On-axis versus off-axis Transmission Kikuchi Diffraction technique: application to the characterisation of severe plastic deformation-induced ultrafine-grained microstructures.

A new configuration for Transmission Kikuchi Diffraction (TKD) in a scanning electron microscope is presented; called 'on-axis TKD'. Compared to the usual off-axis configuration, the scintillator is placed perpendicular to the incident beam under the electron-transparent sample, not in vertical position. In this way, the setup benefits from intense forward scattered electrons enabling short acquisition times. At equivalent diffraction pattern quality, the electron dose needed on the sample is estimated to be 20 times lower in comparison to the off-axis configuration. The technique is particularly suited to the characterisation of severe plastic deformation induced ultrafine grained microstructures. The evolution of the microstructure of an Al-Mg alloy deformed by high pressure tube twisting was analysed. It is shown that the grain refinement was in the steady state stage for a shear strain of 24 with a mean grain size of 120 nm.

The pancreas and oxygen consumption (Part 2). Steroids do not modify resting pancreatic oxygen consumption in dogs: a preliminary report.

In order to evaluate the effect of methylprednisolone sodium succinate (MPSS) on the alteration of pancreatic oxygen consumption (VO2) in hypovolemic shock, MPSS was administered to four normal canines and three hypovolemic animals. All were treated according to the protocol used in the initial report. (The Pancreas and Oxygen Consumption 1: Pancreatic Oxygen Consumption in Normo- and Hypovolemic Dogs.) All seven underwent a splenectomy at the beginning of the experiment. Pancreatic VO2, obtained by adding up VO2 for the head (minus the uncinate process) and tail of the pancreas, was equal to the product of regional blood flow, Q, determined electromagnetically on the gastroduodenal (GDA) and splenic (SA) arteries, times O2 extraction, (a-v)O2; O2 content (in mL%) was measured in the femoral artery (RFA), in the splenic (SV) and superior pancreaticoduodenal (SPDV) veins. Similar determinations were carried out on the right hind limb that served as a control. Recordings were made for 4 h in both groups, the first hour determinations (five in all) serving as reference values. Methylprednisolone did not appear to alter pancreatic VO2, which showed a significant increasing trend from + 77% 1 h after MPSS had been given, to + 98% 3 h later (vs + 56 and + 92%, respectively, in the control group). As in the control group, these increases were owing to augmented O2 extraction by the pancreas. No significant change was noted between the head and tail of the pancreas. In the hind limb, VO2 increased significantly the first 2 h and differed from control VO2 at the end of the first hour only.

The pancreas and oxygen consumption. 1. Pancreatic oxygen consumption in normo- and hypovolemic dogs.

Pancreatic oxygen consumption (VO2) was studied in hypovolemic shock: 4 dogs served as controls and 4 others were kept at 50 mm Hg of mean arterial blood pressure. All 8 were studied for a period of 3 h. Pancreatic VO2 was obtained by adding up VO2 for the head (minus the uncinate process) and tail of the pancreas both equal to the product of regional blood flow times O2 extraction. Regional blood flows were measured electromagnetically on the gastroduodenal (GDA) and the splenic (SA) arteries, whereas O2 extraction was derived from total hemoglobin (THb) and oxygen saturation of hemoglobin (%O2 Hb) determined on the right femoral artery (RFA), the superior pancreaticoduodenal (SPDV), and splenic (SV) veins. A splenectomy was performed in all 8 dogs. Controls showed a significantly elevated pancreatic VO2 from the first hour of observation on (+56% after 1 h, +92% after 3), whereas pancreatic VO2 remained strictly unchanged throughout shock (+2% and +6%, at one and 3 h, respectively), despite significant increases in O2 extraction. These findings give support to the deleterious effects of hypovolemia to the pancreas and that pancreatic O2 extraction indicates metabolic damage to be less severe than observed in experimental bile-trypsin-induced acute pancreatitis.

Steroids do not alter pancreatic blood supply in hypovolemic dogs: implications on steroid action in acute pancreatitis.

A recent report from our laboratory showed that pancreatic inflammation induced by hypovolemic shock can be explained to some extent by spoliation in pancreatic perfusion as revealed by electromagnetic flow determinations on the gastroduodenal artery (GDA). On the other hand, when given early in the course of hypovolemic shock, methylprednisolone sodium succinate (MPSS) alleviated pancreatic inflammation as evidenced by gross and histological findings. Five dogs (18-23 kg) were submitted to a 3-hour hypovolemic shock (mean arterial blood pressure, MABP = 50 mm Hg) and received during bleeding 35 mg/kg of MPSS over a 30 min period. Recordings of cardiac output (CO), MABP, regional blood flows in the GDA and superior mesenteric (SMA) arteries were taken every 15 min. The effect of MPSS was appreciated by comparing GDA flow variations in this group with those previously published of a control group comprised of 12 dogs submitted to 3 hours of hypovolemic shock without steroids; operative protocol was in all points similar in both groups. At no time were any significant changes noted when MPSS was added as far as CO and GDA flows were concerned. In other words, the beneficial action of steroids on hypovolemic pancreases cannot be explained by alteration in regional blood flow.

Hypovolemic shock, pancreatic blood flow, and pancreatitis.

Electromagnetic blood flow determinations were carried out on the superior pancreatic duodena (SPDA), the splenic (SA) and the superior mesenteric (SMA) arteries and compared to cardiac output (CO, thermodilution technique) in 12 anesthetized dogs submitted to hypovolemic shock of various duration: 5 dogs underwent a one-hour and 7 a three-hour period of shock. A 50 mm Hg level of mean arterial blood pressure (MABP) was maintained throughout hypovolemia. Dogs were then reinfused. Control preshock values were 4.12 l/min for CO, 38.0 ml/min for SPDA, 405.9 ml/min for SA, and 963.6 ml/min for SMA. SPDA, SA and SMA flows expressed as % of CO amounted to 0.9, 9.8 and 23.4% respectively. No significant changes in SPDA and SMA flows were noted within the first hour of shock. However, from the end of the second hour on, both flows differed significantly (P less than 0.01), SMA increasing from -75.6% of its control value at the end of bleeding to -61.0%, and SPDA decreasing from -75.6 to -86.9%. Similar observations were made when respective flows were considered as % of CO. The SA behaved somewhat in an intermediate fashion. This relative spoliation in pancreatic blood supply as hypovolemia proceeds supports an ischemic etiology of acute pancreatitis (AP), which could account for some of the so-called idiopathic cases of AP.

Experimental models for gastric leiomyosarcoma. The effects of N-methyl-N'-nitro-N-nitrosoguanidine in combination with stress, aspirin, or sodium taurocholate.

A series of experiments was devised to determine possible modifying effects of stress, aspirin, and sodium taurocholate on the activity of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) in the Buffalo rat stomach. MNNG is a well known, direct-reacting carcinogen, and has been a reliable agent for the experimental production of gastric adenocarcinoma. The authors were able to produce adenocarcinomas in rats, but found a great number of gastric leiomyosarcomas. These occurred only in the groups given MNNG in combination with stress, aspirin, or sodium taurocholate, and did not occur in experimental groups given either MNNG, stress, aspirin, or sodium taurocholate alone, and did not occur in the control group.

Effect of N-methyl-N'-nitro-N-nitrosoguanidine on the gastric mucosal barrier in rats.

The gastric mucosal barrier to hydrogen ion (H+) after the administration of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) on the rat stomach was studied. Increased H+ back-diffusion was observed 3 hr after oral doses of 1 mg of MNNG over a 3-day period. MNNG in concentrations of 250 microgram/ml, 167 microgram/ml, 86 microgram/ml, and 50 microgram/ml in the presence of acid caused increased H+ back-diffusion across the gastric mucosa within 1 hr. Gastric mucosal barrier disruption by MNNG may play a pathogenic role in gastric carcinogenesis.