Results of the 1991 survey of the American Association of Academic Chief Residents in Radiology.
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Humans↗
Biomedical subjects
M A Perry
Publications and source records attributed to M A Perry.
Effect of aspirin on ulcer site blood flow in cat stomachs.
Radioactive microspheres were used to measure blood flow in the cat stomach during exposure to saline, 0.075 M HCl, and then 15 and 30 min after exposure to 20 or 40 mM aspirin in HCl. At the end of the experiment, the stomach wall was divided into ulcerated regions and adjacent nonulcerated areas. When exposed to saline, both regions had similar blood flow: 27 +/- 5 and 25 +/- 5 ml.min-1.100 g-1 (means +/- SE). Addition of acid caused a significant increase in blood flow to 41 +/- 7 ml.min-1.100 g-1 only at those sites that eventually ulcerated in the presence of aspirin. In the adjacent nonulcerated regions, blood flow was 31 +/- 5 ml.min-1.100 g-1 and was not significantly greater than the flow recorded during saline exposure. Aspirin caused ulcer site blood flow to increase dramatically to 89 +/- 12 and 122 +/- 18 ml.min-1.100 g-1 after 15 and 30 min, whereas the adjacent nonulcerated tissue rose to 40 +/- 6 and 44 +/- 5 ml.min-1.100 g-1, respectively. The ulcer site hyperemia with acid alone suggests higher mucosal permeability in these regions allowing back-diffusion of acid and injurious agents. The present data obtained in the cat do not support the notion that ischemia plays a role in initiating nonsteroidal anti-inflammatory drug (NSAID)-induced ulcers, but rather that acute NSAID ulcers are associated initially with a hyperemia.
Animals↗
Leukocyte adhesion in local versus hemorrhage-induced ischemia.
The objective of this study was to compare the leukocyte-endothelial cell adhesive interactions elicited in postcapillary venules by either local ischemia-reperfusion or hemorrhage-reperfusion. Leukocyte rolling, adherence, and emigration were monitored in cat mesenteric venules exposed to an 85% reduction in blood flow (induced by either hemorrhage or local restriction of arterial inflow) for 1 h, followed by 1 h reperfusion. Leukocyte-endothelial cell interactions, venular diameter, and red blood cell velocity were measured during baseline, ischemia, and reperfusion periods. Both local and hemorrhage-induced ischemia reperfusion caused a reduction in leukocyte rolling velocity and increases in leukocyte adherence and emigration. Quantitatively, the adherence and emigration responses in both ischemia models were nearly identical. However, the two models differed in their response to immunoneutralization of the leukocyte adhesion glycoprotein CD11/CD18 with monoclonal antibody (MAb) IB4. The MAb had a more profound effect in attenuating leukocyte adherence and emigration in the local ischemia model. These results indicate that different factors may contribute to leukocyte-endothelial cell adhesive interactions observed in local vs. systemic models of ischemia-reperfusion.
Animals↗
Morphologic assessment of leukocyte-endothelial cell interactions in mesenteric venules subjected to ischemia and reperfusion.
Intravital microscopic studies of the mesenteric microcirculation have demonstrated that leukocyte adherence and emigration in postcapillary venules are a characteristic feature of tissues exposed to ischemia-reperfusion. The objectives of this study were to determine whether: (1) neutrophils are the predominant leukocytes that adhere and emigrate in postischemic mesenteric venules, and (2) leukocyte adherence and/or emigration are a prerequisite for reperfusion-induced increases in venular permeability. Leukocyte kinetics in cat mesenteric venules (25-35 microns diameter) were evaluated using both intravital microscopy and quantitative morphometry. The intestine and mesentery were exposed to 60 min of ischemia, followed by 60 min reperfusion. Some animals were pretreated with a monoclonal antibody (MoAb IB4) against the leukocyte adhesion glycoprotein, CD11/CD18. Vessels observed by intravital microscopy and adjacent venules of similar diameter were excised and processed for light (LM) and electron microscopy (EM). Horseradish peroxidase (HRP), administered intravenously, was used to assess vascular permeability by EM. By LM, the control (nonischemic) mesentery is sparsely populated by plasma cells, mast cells, and leukocytes; 30-50% of the resident population is neutrophils. Ischemia-reperfusion led to a significant increase in the number of extravascular cells, with neutrophils accounting for greater than 80% of the total cell population. Control and ischemic venules demonstrated no leakage of HRP into the interstitium. However, venules exposed to ischemia and reperfusion demonstrated HRP leakage between endothelial cells and into the surrounding interstitium; neutrophils were adherent to the luminal surface of the endothelium, transmigrating the vessel wall, and in the surrounding interstitium. Animals pretreated with MoAb IB4 presented the same cell profile as nonischemic controls, with no adherent or transmigrating neutrophils. However, some HRP leakage was noted following reperfusion in venules treated with MoAb IB4. The results of this study indicate that: (1) neutrophils are the predominate leukocytes that adhere and emigrate in postischemic venules, and (2) inhibition of leukocyte adhesion does not completely prevent the venular dysfunction associated with ischemia-reperfusion.
Animals↗
Role of CD11/CD18 in shear rate-dependent leukocyte-endothelial cell interactions in cat mesenteric venules.
In vivo microscopy was used to assess the relationships among shear rate (and shear stress), leukocyte rolling velocity, and leukocyte adherence in a cat mesentery preparation. Shear rate in individual venules and arterioles of 25-35 microns diameter were varied over a wide range by graded occlusion of an arterial loop. There was a linear decline in leukocyte rolling velocity (Vwbc) as red cell velocity (Vrbc) was reduced. The ratio Vwbc/Vrbc remained constant despite variations in shear stress from 5-25 dyn/cm2. A reduction in shear stress was associated with an increased leukocyte adherence, particularly when Vwbc was reduced below 50 microns/s. Reduction in wall shear rate below 500 s-1 in arterioles allowed 1-3 leukocytes to adhere per 100 microns length of vessel, while venules exposed to the same shear rates had 5-16 adherent leukocytes. In arterioles, leukocyte rolling was only observed at low shear rates. At shear rates less than 250 s-1 leukocyte rolling velocity was faster in arterioles than venules, and the ratio Vwbc/Vrbc for arterioles was 0.08 +/- 0.02, which was fourfold higher than the ratio obtained in venules at similar shear rates. Pretreatment with the CD18-specific antibody (mAb) IB4 increased leukocyte rolling velocity in venules by approximately 20 microns/s at red cell velocities below 2,000 microns/s. mAb IB4 largely prevented the leukocyte adherence to arterioles and venules, and increased the ratio Vwbc/Vrbc observed in venules at low shear elicit a CD18-dependent adhesive interaction between leukocytes and microvascular endothelium, and that differences in shear rates cannot explain the greater propensity for leukocyte rolling and adhesion in venules than arterioles.
Animals↗
Ethanol enhances leukocyte-endothelial cell interactions in mesenteric venules.
In vivo studies have implicated neutrophils in the gastric mucosal injury produced by intraluminal administration of ethanol. However, in vitro studies indicate that ethanol inhibits various neutrophil functions such as adherence, chemotaxis, and degranulation. The aim of the present study was to assess whether ethanol, at clinically relevant concentrations, is proinflammatory in vivo. Ethanol (0.2, 1.0, 2.0, and 4.0%) was applied to the surface of the cat mesentery, and neutrophil adherence to venules (30 microns diam) and extravasation into the interstitium were quantitated using intravital microscopy. Hemodynamic parameters were also measured (venular diameter, red blood cell velocity, and leukocyte rolling velocity) or calculated (venular blood flow and wall shear stress). In this model ethanol produced a dose-dependent increase in neutrophil adherence and extravasation. The increase in leukocyte-endothelial cell interactions could not be attributed to alterations in hemodynamic factors. Pretreatment of animals with a monoclonal antibody (MoAb IB4) directed to the neutrophil CD11/CD18 adherence complex completely prevented the ethanol-induced neutrophil adherence and extravasation. Pretreatment with a leukotriene B4 (LTB4)-receptor antagonist (SC 41930) or a platelet-activating factor (PAF)-receptor antagonist (WEB 2170) did not alter the ethanol-induced neutrophil-endothelial interactions. We conclude that ethanol is proinflammatory at concentrations which may be achieved in the mucosal interstitium during acute alcohol intoxication. The ethanol-induced leukocyte adherence and extravasation is dependent on the expression of adhesive glycoproteins. The inflammatory mediators, PAF and LTB4, do not appear to play an important role in the leukocyte-endothelial cell interactions initiated by ethanol.
Animals↗
Role of blood flow in gastric acid secretion.
The relationship between gastric acid secretion and blood flow has been investigated with a variety of different blood flow techniques including aminopyrine clearance, hydrogen gas clearance, intravital microscopy, laser-Doppler flowmetry, radioactive microspheres, and the elimination of inert gases. The most commonly used technique, aminopyrine clearance, predicts that increasing acid secretion is accompanied by a parallel increase in blood flow. However, the efficiency of clearance of aminopyrine is low in the nonsecreting stomach and increases as secretion rate increases. This precludes the use of aminopyrine clearance as a reliable measure of gastric mucosal blood flow at all but the highest steady-state level of acid secretion and casts doubt on the findings with this technique. Other methods for measuring blood flow indicate that there is no simple relationship between secretion and flow, with some studies finding that secretion and flow change in parallel and others finding that secretion varies quite independently of flow to the mucosa. One consistent finding is a strong correlation between stimulated acid secretion and gastric oxygen consumption. Both acid secretion and oxygen consumption fall if celiac blood flow is reduced below a critical value, which in the anesthetized dog stomach is approximately 30-40 ml.min-1.100 g-1. Driving blood flow above this value does not increase oxygen consumption and acid secretion, i.e., they reach a plateau. The shape of this relationship with its flow-dependent and flow-independent portions is used to explain the apparently contradictory findings in the literature regarding gastric acid secretion and blood flow.
Aminopyrine↗
Gradual reintroduction of oxygen reduces reperfusion injury in cat stomach.
Recent studies have shown that oxygen-derived free radicals are responsible for a major portion of ischemia-reperfusion injury in the stomach. The oxygen radicals are produced during reperfusion when oxygen delivery to the tissue increases. In the present study we investigate the effect on mucosal injury of regulating the rate of reintroduction of oxygen to the stomach after ischemia. Local gastric ischemia was achieved by reducing celiac artery pressure to 30 mm Hg for 1 h. Ischemic injury was assessed by measuring the loss of 51Cr-labeled red blood cells across the gastric mucosa. Mucosal blood loss was negligible before and during the ischemia period but increased to 0.178 ml.min.-1.100 g-1 during reperfusion. When blood flow to the stomach was gradually returned to normal after ischemia by increasing celiac artery pressure by 10 mmHg every 10 min, the mucosal blood loss was reduced to 0.013 ml.min.-1.100 g-1. If the stomach was vascularly perfused with low PO2 (34 mmHg) blood for 1 h after ischemia before being returned to normal arterial perfusion, the mucosal blood loss was also reduced to 0.063 ml.min.-1.100 g-1. When the stomach was made hypoxemic for 1 h rather than ischemic by perfusing the vasculature with low PO2 (29 mmHg) blood then reperfused with normoxic blood, there was very little mucosal bleeding (0.014 ml.min.-1.100 g-1). The data indicate that gastric mucosal bleeding after ischemia is reduced if the tissue is returned slowly to a normal PO2. These findings support the concept that reperfusion injury is due largely to the production of oxygen radicals.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Bronchopulmonary dysplasia: discharge planning and complex home care.
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Aftercare↗
Role of neutrophils in hemorrhagic shock-induced gastric mucosal injury in the rat.
Gastric mucosal clearance of 51Cr-labeled red blood cells (51Cr-RBC) was measured in rats during a 30-min control period, a 30-min ischemic period (hemorrhage to 27 mmHg arterial pressure), and a 60-min reperfusion period (reinfusion of shed blood). In untreated (control) rats, a dramatic rise in the leakage of 51Cr-labeled red blood cells into the gastric lumen was observed during the reperfusion period. Treatment with neutrophil antiserum attenuated 51Cr-labeled red blood cell flux into the gastric lumen. Using the radioactive microsphere technique, neutrophil-depleted animals were shown to have higher blood flows in the ischemic period than the untreated rats. Bleeding of untreated rats to a mean arterial pressure of 40 mmHg resulted in blood flows that were not different from those in antiserum-treated rats bled to 27 mmHg and leakage of 51Cr-labeled red blood cells similar to that measured in antiserum-treated rats. The results of this study indicate that neutrophils play an important role in hemorrhagic shock-induced gastric bleeding.
Animals↗
Gastric injury induced by hemorrhage, local ischemia, and oxygen radical generation.
Gastric mucosal injury caused by local intra-arterial generation of oxygen-derived free radicals was compared with gastric injury caused by 30 min of hemorrhage-induced ischemia (systemic pressure of 30 mmHg) or local ischemia (celiac artery pressure of 30 mmHg). The index of injury was the loss of 51Cr-labeled red cells across the gastric mucosa. Generation of oxygen radicals in the celiac artery caused a rapid increase in mucosal blood loss during the period of radical generation (0.029 +/- 0.013 ml X min-1 X 100 g-1, mean +/- SE), and this loss was maintained after radical production ceased (0.041 +/- 0.018 ml X min-1 X 100 g-1). Local ischemia produced similar mucosal injury; however, this occurred after reperfusion of the stomach (0.038 +/- 0.006 ml X min-1 X 100 g-1) and not during the ischemic episode (0.001 +/- 0.0003 ml X min-1 X 100 g-1). Hemorrhage-induced ischemia produced a threefold greater mucosal blood loss (0.133 +/- 0.048 ml X min-1 X 100 g-1) than local ischemia. The results of this study indicate that oxygen radicals generated enzymatically in the blood supply to the stomach cause mucosal bleeding of similar magnitude to that observed after local ischemia and that gastric ischemia induced by systemic hypotension produces more severe gastric injury than the same level of local hypotension.
Animals↗
Proarrhythmic effects of an oxygen-derived free radical generating system on action potentials recorded from guinea pig ventricular myocardium: a possible cause of reperfusion-induced arrhythmias.
Standard microelectrode techniques were used to study the effects of a free radical generating system on action potentials recorded from guinea pig ventricular myocardium. Free radicals were generated by mixing xanthine oxidase (0.02-0.04 mu/ml) with the superfusate-modified Locke's solution containing purine 2.3 mM. The system was validated by demonstrating that it could reduce cytochrome C at a rate of 15.9 +/- 1.5 mol/l/min. This rate was decreased to 3.0 +/- 0.3 (p less than 0.001) in the presence of superoxide dismutase (12 mg/100 ml), and the reaction was absent if xanthine oxidase and purine were premixed for 60 minutes prior to adding cytochrome C. Superfusion of guinea pig ventricular strips with the free radical generating system (20-30 minutes) resulted in a highly significant reduction in resting potential from -79.3 +/- 1.8 mV to -70.9 +/- 1.4 mV (p less than 0.0001, n = 6) and in action potential amplitude from 110.9 +/- 2.2 mV to 101.7 +/- 4.0 mV (p less than 0.0001). There was an accompanying fall in maximum rate of depolarization (Vmax) from 254.1 +/- 17.7 V/sec to 207.1 +/- 18.6 V/sec (p less than 0.01) and no significant change in action potential duration. These changes were accompanied by spontaneous activity in 3 of 6 preparations and reversed after 20-30 minutes washing in Locke's solution. They were largely abolished by adding superoxide dismutase (12 mg/100 ml) to the superfusate and completely absent if the xanthine oxidase and purine were premixed for 60 minutes before superfusing the myocardium. We conclude that the phenomena observed may contribute to the genesis of reperfusion arrhythmias.
Action Potentials↗
Descending noradrenergic pathways involved in the A5 depressor response.
The objective of the present study was to analyze the anatomical basis of the A5 depressor response and to test if the putative neurotransmitter noradrenaline is involved in the response. Two approaches were used; one was neuroanatomical and the other was pharmacological. First, the retrograde transport method in which two fluorescent markers (Fast blue and rhodamine microspheres) was used in combination with the indirect immunofluorescence technique to establish that A5 catecholamine neurons project to both the spinal cord and the region of the nucleus tractus solitarii (NTS). Second, we analyzed the effects of 6-hydroxydopamine (6-OHDA) lesions of the spinal cord and/or NTS area on the A5 depressor response. This response was elicited by a 80-nl microinjection of L-glutamate (500 mM) into the A5 region in pentobarbital anesthetized rats; it was characterized by a decrease in blood pressure and heart rate. After destruction of various noradrenergic terminal fields we have found that intraspinal injections of 6-OHDA caused a 30% reduction in the blood pressure component of the A5 depressor response and a transient depression of the bradycardic response. This result suggests that only a small portion of the A5 depressor response depends on the descending A5 spinal pathway. Injections of 6-OHDA into the NTS region caused a transient depression of the A5 depressor response, and by 7-14 days postinjection, the response returned to normal. After combined 6-OHDA injections into the spinal cord and NTS area, the blood pressure and heart rate components of the A5 depressor response were reduced to 80% of the control level at 3 days postinjection. By 14 days, even with severe depletion of noradrenaline in the spinal cord (96%) and a moderate depletion of noradrenaline in the NTS (50%), the A5 response was restored to about 80% of its original magnitude, suggesting some type of functional recovery occurs in this system. Third, the blood pressure decrease elicited by L-glutamate stimulation of the A5 cell group was unaffected by pharmacological blockade of the heart. In addition, this response appeared to be normal in rats that had both their autonomic supply to the heart blocked pharmacologically and their spinal cord noradrenaline levels depleted (14 days after intraspinal 6-OHDA injections). These data suggest that the major A5 depressor response operates mainly by inhibition of the sympathetic outflow involved in control of total peripheral resistance and that this system is controlled by a descending spinal pathway which probably does not use noradrenaline as a neurotransmitter.
Adrenergic Fibers↗
Charge selectivity of rat intestinal capillaries. Influence of polycations.
The role of fixed anionic sites on the intestinal capillary wall in transvascular protein exchange was assessed by neutralizing the negative charges with polycations. The studies were performed in anesthetized rats with an intestinal lymph cannula. Intestinal lymph flow and lymph and plasma total protein concentrations were measured at regular intervals before and after intravenous infusion of either protamine sulfate, poly-L-lysine, or poly-ethyleneimine. Protamine sulfate infusion produced an eightfold increase in lymph flow and a fivefold increase in lymph protein clearance. Lymph flow increased 4.6-fold and lymph protein clearance increased 3.6 times over control in rats receiving the poly-L-lysine infusion. Polyethyleneimine infusion produced results comparable in magnitude to protamine sulfate; however, the animals were unable to tolerate this agent. The enhanced transcapillary protein fluxes produced by the polycation infusions suggest that fixed anionic sites normally impede the egress of proteins from the intestinal vasculature.
Animals↗
Role of oxygen radicals in ischemia-induced lesions in the cat stomach.
Ischemia in a stomach that contains acid may produce severe gastric mucosal injury. The extent to which oxygen-derived free radicals are involved in the pathogenesis of this injury was investigated in the present study. Local gastric ischemia was achieved by reducing celiac artery pressure to 30 mmHg for 1 h. Ischemic injury was assessed by recording the loss of 125I-albumin and 51Cr-red cells across the gastric mucosa. Cats were treated with a xanthine oxidase inhibitor (allopurinol), a superoxide radical scavenging enzyme (superoxide dismutase), and a scavenger of hydroxyl radicals (dimethyl sulfoxide). The damage associated with ischemia only occurred during reperfusion of the stomach and was worst in the antrum. The level of xanthine oxidase in the antrum was twice that of the corpus. Treatment with allopurinol, superoxide dismutase, and dimethyl sulfoxide reduced 51Cr-red cell loss to 15%, 25%, and 21% of control (untreated) animals, respectively. The data indicate that oxygen-derived free radicals play a role in ischemic injury to the stomach and that the hydroxyl radical, a secondary radical produced from the superoxide anion, appears to be the major oxygen radical contributing to ischemic damage.
Allopurinol↗
Measurement of capillary pressure in humans using a venous occlusion method.
The venous occlusion technique was used to measure capillary pressure in the forearm and foot of man over a wide range of venous pressures. In six recumbent subjects venous pressure (Pv) in the forearm (mean +/- SE) was 9.3 +/- 1.4 mmHg and the venous occlusion estimate of capillary pressure (Pc) was 17.0 +/- 1.6 mmHg, whereas in another six subjects Pv in the foot was 17.1 +/- 1.2 mmHg and Pc was 23.4 +/- 2.5 mmHg. Venous pressure in the limbs was increased either by changes in posture or by venous congestion with a sphygmomanometer cuff. On standing Pv in the foot increased to 95.2 +/- 1.5 mmHg and Pc rose to 112.8 +/- 3.1 mmHg. The relationship established between venous pressure and capillary pressure in the forearm is Pc = 1.16 Pv + 8.1, whereas in the foot the relationship is Pc = 1.2 Pv + 1.6. The magnitude and duration of the changes in capillary pressure were also recorded during reactive hyperemia. The venous occlusion method of measuring capillary pressure is simple and easily applied to studies in humans.
Blood Pressure↗
Relationship of blood flow and oxygen consumption to ischemic injury in the canine small intestine.
The relationship of blood flow and oxygen uptake to ischemic intestinal injury was investigated by measuring the clearance of 131I-albumin from the blood to the lumen of isolated, perfused segments of canine jejunum. Reductions in blood flow for 2 h to various levels confirmed the previously demonstrated relationship of oxygen uptake to blood flow, i.e., oxygen uptake was flow-independent at blood flows above 30 ml/min X 100 g, and flow-dependent at levels below this. Blood flows above this threshold did not change the level of albumin clearance seen under control conditions (0.022 +/- 0.003 ml/min X 100 g). However, increases in the mucosal permeability to albumin were seen after blood flow was reduced to levels where oxygen uptake was decreased by more than 50%. These findings indicate that the ability of the small intestine to maintain oxygen consumption during low flow states may be an important factor in providing protection from ischemic injury, even during prolonged periods of hypoperfusion.
Animals↗
Permselectivity of the peritoneal membrane.
To investigate the osmotic barrier characteristics of the peritoneal membrane during conditions similar to peritoneal dialysis in man, yet transperitoneal fluid movement was measured in 20 cats following intraabdominal placement of isotonic saline and hypertonic solutions of NaCl, glucose, raffinose, and inulin. Also, isooncotic solutions of hemoglobin and albumin and two sulfated high-molecular-weight dextrans were investigated. Transperitoneal fluid movement was measured by a volume recovery method. Oncotic pressures of test solutions and plasma were measured by osmometry. Peritoneal osmotic conductances were calculated from the rate of transperitoneal water movement and the difference in osmotic pressures between the test solution and isotonic saline. The average glucose osmotic conductance per unit body surface are was found to be 2.3 +/- 0.18 x 10(-3) ml . min-1 . mm Hg-1 . m-2, in good agreement with previous reports, and the glucose osmotic reflection coefficient (sigma) was estimated to be 0.02. All the osmotic conductances measured could be fitted to a peritoneal equivalent pore radius of approximately 6 nm according to current hydrodynamic theories. The peritoneal membrane filtration coefficient was estimated to be 0.12 ml . min-1 . mm Hg-1 . m-2, of which 0.5-1% was found to be due to transcellular water flow. In conclusion the results of this study indicate that the peritoneum is a highly selective membrane with restrictive properties comparable to those reported for continuous capillary beds.
Animals↗