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Biomedical subjects

H J Weiss

Publications and source records attributed to H J Weiss.

At least 127 records · Page 7Linked to original sources
PubMed1975

Content and thrombin-induced release of acid hydrolases in gel-filtered platelets from patients with storage pool disease.

The levels of four acid hydrolases, beta-N-acetyl glucosaminidase, beta-glucuronidase, beta-galactosidase, and acid phosphatase, and the extent of their release (release II) by thrombin was determined in platelets from nine normal subjects, nine patients with storage pool disease, and in normal platelets which had been exposed to aspirin. The levels of all four hydrolases were normal in patients with SPD. However, release of three of these hydrolases (acid phosphatase was an exception) by low concentrations of thrombin (0.015 and 0.04 U/ml) was decreased in the patients as a group, although considerable variation in the extent of release of each enzyme was noted. In contrast, aspirin failed to inhibit release II in normal platelets (except for a slight impairment in the release of beta-N-acetyl glucosaminidase), although release I (serotonin, ATP and ADP) was inhibited. All release defects could be overcome by using higher concentrations of thrombin (0.2 U/ml). The normal levels of acid hydrolases in the platelets of patients with SPD (who are deficient in the platelet dense granules) suggest that these enzymes are not normally stored in the dense granules, but rather in alpha-granules. The findings also support the conclusions of previous studies that the release reaction is impaired in SPD. This release defect appears to be different from that seen in normal platelets after exposure to aspirin.

Acetylglucosaminidase↗
PubMed1974

Acetylenic analog of arachidonate that acts like aspirin on platelets.

Development of irreversible platelet aggregation and the accompanying release of platelet-bound serotonin and production of prostaglandins is suppressed by 5,8,11,14-eicosatetraynoic acid (TYA). These findings may be explained by an ability of TYA to inhibit the enzymatic conversion of arachidonate to a newly recognized factor, labile aggregation-stimulating substance, which induces platelet aggregation, and to prostaglandins E(2) and F(2alpha).

Adenosine Diphosphate↗
PubMed1974

Disseminated intravascular coagulation as a complication of abdominal aortic aneurysm repair.

A retrospective review was done of all patients undergoing surgical repair of abdominal aortic aneurysm (AAA) on whom coagulation studies were obtained. Those patients with laboratory documented disseminated intravascular coagulation (DIC) were selected and their clinical records reviewed. This included 7 patients studied in the periods 1964-1965 and January 1971-July 1973. Of these 7 cases, 4 occurred in patients undergoing emergency operation for ruptured aneurysm and 3 were in elective cases. All 7 patients exhibited clinical evidence of abnormal bleeding, while 6 of the 7 progressed rapidly to renal shutdown. The seventh patient recovered spontaneously. Of the 6 patients with full blown clinical and laboratory evidence of DIC, 2 recovered. Both cases received heparin therapy and multiple hemodialyses. A third patient was started on heparin but died at 36 hours in heart failure. All 3 patients receiving heparin showed clinical cessation of abnormal bleeding and disappearance of soluble fibrin monomer complexes within 24 hours of starting therapy. The study suggests a higher incidence of DIC than has previously been appreciated in both the emergency and elective repair of AAA. The prompt recognition and treatment of this complication may reverse the abnormal intravascular clotting, minimize its more serious results and avoid futile and dangerous operative intervention.

Aged↗
PubMed1974

Studies of platelet 5-hydroxytryptamine (serotonin) in storage pool disease and albinism.

Platelets in patients with storage pool disease are markedly deficient in a nonmetabolic (storage) pool of ADP that is important in platelet aggregation. They are also deficient in ATP, although to a lesser degree. In seven patients with this disorder, including one with albinism, platelet 5-hydroxytryptamine (5-HT) levels were reduced in proportion to the reduction in ATP (r = 0.94). Their platelets show diminished capacity to absorb [(14)C]5-HT, and the type of defect was similar to that produced in normal platelets by reserpine, a drug known to inhibit the uptake of 5-HT by the platelet dense granules. Storage pool-deficient platelets also converted more [(3)H]5-HT to [(3)H]5-hydroxyindoleacetic acid than did normal platelets, and the platelets in one of two patients studied contained increased amounts of 5-HT metabolites. The above findings, together with those reported previously, support the conclusion that the capacity of the dense granules (which may be either diminished or functionally abnormal) for storing 5-HT is decreased in storage pool disease; as a result, the 5-HT that enters the platelet may be more exposed to monoamine oxidases present on mitochondrial membranes. This diminished storage capacity (for 5-HT) may also explain why preincubating platelet-rich plasma with 5-HT for 45 min without stirring inhibits subsequent platelet aggregation by 5-HT to a greater degree in patients with storage pool disease than in normal subjects. The latter finding is also consistent with the theory that the aggregation of platelets by 5-HT is mediated by the same receptors on the plasma membrane that are involved in its uptake. The diminished release of platelet-bound [(14)C]5-HT by collagen that we found in these patients, as well as findings in previous studies, suggests that the release reaction may also be abnormal in storage pool disease.

Adenosine Diphosphate↗
PubMed1973

Von Willebrand factor: dissociation from antihemophilic factor procoagulant activity.

Factor VIII corrects both the clotting defect in hemophilia A and an abnormality of platelet aggregation in von Willebrand's disease. These two activities of factor VIII (antihemophilic factor and von Willebrand factor) are both detected in the void volume when human plasma or cryoprecipitate is chromatographed on Bio-Gel 5M under conditions of isotonic salt concentration. In contrast, antihemophilic factor procoagulant activity is detected with proteins of lower molecular weight when the chromatography is performed with a buffer containing 0.8M NaCl. In this way, the two activities of factor VIII can be dissociated. It remains to be determined whether these components are separate molecules associated as a complex of high molecular weight in plasma or whether they are subunits of a complex macromolecule.

Animals↗