory studies show that pre-exercise ingestion of foods rich in dietary fibre, fat and protein, as well as strongly hypertonic drinks, may cause upper GI symptoms such as stomach ache, vomiting and reflux or heartburn There is no evidence that the ingestion of nonhypertonic drinks during exercise induces GI distress and diarrhoea In contrast, dehydration because of insufficient fluid replacement has been shown to increase the frequency of GI symptoms Lower GI symptoms, such as intestinal cramps, diarrhoea — sometimes bloody — and urge to defecate seem to be more related to changes in gut motility and tone, as well as a secretion These symptoms are to a large extent induced by the degree of decrease in GI blood flow and the secretion of secretory substances such as vasoactive intestinal peptide, secretin and peptide-histidine-methionine Intensive exercise causes considerable reflux, delays small intestinal transit, reduces absorption and tends to increase colonic transit The latter may reduce whole gut transit time The gut is not an athletic organ in the sense that it adapts to increased exercise-induced physiological stress However, adequate training leads to a less dramatic decrease of GI blood flow at submaximal exercise intensities and is important in the prevention of GI symptoms
155 citations
TL;DR: Mechanisms of ischemic injury and the central role of vasoconstriction are discussed and the importance of EMT in the management of intestinal ischemia is discussed.
101 citations
TL;DR: Seromuscular enzymes, particularly creatinine phosphokinase, were more likely to be elevated during intestinal ischemia, and were not influenced by the extent and reversibility of the ischemic injury.
Abstract: Because the intestinal mucosa is most sensitive to ischemia, serum levels of mucosal enzymes, such as diamine oxidase, may be most likely to indicate intestinal ischemia. Our aim was to compare serum levels of mucosal (diamine oxidase, alkaline phosphatase) and seromuscular (creatinine phosphokinase, lactic dehydrogenase, serum glutamic oxaloacetic transminase) enzymes during intestinal ischemia of varying extent and duration in dogs. Group 1 (n = 6) underwent sham laparotomy. Group 2 (n = 8) had 50% of the small intestine devascularized. Group 3 (n = 8) had the superior mesenteric artery occluded for 2 hours and released. Group 4 (n = 8) had the superior mesenteric artery ligated. Serum samples were obtained before and 2, 4, 8, and 24 hours after operation, and histologic specimens were examined at 4 hours. Creatinine phosphokinase levels became elevated within 4 hours of ischemic injury in group 2 (223 +/- 197 vs. 68 +/- 26, p less than 0.05) and group 4 (212 +/- 136 vs. 76 +/- 29, p less than 0.05). Significant elevation of serum enzymes levels, except diamine oxidase, occurred in groups 2, 3, and 4 at 24 hours, including those with normal histology after temporary superior mesenteric artery occlusion. Thus seromuscular enzymes, particularly creatinine phosphokinase, were more likely to be elevated during intestinal ischemia. Enzyme levels were not influenced by the extent and reversibility of the ischemic injury.
94 citations
01 May 1993
TL;DR: The authors in this paper showed that preventive therapy using either enteral IgA supplementation, breast milk feeding, antibiotic prophylaxis, or exogenous steroid administration have reduced the incidence of this overwhelming disease in small randomized trials.
Abstract: Necrotizing enterocolitis (NEC) is a devastating gastrointestinal disease of premature neonates that accounts for 3000 to 4000 deaths each year in the United States. The pathogenesis is not well understood, however theories suggest that prematurity, enteral feeding, bacterial colonization, and intestinal ischemia contribute to the intestinal injury. Furthermore, recent studies have shown that platelet activating factor and perhaps other inflammatory mediators mediate bowel necrosis in animals and possibly in humans. Although no specific intervention for NEC treatment exists, preventive therapy using either enteral IgA supplementation, breast milk feeding, antibiotic prophylaxis, or exogenous steroid administration have reduced the incidence of this overwhelming disease in small randomized trials. These modalities and perhaps PAF antagonists or other inflammatory mediator inhibitors may reduce the incidence or severity of NEC in the next several years.
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TL;DR: HEMORRHAGE and retransfusion represent the principal method by which experimental normovolemic shock is induced in the laboratory animal and the animal awakens from anesthesia much like an animal subjected to a nonshocking surgical procedure of comparable duration.
Abstract: HEMORRHAGE and retransfusion represent the principal method by which experimental normovolemic shock is induced in the laboratory animal. When the preparation is lethal, the time interval between retransfusion and death is usually very short, ranging from 2 to 12 hours. To bring about this situation one has to maintain a dog in hypovolemia with a blood pressure at 35 to 40 mm/Hg for two to four hours.1After retransfusion of blood the outcome is rather clear cut; the animal either dies or recovers completely. In the latter instance the animal awakens from anesthesia much like an animal subjected to a nonshocking surgical procedure of comparable duration: the rapid clinical recovery is reflected by the lack of significant metabolic or pathological alterations. From 100% survival after 60 to 90 minutes of hypovolemia, to 100% mortality after four hours of hypovolemia, the difference in duration of the hypovolemic phase and the
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TL;DR: The constant gastric reflux of chyme with its altered enzymic activity may offer a pathogenetic link between the intestinal lesion and the gastric stress ulcers seen in most of the dogs surviving intestinal ischemic shock.
48 citations
TL;DR: Increase of lysosomal enzymes in the cytoplasm has been demonstrated biochemically in genetic muscular dystrophy and shortly after ligation of the blood supply of a liver lobe, however, Slater and Greenbaum were unable to detect rapid release ofLysosome enzymes after induction of acute liver necrosis.
Abstract: Increasing attention has been given to the role of the lysosome in the pathogenesis of disease and tissue injury including shock. Lysosomes were described by de Duve1in 1955 as biochemically inactive acid hydrolases, surrounded by an intact membrane. If the membrane becomes permeable or disrupted these enzymes are activated. Under certain conditions, concentrated lysosomal preparations can hydrolyse phosphate esters, ribonucleic acid (RNA), and microsomal and mitochondrial membrane components, causing loss of oxidative phosphorylation.2For these reasons it has been suggested that lysosomes may play a major role in tissue destruction and may be the cause of irreversibility in shock. Increase of lysosomal enzymes in the cytoplasm has been demonstrated biochemically in genetic muscular dystrophy,3and shortly after ligation of the blood supply of a liver lobe.4Slater and Greenbaum,5however, were unable to detect rapid release of lysosomal enzymes after induction of acute liver necrosis.
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