Ultrasound evaluation of the impact of cricoid pressure versus novel 'paralaryngeal pressure' on anteroposterior oesophageal diameter.

To assess the degree to which cricoid pressure (Sellick manoeuvre) actually compresses the oesophagus, we measured the effect of cricoid pressure and paralaryngeal pressure on the outer anteroposterior diameter of the upper oesophagus with ultrasound in 39 healthy volunteers. The mean (SD) outer anteroposterior oesophageal diameter was 0.77 (0.11) cm with no pressure, 0.79 (0.13) cm with the application of cricoid pressure of 30 N and 0.68 (0.12) cm with the application of paralaryngeal pressure of 30 N (p < 0.0001). If cricoid pressure does not reduce the anteroposterior diameter of the oesophagus, it is difficult or impossible to explain the efficacy of the Sellick manoeuvre. However, paralaryngeal pressure decreases this diameter and has the potential to occlude the upper oesophagus.

Is blood the ideal submucosal cushioning agent? A comparative study in a porcine model.

BACKGROUND AND STUDY AIMS: Creation of a submucosal cushion before endoscopic mucosal resection (EMR) significantly reduces perforation risk. We evaluated six solutions as cushioning agents in live pigs. MATERIAL AND METHODS: 5 ml of normal saline, normal saline plus epinephrine, albumin 12.5 %, albumin 25 %, hydroxypropyl methylcellulose, and the pig's own whole blood were endoscopically injected into the porcine esophageal submucosa. Blood was obtained from a peripheral vein immediately before injection. Injections were made every 4 cm from the gastroesophageal junction. The time from completion of the injection to disappearance of the cushion was recorded. Endoscopy was repeated at 48 hours post injection. Two EMRs were performed after blood injection. Statistical analysis employed one-way analysis of variance followed by pairwise T test comparisons using the Bonferroni correction. RESULTS: Five animal experiments were completed. The mean time to dissipation of the submucosal cushion was shortest for saline plus epinephrine sites (2.87 minutes, SD 2.21) followed by the saline (4.8 minutes, SD 1.56), albumin 12.5 % (5.68 minutes, SD 3.48), albumin 25 % (7.83 minutes, SD 2.02), hydroxypropyl methylcellulose (9.77 minutes, SD 1.55), and blood sites (38.6 minutes, SD 6.07). Injection of blood resulted in significantly longer mucosal elevation than any other solution ( P < 0.0007). Blood from the cushion did not hamper visualization and facilitated EMR. CONCLUSION: Blood produces the most durable cushion compared with standard agents, also having the advantages of being readily available and without cost. Albumin 25 % provides as durable a cushion as hydroxypropyl methylcellulose.

Stimulation of the gastrin-cholecystokinin(B) receptor promotes branching morphogenesis in gastric AGS cells.

Epithelial organization is maintained by cell proliferation, migration, and differentiation. In the case of the gastric epithelium, at least some of these events are regulated by the hormone gastrin. In addition, gastric epithelial cells are organized into characteristic tubular structures (the gastric glands), but the cellular mechanisms regulating the organization of tubular structures (sometimes called branching morphogenesis) are uncertain. In the present study, we examined the role of the gastrin-cholecystokinin(B) receptor in promoting branching morphogenesis of gastric epithelial cells. When gastric cancer AGS-G(R) cells were cultured on plastic, gastrin and PMA stimulated cell adhesion, formation of lamellipodia, and extension of long processes in part by activation of protein kinase C (PKC) and phosphatidylinositol (PI)-3 kinase. Branching morphogenesis was not observed in these circumstances. However, when cells were cultured on artificial basement membrane, the same stimuli increased the formation of organized multicellular arrays, exhibiting branching morphogenesis. These effects were reversed by inhibitors of PKC but not of PI-3 kinase. We conclude that, in the presence of basement membrane, activation of PKC by gastrin stimulates branching morphogenesis.

Gastrin-cholecystokinin(B) receptor expression in AGS cells is associated with direct inhibition and indirect stimulation of cell proliferation via paracrine activation of the epidermal growth factor receptor.

BACKGROUND: Activation of the gastrin-cholecystokinin(B) (CCK(B)) receptor stimulates cell proliferation and increases production of ligands for the epidermal growth factor receptor (EGF-R). AIMS: To determine the role of gastrin-CCK(B) activation in stimulation of cell proliferation via paracrine activation of EGF-R. METHODS: AGS cells were transfected with the gastrin-CCK(B) receptor (AGS-G(R) cells) or with green fluorescent protein (AGS-GFP cells). Proliferation was determined by [(3)H] thymidine incorporation, flow cytometry, and cell counting. RESULTS: Gastrin inhibited proliferation of AGS-G(R) cells by delaying entry into S phase. However, when AGS-G(R) cells were cocultured with AGS-GFP cells, gastrin stimulated proliferation of the latter. Immunoneutralisation and pharmacological studies using metalloproteinase and kinase inhibitors indicated that the proliferative response was mediated by paracrine stimulation of EGF-R and activation of the mitogen activated protein kinase pathway through release of heparin binding EGF. CONCLUSIONS: Gastrin can directly inhibit, and indirectly stimulate, proliferation of gastric AGS cells.

The impact of Clostridium difficile on a surgical service: a prospective study of 374 patients.

OBJECTIVE: To evaluate the epidemiology of Clostridium difficile colitis (CDC) in a subset of patients admitted specifically to a surgical service. SUMMARY BACKGROUND DATA: CDC is an increasingly prevalent nosocomial infection that can prolong hospitalization and adversely affect patient outcome. Although this disease has been investigated extensively in patients admitted to medical services, the incidence and risk factors for the development of this disease in patients admitted to a surgical service have not been studied. METHODS: Over a 5-month period, 374 patients admitted to the general, vascular, thoracic, and urologic surgery services were monitored for the development of symptomatic CDC (defined as >3 bowel movements per 24 hours and a positive cytotoxin assay or culture). RESULTS: Twenty-one patients developed CDC (incidence, 5.6%). Factors that independently predisposed to infection included admission from a skilled care facility, use of the antibiotic cefoxitin, and an operative procedure for bowel obstruction. Other factors associated with CDC included colectomy, treatment with any antibiotic, nasogastric tube suction, advanced age, and prior antibiotic treatment. Abdominal pain and fever were also more common in patients with CDC. Morbidity included prolonged hospitalization in all patients and urgent colectomy in one. CONCLUSIONS: CDC frequently affects surgical patients, producing morbidity ranging from mild diarrhea to life-threatening illness. A variety of factors, many of which are associated with intestinal stasis, predispose to the development of CDC.

[A case of bilateral internal carotid artery and right vertebral artery occlusion]. / Przypadek pacjenta z obustronna niedroznoscia tetnic szyjnych wewnetrznych oraz prawej tetnicy kregowej.

The authors discuss a case of a 46 year-old man with bilateral internal carotid artery and right vertebral artery occlusion in unexpectedly good clinical state. The clinical diagnosis is documented by angiographic and doppler findings and brain CT scan.

Platelet attachment stimulates endothelial cell regeneration after arterial injury.

BACKGROUND: Arterial injury is associated with endothelial disruption and attachment of platelets to an exposed subintimal layer. A variety of factors released by platelets may affect the ability of endothelial cells bordering an injury to regenerate. In this study an organ culture model of arterial injury was used to investigate the relationship between attachment of platelets to a superficial arterial injury and endothelial regeneration. METHODS: A defined superficial endothelial injury was made in whole vessel wall explants of rabbit thoracic aorta. Injured explants were treated with either fresh whole platelets, the supernatant of platelets aggregated by collagen, or basic fibroblast growth factor. Four days after injury and treatment, the average distance of endothelial regeneration was determined. RESULTS: A dramatic increase in the rate of endothelial cell regeneration was observed when injured vessels were exposed to fresh whole platelets (p = 0.003). This increase in regeneration was comparable to that observed with fibroblast growth factor. No increase in the regenerative rate was found after exposure of explants to the supernatant of aggregated platelets (p = 0.69). CONCLUSIONS: Platelets stimulate endothelial regeneration at a rate equal to that observed with the potent endothelial mitogen basic fibroblast growth factor. Because this effect was not demonstrated with the supernatant of aggregated platelets, endothelial regeneration may be dependent on attachment of the platelets to the area of injury.

Evaluation of myocardial viability following ischemic and reperfusion injury using phosphorus 31 nuclear magnetic resonance spectroscopy in vivo.

Recovery of myocardial high-energy phosphate (HEP) metabolism after coronary occlusion and reperfusion may vary with ischemic duration and may provide information about the extent of tissue viability. To evaluate the differences between varying durations of ischemia and to attempt to identify metabolic indexes of salvaged viable tissue, intact New Zealand white rabbits underwent either 30 (group 1; n = 8) or 60 (group 2; n = 8) minutes of coronary occlusion followed by reperfusion. HEP metabolism was evaluated with cardiac gated phosphorus 31 (31P) nuclear magnetic resonance (NMR) spectroscopy with a 2.0 T spectrometer. While similar HEP changes were observed during ischemia in both groups, differences in HEP recovery between groups were seen following reperfusion. Group 1 animals demonstrated a gradual decrease in inorganic phosphates (Pi) (p less than 0.05 versus group 2), an immediate recovery of phosphocreatine (PCr) (p = ns versus baseline), and a gradual increase of adenosine triphosphate (ATP) to pre-ischemic levels. Group 2 animals had elevated levels of Pi (p less than 0.05 versus baseline; p less than 0.05 versus group 1), slow recovery of PCr, and continued reduction of ATP (p less than 0.05 versus baseline; p less than 0.05 versus group 1). Group 1 rabbits had a greater extent of viable myocardium than group 2 (77.1 +/- 9.7% of risk area versus 39.4 +/- 9.4%; p less than 0.001). Significant correlations were found between PCr and Pi reperfusion values and myocardial viability (r = 0.59, p less than 0.05; r = 0.73, p less than 0.01, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of diltiazem on phosphate metabolism in ischemic and reperfused myocardium using phosphorus31 nuclear magnetic resonance spectroscopy in vivo.

Diltiazem may provide a protective effect to ischemic and reperfused myocardium through preservation of high-energy phosphate metabolism. To test this hypothesis, rabbits had a 1.3 cm solenoidal coil placed over the myocardium to be rendered ischemic. Data were acquired with a 22 cm bore nuclear magnetic resonance spectrometer at 2.0 T. Animals were treated with diltiazem (200 micrograms/kg intravenous bolus of drug followed by a 15 micrograms/kg/min continuous intravenous infusion, n = 10) or by an equal volume of saline (n = 6). The left circumflex artery was occluded and reperfused using a reversible snare while electrocardiogram-gated spectra were accumulated. Levels of phosphocreatine were decreased during occlusion in both groups; however, this decrease was attenuated in the diltiazem treated animals compared to control (in relative percent area: 7.8 +/- 1.0 to 2.5 +/- 0.5, p less than 0.01). Levels of phosphocreatine promptly returned to baseline following reperfusion and there was no difference between the two groups. The inorganic phosphate metabolites of high-energy phosphate consumption increased with occlusion, though more so in the control group compared with the diltiazem-treated rabbits (in relative percent area: 72.5 +/- 0.9 to 55.4 +/- 1.3, p less than 0.01). With reperfusion, levels of inorganic phosphates returned toward baseline in both groups; however, the diltiazem group had a more complete recovery relative to control (in relative percent area: 38.8 +/- 2.1 to 47.6 +/- 2.7, p less than 0.05). Levels of adenosine triphosphate decreased in both groups relative to baseline; however, the amount of decrease was similar in the two groups. With reperfusion there was a definite though incomplete recovery of levels of adenosine triphosphate in the diltiazem-treated group (in relative percent area: 10.7 +/- 1.0 at occlusion, 12.3 +/- 0.4 during reperfusion, p less than 0.05), but in the control group levels of adenosine triphosphate remained depressed (in relative percent area: 9.8 +/- 0.6 at occlusion, 9.8 +/- 0.8 during reperfusion, p = NS). During ischemia there was a trend toward attenuation of intracellular acidosis in the diltiazem group; however, this trend did not reach statistical significance. These data indicate that diltiazem provides a protective effect on myocardial high-energy phosphate metabolism during regional ischemia and reperfusion in the intact animal.