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G Escolar

Publications and source records attributed to G Escolar.

At least 127 records · Page 7Linked to original sources
PubMed1993

[Potentiation of the antiplatelet effect of dipyridamole and aspirin by erythrocytes. Study under flow conditions].

PURPOSE: To assess, by means of a morphometric method, the interaction of platelets with subendothelium, as induced by perfusion with the Baumgartner system, and to compare the antiplatelet effect of acetylsalicylic acid (ASA) and dipyridamole (DIP) and the combination of both drugs. MATERIAL AND METHODS: Blood samples were drawn from healthy volunteers and platelet-rich plasma specimens were prepared at a concentration of 4 x 10(8)/mL. Abdominal aorta segments were obtained from New Zealand rabbits, they being deprived of endothelium by alpha-chymotrypsin. Red cells and platelets were separately or conjointly treated on reconstituted whole blood using ASA and DIP at therapeutic doses, separately or in association. Perfusion experiences were carried out in Baumgartner's annular chamber. Upon finishing the studies, the aorta segments were morphometrically evaluated by an optic analysis system attached to a computer with an automatic image recognition programme. The statistical analysis was performed with Student's t test, differences between groups of p < 0.05 being assigned significance. RESULTS: Treatment with the association ASA-DIP was the only one to significantly reduce interaction, as both the size of aggregates and the extent of the covered surface decreased when whole blood was treated, and only the covered surface did when red cells were separately treated. When treating only platelets, the reduction of aggregates had no significance. CONCLUSION: The synergism of ASA and DIP in antiplatelet therapy was confirmed, as well as the important enhancing effect exerted by red cells.

Adenosine↗
PubMed1993

Platelet activation on hemodialysis: influence of dialysis membranes.

During hemodialysis, platelets are activated and release alpha-granule-specific proteins. GMP-140 is a glycoprotein stored in the alpha-granules of platelets, which is selectively expressed on the plasma membrane of activated platelets. Using a specific monoclonal antibody against this protein (CD 62), we have evaluated the influence of different dialysis membranes on hemodialysis-induced platelet activation in vivo by flow cytometry in nine patients with end-stage renal disease on maintenance hemodialysis. Five membranes were evaluated: Cuprophane, cellulose acetate, polymethylmethacrylate, polysulphone and polyacrylonitrile (AN-69). Blood samples were obtained before hemodialysis and from the inlet and outlet lines five minutes after the beginning of hemodialysis. A significant increase in the GMP-140 expression was observed in samples obtained from the outlet line compared with samples obtained from the inlet line for all membranes evaluated, but the extent of this increase depended on the type of membrane used: Cuprophane 13.95 +/- 3.94%, cellulose acetate 7.4 +/- 4.52%, polymethylmethacrylate 6.93 +/- 4.6%, polysulphone 3.83 +/- 2%, and AN-69 2.14 +/- 2.19% (mean +/- SD). Cuprophane induced the highest degree of platelet activation (P < 0.05). Cellulose acetate and polymethylmethacrylate induced more platelet activation than polysulphone or AN-69 (P < 0.05). These data demonstrate that all hemodialysis membranes induce platelet activation but to a variable extent, cuprophane being the most activating membrane, cellulose acetate and polymethylmethacrylate showing an intermediate potential of activation, while the more biocompatible membranes, polysulphone and AN-69, inducing the lowest degree of platelet activation.

Adult↗
PubMed1993

Abnormal cytoskeletal assembly in platelets from uremic patients.

The mechanisms involved in the hemostatic abnormality of uremic patients remain obscure. We have explored the response of normal and uremic platelets to surface activation at the ultrastructural level and analyzed changes in the composition of proteins associated with normal and uremic platelet cytoskeletons after stimulation with thrombin (0.01 and 0.1 U/ml). Cytoskeletons were obtained by extraction with Triton X-100, processed by sodium dodecylsulfate-polyacrylamide gel electrophoresis, and the presence of cytoskeletal proteins analyzed by densitometry. Under static conditions, uremic platelets spread with difficulty on formvar-coated grids. The percentage of platelets that spread fully on this polymer surface was statistically reduced compared with that of control platelets (11 +/- 1.4 vs. 21 +/- 1.6; P < 0.05). An impairment of cytoskeletal organization was observed in resting uremic platelets but abnormalities were more evident after thrombin activation. The incorporation of actin into the cytoskeletons of thrombin-stimulated uremic platelets was significantly reduced with respect to controls (6 +/- 3% vs. 29 +/- 5%; P < 0.01 after 0.01 U/ml and 28 +/- 9% vs. 59 +/- 10%; P < 0.05 after 0.1 U/ml). Decreased associations of actin-binding protein (P < 0.01), alpha-actinin (P < 0.05), and tropomyosin (P < 0.05) with the cytoskeletons of uremic platelets were also noted. No difference was observed for the incorporation of myosin into the cytoskeletons of activated uremic platelets. These results suggest functional and biochemical alterations of the platelet cytoskeleton in uremia, which may contribute to the impairment of platelet function observed in uremic patients.

Adult↗
PubMed1993

[Effect of PAF (platelet-activating factor) on hemostasis. Studies on endothelial cells and platelets].

PURPOSE: To evaluate the direct action of PAF on the pro-coagulant activity of cultured vascular endothelial cells; to analyse by photometric methods the thrombogenic effect of PAF on platelets, and to assess platelet deposition on vascular endothelium. MATERIAL AND METHODS: Human endothelial cells were isolated from umbilical cord vein and incubated for three minutes at 22 degrees C with different PAF concentrations (10(9) M to 10(-7) M) in order to assess the influence of this lipidic mediator on the procoagulant activity of the cells. The effect of PAF on platelet aggregation was assessed by aggregation studies using arachidonic acid (AA) and different PAF and Lyso-PAF concentrations (10(-8) M to 10(-4) M). Serotonin (5-HT) release was tested in platelet rich plasma (PRP) samples highly sensitive to PAF. PRP samples were incubated for 30 minutes at 22 degrees C with 100 microCi 3H-5-HT. Platelets were activated with 10(-7) M to 10(-9) M PAF concentrations, the percentage of 3H-5-HT released into the extra-platelet medium being calculated. Baumgartner's continuous perfusion model was used to study platelet deposition on the vascular endothelium. The morphometric evaluation was carried out by a planimeter assembled to a data processor with a programme devised for analysing the platelet-subendothelium interaction. RESULTS: Evaluation of the procoagulant activity on the cell surface: The expression of the procoagulant activity showed no variations with respect to the controls under different concentrations of PAF. Platelet aggregation and release studies: Normal values of platelet aggregation (80% to 100%) were found when using AA, however, there were great case to case variations under different PAF concentrations. Serotonin release was less marked than aggregation itself. The use of Lyso-PAF failed to elicit platelet aggregation and serotonin release in any case. Morphometric evaluation: The results attained showed that perfusion carried out with 10(-8) M PAF concentration showed contact, adhesiveness and thrombus formation figures similar to those of control perfusion. CONCLUSIONS: Human platelets are not too sensitive to PAF activity, only high PAF concentrations being capable of inducing platelet aggregation and 5-HT release with ample variability. This suggests the existence of a heterogeneous platelet population with PAF receptors. Low PAF concentrations do not modify the haemostatic function, and only those PAF concentrations inducing maximal release and aggregations could reduce the interaction of platelets with vascular subendothelium and the formation of thrombi.

Blood Platelets↗
PubMed1992

Recombinant human erythropoietin treatment improves platelet function in uremic patients.

The effect of recombinant human erythropoietin (rHuEPO) on primary hemostasis was tested in 19 hemodialyzed patients. Bleeding time, platelet aggregation and platelet interaction with vessel subendothelium (SE) under flow conditions were determined before treatment and after patients reached hematocrits greater than or equal to 30%. Two thrombotic events (an acute myocardial infarction and an AV fistula clotting) were recorded during the early stages of treatment. A shortening of average bleeding times (P less than 0.01), an increase in platelet count (P less than 0.01) and an improvement of platelet aggregation (P less than 0.01) and of platelet-SE interaction (P less than 0.01) were observed. A low correlation index was found between hematocrit and bleeding time (r = -0.351, P less than 0.05). To assess a possible effect of rHuEPO on platelet function, the same parameters were evaluated before and after receiving three doses of rHuEPO (40 U/kg i.v. post-hemodialysis) in 14 of the patients. No changes in platelet or erythrocyte counts were observed, the mean bleeding time remained unchanged, but platelet aggregation induced by arachidonic acid (P less than 0.05), ADP (P less than 0.01) and ristocetin (P less than 0.05) improved. Perfusion studies confirmed moderate but significant increases in the parameters that quantify platelet-SE interaction (P less than 0.05). Improvement of ADP-induced aggregation correlated with the increase of platelet adhesion to SE (r = 0.675, P less than 0.05). We conclude that rHuEPO treatment improves primary hemostasis in uremia through an increase of red cell mass but also through a beneficial effect on platelet function, which is independent of the hematocrit rise.

Adult↗
PubMed1992

A variant of Glanzmann's thrombasthenia which fails to express a GPIIb-IIIa related epitope that is recognized by a specific monoclonal antibody (C17).

Binding of different antibodies to the GPIIb-IIIa complex in resting (AP2, EDU3, C17) or activated platelets (PAC1) was studied by flow cytometry in a patient with a platelet defect involving GPIIb-IIIa related functions. The patient has a mild history of bleeding. Aggregation induced by ADP and collagen were absent but normal response was obtained with ristocetin. Platelets from the patient do not bind fibrinogen. Perfusion studies with flowing blood showed that patient's platelets have a marked impairment in the process of spreading and aggregate formation on vascular subendothelium. Electrophoretic studies in SDS-polyacrylamide gels demonstrated the presence of normal amounts and normal mobility of GPIIb-IIIa. Fibrinogen was present in the patient's platelets (68-74% of controls). The binding of AP2 and EDU3 to patient's resting platelets was normal as assessed by flow cytometry. In contrast, a decreased presence of the C17 antigen (10 fold lower than control platelets) was detected in resting platelets and a markedly reduced binding of PAC1 was found in thrombin activated platelets. These studies suggest that C17 recognizes an epitope of the GPIIb-IIIa in resting platelets that is implicated in the regulation of adhesive and cohesive properties of GPIIb-IIIa. Studies on this patient might be helpful for the understanding of GPIIb-IIIa functions.

Adenosine Diphosphate↗
PubMed1992

Hemostatic effect of platelet von Willebrand factor.

In type III von Willebrand disease (vWD) patients, the bleeding time was only partially corrected or not modified after cryoprecipitate infusion, although the levels and the multimeric structure of plasma von Willebrand factor (vWF) were normal. However, the adhesion of normal platelets on the vessel wall subendothelium in the presence of postinfusion patient plasma improved more significantly than the bleeding time. These results suggest a role of the vWF released from normal platelets which is absent in type III vWD platelets. In 5 patients transfusion of normal platelet concentrates performed 1 h after cryoprecipitate infusion without modification of the bleeding time (> 30 min) normalized this parameter, and platelet adhesion to the subendothelium elicited a marked improvement. These last results confirm the suggestion that platelet vWF plays an important 'in vivo' role in the hemostatic process, particularly in patients suffering from severe vWD.

Animals↗
PubMed1992

Plasma from systemic lupus erythematosus patients with antiphospholipid antibodies promotes platelet aggregation. Studies in a perfusion system.

The possible platelet-aggregating effect of plasma from systemic lupus erythematosus (SLE) patients (n = 19) was investigated under flow conditions. Aliquots of the SLE plasmas with (n = 10) or without (n = 9) anticardiolipin antibodies (ACAs) were added to anticoagulated blood (1:20, vol/vol). Plasma from normal donors was used as a control. Blood was incubated for 15 minutes at 37 degrees C and then perfused through annular chambers containing denuded arterial segments. Perfusions were performed for 10 minutes at a shear rate of 800 sec-1. The interaction of platelets with vessel subendothelium (SE) was morphometrically evaluated in thin sections. In control experiments, the percentage of the SE covered with platelets was 23.6 +/- 4.3% (mean +/- SD). Large aggregates (more than 5 microns in height) covering 11.8 +/- 5.7% of the exposed SE were noted. The deposition of platelets was statistically increased (38.5 +/- 7.6%, p less than 0.01 versus control) in the presence of SLE plasmas with demonstrated antiphospholipid antibodies (APAs). The formation of large aggregates was also augmented (30.3 +/- 5.9%, p less than 0.01 versus control). A similar response was obtained after addition of affinity-purified immunoglobulin G and immunoglobulin M fractions from two patients with ACAs. SLE plasmas with no detectable APAs did not influence the morphometric parameters studied. Results of the present study indicate that the presence of APAs in SLE plasma promotes platelet aggregation under flow conditions. These observations may help to explain the pathophysiology of the thrombotic events occurring in patients with APAs.

Adolescent↗
PubMed1992

Contribution of perfusion techniques to the evaluation of the hemostatic effectiveness of platelet concentrates.

Perfusion systems allowing the morphometric analysis of platelet interactions with vessel subendothelium under flow conditions have been applied to evaluate the quality and function of stored platelets. Studies performed in vitro indicate that despite the existence of storage lesions, platelets in concentrates stored for up to 5 days retain their ability to interact with the subendothelium. Perfusion studies ex vivo with nonanticoagulated blood from anemic-thrombocytopenic patients have shown the critical hemorrheological role of red blood cells facilitating platelet interactions with subendothelium. Similar studies performed on severely thrombocytopenic patients who received transfusions of platelets stored at 4 degrees C indicate that incompletely viable platelets can contribute to primary hemostasis through procoagulant mechanisms. The latter results suggest that storage lesions which contribute to impairment of platelet function may result in enhancement of platelet procoagulant activities. Perfusion techniques have contributed to the evaluation of the hemostatic effectiveness of platelet concentrates. These techniques will provide a useful model to test the impact of new storage technologies on platelet hemostatic function.

Animals↗
PubMed1992

The role of subendothelial laminin and platelet laminin receptors in haemostasis.

Laminin (LM) is a basement membrane glyco-protein which exhibits a number of biological activities, including the promotion of cell attachment and migration. In a static system, platelets attach to LM without spreading. In order to elucidate the mechanisms mediating platelet-LM interactions under flow conditions, we studied the effects of blocking subendothelial LM and its platelet receptor. We measured the extent of platelet adhesion to the endothelial cell extracellular matrix (ECM) using a parallel plate perfusion chamber. To do this, we performed the following experiments: i) blockade of subendothelial LM by incubation of ECM with an anti-LM antibody (Ab); ii) blockade of the platelet receptor for LM with: a) an anti-67 KDa receptor Ab; and b) three different LM-derived peptides (CFALRGDNP, IKVAV and CDPGYIGSR). In i) perfusates consisted of whole blood, whereas in ii) perfusates were prepared with washed platelets pre-incubated with Ab or peptides and reconstituted with plasma and washed red blood cells. Perfusions were carried out at 800 s-1 shear rate. Platelet deposition was morphometrically evaluated by a computerized system. Our results indicated that when ECM was pre-incubated with an anti-LM Ab (100 micrograms/ml, 30 min, 37 degrees C) a reduction of the surface coverage (SC) of 23.3 +/- 2.3% (p less than 0.01) was observed. When washed platelets were pre-incubated with an anti-67 KDa receptor Ab (40 micrograms/ml, 30 min, 37 degrees C) their interaction with ECM was decreased by 22.3 +/- 2.1% of SC (p less than 0.005). In other experiments platelets were pre-incubated with CFALRGDNP, IKVAV and CDPGYIGSR (200 micrograms/ml, 30 min, 37 degrees C).(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1992

Morphological study of gastric lesions developing in the rat under several damaging conditions: modifications induced by pretreatment with zinc acexamate.

Lesions developing in the gastric mucosa of the rat after exposure to different gastric damaging agents (100 mg/kg aspirin, and 70% or 100% ethanol) were assessed by scanning electron microscopy. The severity of the lesions was quantified according to morphological criteria. Modifications in the severity of these lesions induced by pretreatment with zinc acexamate were also analyzed. The scanning electron microscope revealed that with the exception of absolute ethanol, which caused distinctive morphological features, lesions found under the different experimental agents shared a common pattern of progression. Ultrastructural lesions on surface epithelial cells preceded further alterations of parietal cells. After the integrity of the epithelial cells was lost, detachment of the parietal cells occurred, probably, through peptic digestion of the connections between cells and their extracellular matrices. Pretreatment of animals with zinc acexamate increased the presence of mucus on the gastric surface and significantly prevented the progression of lesions towards the severest stages. Ultrastructural damage of surface epithelial cells was not influenced by this treatment, but detachment of damaged cells was clearly diminished. These data confirm the protective effect of zinc acexamate against gastric aggressions. Moreover, our studies confirm the notion that mucus secretion and maintenance of continuity on the gastric lumen by surface epithelial cells is of critical importance in preventing the gastric damage induced in these experimental models.

Aminocaproates↗
PubMed1992

[The effect of low-dose acetylsalicylic acid on platelet aggregation parameters in vitro].

In order to elucidate whether a single dose of 150 mg acetylsalicylic acid three times a day, provokes significant changes into platelet aggregation, we analyzed a group of 50 patients who underwent coronary revascularization. During 48 hours before surgery, all patients received 100 mg dipyridamole orally every 6 hours and 1 hour after the end of the operation 100 mg dipyridamole via nasogastric tube. Patients were then randomized into three groups to receive 3 times a day a capsule containing: 50 mg acetylsalicylic acid, 50 mg acetylsalicylic acid plus 75 mg dipyridamole or placebo. Before the antiplatelet therapy was started, the day of the operation and 5 days after the onset of the treatment, blood samples were taken to determine platelet aggregation (turbidimetric technique) and the thromboxane A2 liberation. The three groups were comparable for all the studied clinical and angiographic variables. Preoperative dipyridamole did not provoke significant changes in platelet aggregation (acetylsalicylic acid group 86.5 +/- 10% vs 71 +/- 28.8%; acetylsalicylic acid + dipyridamole group 81.5 +/- 7.8% vs 75.3 +/- 22.7%; placebo group 83.7 +/- 8.9% vs 70 +/- 21.5%). After 5 days of treatment with acetylsalicylic acid, both groups under active treatment showed a significant (p less than 0.001) decrease of aggregability (acetylsalicylic acid 12.8 +/- 4.4%; acetylsalicylic acid + dipyridamole 20.5 +/- 17%; placebo 72 +/- 21.5%).(ABSTRACT TRUNCATED AT 250 WORDS)

Aspirin↗
PubMed1991

Dipyridamole induces changes in the thrombogenic properties of extracellular matrix generated by endothelial cells in culture.

Dipyridamole (DIP) is a drug widely used as an antiplatelet agent, which also has effects on endothelial cells. In this study, the effects of treating confluent endothelial cell monolayers (EC) with DIP on EC viability (trypan blue exclusion test) and metabolic activity (3H-thymidine incorporation) were examined. Platelet reactivity of the extracellular matrix (ECM) produced by untreated and DIP-treated ECs was determined morphometrically by a perfusion technique. Levels of ECM-associated von Willebrand factor (vWF) and fibronectin (FN) were also quantified (ELISA). The present results indicate that treatment of EC with 10 microM DIP did not reduce EC viability but that the incorporation of labelled nucleotides was significantly decreased (p less than 0.01). Platelet deposition onto the ECM generated by DIP-treated cells, perfused at a shear rate of 1300 sec-1, differed significantly with respect to controls (p less than 0.05), and platelet adhesion was also reduced (25% less, p less than 0.05). This effect was shear rate dependent, as no differences were noted when the ECMs were perfused at 300 sec-1 shear rate. Levels of VWF and FN associated with ECM remained unchanged with respect to controls. These results suggest that treatment with DIP alters EC metabolic activity, which in turn, influences the reactivity of the ECM generated by treated cells.

Cell Count↗
PubMed1991

Hemostatic effect of normal platelet transfusion in severe von Willebrand disease patients.

Platelet von Willebrand factor (vWF) has been suggested to play an important role in the hemostatic process. Clinical and experimental data indicate that bleeding time (BT) and platelet-vessel wall interaction cannot be normalized unless the defect of platelet vWF is also corrected. We have examined the effect of normal platelet concentrate transfusion 1 hour after cryoprecipitate infusion in five type III von Willebrand disease (vWD) patients. The cryoprecipitate infusion attained normal circulating levels of ristocetin cofactor, vWF antigen, and factor VIII activity. In two patients, cryoprecipitate infusion did not modify the BT (greater than 30 minutes), whereas in the remaining three patients BT was only partially corrected (from greater than 30 to 12, 18, and 21 minutes). However, the immediate platelet transfusion completely corrected the BT in four cases, and in one case it shortened the BT to 8.30 minutes (n = 3 to 8 minutes). In the perfusion study, cryoprecipitate infusion only resulted in a slight increase in platelet deposition (surface coverage range: 2.4% to 11.3%), whereas the platelet concentrate transfusion elicited a more marked improvement (range: 8.2% to 26.4%; P less than .02 v post-cryoprecipitate). These results suggest an important in vivo role of the platelet vWF in supporting platelet-vessel wall interaction. They also give support to the occasional addition of normal platelet transfusion to the cryoprecipitate infusion for the control of serious bleeding episodes resistant to cryoprecipitate in severe vWD patients.

Bleeding Time↗
PubMed1991

Evaluation of the transfusion effectiveness of various platelet concentrates by means of an in vitro perfusion technique.

An in vitro perfusion technique was used for the assessment of the effectiveness of platelet concentrates (PCs) administered to patients with bone marrow failure. Denuded rabbit arterial segments mounted in annular chambers were exposed to nonanticoagulated blood drawn directly from the antecubital vein. This perfusion system allows the direct visualization of platelet-subendothelium interactions. The deposition of platelets on exposed subendothelium and the presence of fibrin were evaluated morphometrically. Perfusions were performed before and 10 and 120 minutes after the transfusion of PCs that had been obtained by apheresis and administered immediately after collection (A) or separated by centrifugation of blood units and transfused 24 hours after storage at 22 degrees C (B) or 4 degrees C (C). Bleeding times were also determined systematically. The deposition of platelets on the subendothelium increased significantly (p less than 0.01) 10 minutes after transfusions of A and B PCs, but the presence of fibrin did not differ from pretransfusion values. Two hours after the administration of A or B PCs, the improvement of platelet deposition persisted. By then, the presence of fibrin increased markedly (p less than 0.01). The deposition of platelets was not modified after the transfusion of C PCs, but the presence of fibrin was augmented significantly at both posttransfusion times. Comparisons between bleeding times and morphometric results pointed to a possible role of fibrin formation in contributing to primary hemostasis.

Bleeding Time↗
PubMed1991

Comparison between human umbilical artery and rabbit abdominal aorta as substrata for platelet adhesion and platelet thrombus formation under flow conditions.

Rabbit abdominal aortas and human umbilical arteries are currently used as substrata for the study of platelet adhesion and aggregate formation under flow conditions. Using immunohistochemical and ultrastructural methods, we have analyzed both vessel surfaces. The reactivity towards platelets of the subendothelium (SE) exposed on these vessels after mechanical or enzymatic digestion (alpha-chymotrypsin) was morphometrically quantified and the nature of the interaction studied in the electron microscope. After mechanical damage, the ultrastructural study of rabbit aortas showed a clearly defined internal elastic lamina (IEL). In contrast, umbilical vessels lacked a consistent IEL and masses of amorphous material often located deeper in the media were the main constitutents of the SE. Immunohistochemical labeling of the von Willebrand factor bound to both types of vessel differed considerably. Quantification of platelet interactions after perfusion of citrated blood showed qualitative differences between mechanically damaged rabbit or human vessels. Enzymatic digestion produced a more thrombogenic surface on rabbit aortas (p less than 0.01 vs. nondigested), but decreased their reactivity towards platelets on umbilical arteries (p less than 0.01 vs. nondigested). The ultrastructural study of the interacting platelets revealed that aggregates, when present, were found on the extracellular matrix underlying endothelial cells of rabbit aortas, but interacting with fibrillar structures probably derived from cell elements of the media in the case of umbilical arteries. These findings indicate that rabbit aortas and umbilical arteries possess structural characteristics that result in different thrombogenic properties with respect to circulating platelets.

Aorta, Abdominal↗
PubMed1991

Experimental reactivation of chronic gastric lesions exposed to different aggressive conditions.

Experimental reactivation of chronic gastric lesions induced by acetic acid injection to the rat stomach was produced after exposure of the animals to different secondary damaging conditions. On day 18 after the initial injury, animals (n = 100) were distributed in five groups. One of them was used as control and the remainder were subjected to absolute ethanol, stress, pyloric ligation or aspirin. Measurements of gastric acid secretion were performed. Pyloric ligation resulted in the maximal rate of acid secretion. Computerized morphometric analysis of the gastric injuries showed a significant association (70%, p less than 0.01) of hemorrhagic lesions with the primary site of chronic injury in animals subjected to pyloric ligation. No significant association was observed after absolute ethanol (30%), aspirin (30%) or stress (35%). The presence of hemorrhage associated with the original gastric lesions was more dependent on the disorganization of the lamina propria and proliferation of chief cells in the margins of the mucosal scar than on the severity of extent of the chronic lesions. These results indicate that local conditions at the level of gastric mucosa together with an increased presence of acid in the gastric lumen provide favorable conditions for the reactivation of primary chronic lesions in the rat.

Acetates↗