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At least 1,063 records · Page 59Linked to original sources
PubMed2003

Influence of platelet count, acetylsalicylic acid, von Willebrand's disease, coagulopathies, and haematocrit on results obtained using a platelet function analyser in dogs.

The platelet function analyser PFA-100 aspirates blood in vitro from a sample reservoir in disposable test cartridges through a microscopic aperture cut into a biologically active membrane at the end of a capillary. In different cartridges the membrane is coated with collagen and adenosine diphosphate (ADP) or collagen and epinephrine (adrenaline) inducing a platelet plug and closure of the aperture. The closure time and total volume of blood flow through the capillary until closure of its aperture were measured. The correlation between platelet count in samples of thrombocytopenic dogs and results of the collagen/ADP cartridge (closure time: r(S)=-0.579; total volume: r(S)=-0.549) was closer than between platelet count and capillary bleeding time. No significant correlation was observed between platelet count and the results obtained with the collagen/epinephrine cartridge. In addition, a higher sensitivity was obtained for the collagen/ADP cartridge. Injection of acetylsalicylic acid into healthy dogs significantly increased closure time and total volume of both types of cartridges (P<0.01). Two dogs with von Willebrand's disease had abnormal values. In contrast, coagulopathies did not significantly influence the results of the platelet function analyser (P>0.05). Despite adequate sensitivity of measurements using the collagen/ADP cartridge to assess quantitative and qualitative platelet disorders in dogs, the influence of haematocrit (P<0.0001) will limit the clinical application of the analyser.

Animals↗
PubMed1981

Effects of acetylsalicylic acid and prostaglandin on endotoxin-induced pulmonary platelet sequestration.

Previous experimental studies have shown that soft tissue trauma and endotoxin shock cause pulmonary platelet trapping. In the soft tissue trauma model it has been found that this event can be obviated by pretreatment with aspirin and prostaglandin E1 in combination. This study was made to determine the effect of these two drugs on endotoxin-induced pulmonary platelet trapping. Dogs with 51Cr-tagged platelets were injected with 20 mg endotoxin E. coli. The dogs were kept in shock for 2 hours and then sacrificed. The dogs were kept in shock for 2 hours and then sacrified. The amount of platelet sequestration in the lungs was determined by measuring the 51Cr activity in the lungs. The results of the study showed that prostaglandin alone decreases pulmonary platelet trapping induced by endotoxin, but aspirin, either alone or together with prostaglandin E1, has no positive effect. This could be explained by the fact that acetylsalicylic acid depresses endogenous prostaglandin, and thus decreases the blood concentration of available prostaglandin.

Alprostadil↗
PubMed1983

Manipulation of the local thromboxane and prostacyclin balance in vivo by the antithrombotic compounds dazoxiben, acetylsalicylic acid and nafazatrom.

We have developed an experimental model for the study of local prostaglandin production by platelets and the vessel wall following stimulation 'in vivo'. A nylon thread was inserted into the external jugular vein of rabbits; its presence did not induce an occluding thrombus. Thromboxane (TXB2) values in the blood, sampled through the facial vein, immediately distal to the stimulus, rose and remained high for at least 4 hr, while 6-keto prostaglandin (PG) F1 alpha levels, after a first increase, gradually returned to normal ('exhaustion' of the endothelial cells?). No changes were observed in the contralateral jugular vein without thread. After infusion via the femoral vein of 10 mg/kg dazoxiben, a thromboxane synthetase inhibitor, local TXB2 production was completely abolished, whereas 6-keto PGF1 alpha formation no longer returned to basal values, but tended to increase. This leads to the conclusion that upon inhibition of TXB2 formation endoperoxide metabolism is reoriented 'in vivo' towards prostacyclin, and this mainly at the site where platelets are activated. Injection of 100 mg/kg lysine acetylsalicylic acid resulted in complete inhibition of TXB2 and 6-keto PGF1 alpha formation, the latter, however, slowly recovering with time. The administration of nafazatrom to the animals did not influence the local TXB2 changes, but partially prevented the decline of 6-keto PGF1 alpha with time. The antithrombotic properties of this drug thus could be related to protection of the endothelial cells from 'exhaustion'.

Animals↗
PubMed1974

Comparative effects of proteinase inhibitors, plasminogen antiactivators, heparin and acetylsalicylic acid on the experimental disseminated intravascular coagulation induced by thormbin.

In an experimental study in the rabbit, the modifications of some haemostasis parameters (platelet count, platelet retention and aggregation, platelet factors 3 and 4, platelet and plasma plasmin inhibiting activities, fibrinogen and other plasma factor levels, FDP), and histological findings are compared in both the normal animal and the animal with disseminated intravascular coagulation (DIC) induced by thrombin perfusion after administration of fibrinolytic inhibitors (plasminogen antiactivators and proteinase inhibitors). In the normal animal, the administration of fibrinolytic inhibitors is followed by haemostatic changes similar to those found in thrombophilic states. The modifications are more pronounced with plasminogen antiactivators than with proteinase inhibitors. In the animal with DIC, the administration of fibrinolytic inhibitors enhances the haemostatic and the biological disorders produced by thrombin perfusion. The effect of the plasminogen antiactivators is even more evident. The preventive administration of heparin reduces or abolishes the biological and histological disorders induced by thrombin; its beneficial effect is considerably reduced when thrombin is combined with fibrinolytic inhibitors. The administration of acetylsalicylic acid appears to be ineffective for the prevention of haemostatic and histological changes induced by thrombin perfusion.

Aminocaproates↗
PubMed1993

Acetylsalicylic acid (ASA) protects the prostaglandin-cAMP-system of human hypernephroma cells against irradiation-induced alterations.

There is abundant evidence that inhibitors of prostaglandin (PG) biosynthesis might increase the radioresponse of certain tumour cells. This study investigated specific PG binding sites, eicosanoid production as well as intracellular cAMP levels in cultured human hypernephroma cells derived from 11 patients upon nephrectomy. Scatchard analyses of the binding data revealed specific PGE1-, PGE2- as well as PGI2-binding sites (PGE1: Bmax = 755 +/- 206 fmol mg-1 protein, Kd = 3.7 +/- 2.7 nM PGE2: Bmax = 494 +/- 221 fmol mg-1 protein, Kd = 4.2 +/- 2.5 nM; PGI2: Bmax = 693 +/- 164 fmol mg-1 protein, Kd = 6.0 +/- 4.5 nM). Significant (P < 0.01) increase in PG binding sites expressed on human hypernephroma cells (PGE1: Bmax = 1084 +/- 303 fmol mg-1 protein, Kd = 2.8 +/- 1.3 nM; PGE2: Bmax = 663 +/- 309 fmol mg-1 protein, Kd = 2.2 +/- 1.5 nM; PGI2: Bmax = 1021 +/- 391 fmol/protein, Kd = 4.2 +/- 3.6 nM) and inhibition of PG biosynthesis (TXB2: -82.5%, PGE2: -87.5%. PGD2: -80.6%, PGF2: -81.3%) were found after acetylsalicylic acid (ASA)-treatment (0.5 mg 10(-6) cells for 24 h). Following irradiation (60Co, 1.0 Gy/min-1 over 10(min), PG binding sites (PGE1: Bmax = 266 +/- 153 fmol mg-1 protein, Kd = 5.0 +/- 5.0 nM; PGE2: Bmax = 148 +/- 66 fmol mg-1 protein, Kd = 4.7 +/- 3.6 nM; PGI2: Bmax = 325 +/- 194 fmol mg-1 protein, Kd = 6.8 +/- 7.1 nM) were significantly (P < 0.01) diminished. However, irradiation had no significant effect on PG binding sites in ASA-pretreated cells (PGE1: Bmax = 699 +/- 240 fmol mg-1 protein, Kd = 3.5 +/- 1.8 nM; iloprost: Bmax = 766 +/- 452 fmol mg-1 protein, Kd = 3.2 +/- 2.2 nM). Although there was no significant difference in the basal values for cAMP between control and ASA-treated group cells, the PG-induced cAMP-production was less pronounced in the control group. Taken together, the findings suggest that ASA may modify the radioresponse of cultured human hypernephroma cells by preventing the decrease of PG binding sites induced by irradiation.

Alprostadil↗
PubMed1991

[75 mg roxatidine nocte protects human gastric mucosa against 300 mg acetylsalicylic acid nocte].

In a randomized double-blind parallel study the gastroduodenal tolerability of 300 mg ASS nocte (8 p.m.) has been evaluated in the presence of 75 mg roxatidine nocte (8 p.m.) or placebo in 20 healthy volunteers using upper GI-endoscopy. The treatment periods lasted 14 days. Endoscopic controls were performed at entry, and repeated at day 7 and day 14. At entry the mean endoscopic score averaged 0.9 +/- 0.1 in the ASS/placebo-group and 0.9 +/- 0.1 in the ASS/roxatidine-group. The median values were 1.0 and 1.0. 300 mg ASS nocte induced in the placebo-experiments marked gastroduodenal lesions both at day 7 and day 14 (6.5 +/- 1.2 and 7.9 +/- 0.7, respectively). The median values were 8.0 and 9.0, respectively. Concomitant administration of 75 mg roxatidine nocte afforded significant protection against 300 mg ASS nocte both on day 7 and day 14 (3.3 +/- 1.0 and 3.1 +/- 0.9, respectively) (p less than 0.05). The corresponding median values were 1.0 and 1.0. Our data suggest that coadministration of roxatidine nocte reduces significantly gastroduodenal lesions evoked by acetylsalicylic acid 300 mg nocte.

Adult↗
PubMed1991

[Protection from gastroduodenal adverse effects of acetylsalicylic acid with ranitidine. An endoscopic controlled double-blind study of healthy subjects].

Ranitidine protects against gastroduodenal mucosal damage associated with low-dose ASA therapy/Endoscopically evaluated double-blind study in healthy volunteers In a randomized double-blind crossover study the gastroduodenal tolerability of 300 mg ASA mane (8 a.m.) has been evaluated in the presence of 300 mg ranitidine nocte (8 p.m.) or placebo in 10 healthy volunteers using upper GI-endoscopy. The treatment periods lasted 14 d. Endoscopic controls were performed at entry, and repeated at day 7 and day 14. At entry the mean endoscopic score averaged 0.9 +/- 0.1 in the ASA/placebo-group and 0.8 +/- 0.1 in the ASA/ranitidine-group. 300 mg ASA mane induced in the placebo-experiments marked gastroduodenal ulcerations both at day 7 and day 14 (7.3 +/- 1.3 and 8.2 +/- 2.1, respectively). Concommittant administration of 300 mg ranitidine nocte afforded almost full protection against 300 mg ASA mane both on day 7 and day 14 (1.6 +/- 0.4 and 1.7 +/- 0.5, respectively) (p less than 0.05). These data suggest that nocturnal coadministration of ranitidine 300 mg reduces almost completely gastroduodenal lesions evoked by acetylsalicylic acid 300 mg mane.

Adult↗
PubMed1999

Prevention of small black spots on sugar-coated tablets containing aluminum acetylsalicylic acid.

Sugar-coated tablets containing aluminum acetylsalicylate gradually developed black spots on their surface. A factorial experiment was performed based on an L32 orthogonal array table in an attempt to halt this phenomenon. The factor responsible proved to be talc used to formulate the smooth coating layer over the subcoating layer containing aluminum acetylsalicylate. When HCl-treated talc was used as a filler for the smoothing layer, the black spots were markedly decreased. The spotting mechanism was considered to be due to hydrolysis of aluminum acetylsalicylate in the subcoating layer to salicylic acid and acetic acid, which sublimated into the pores of the smoothing layer. Then, ferrous ion substituted from magnesium ion in the talc molecule center was extracted by salicylic acid, acetic acid, and moisture. Finally, the ferrous ion was oxidized to ferric ion, and this produced an Fe3+ chelate compound together with salicylic acid.

Acetic Acid↗
PubMed1984

Absorption of acetylsalicylic acid from enteric-coated tablets in relation to gastric emptying and in-vivo disintegration.

The absorption of acetylsalicylic (ASA) acid from enteric coated tablets was studied in relation to gastric emptying and in-vivo disintegration. ASA tablets labelled with 51Cr were given to six healthy subjects under fasting and non-fasting conditions. The position and disintegration of the 51Cr-labelled tablets was followed by external radiation measurement and the amount of salicylic acid in blood and urine was analysed. The absorption of ASA from the studied enteric coated tablets was usually correlated with gastric emptying and in-vivo disintegration. However in some cases the absorption can be delayed between 10-20 h even if gastric emptying and disintegration of the tablet have occurred.

Aspirin↗