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Biomedical subjects

G D Lowe

Publications and source records attributed to G D Lowe.

At least 289 records · Page 16Linked to original sources
PubMed1984

Protein C, an anticoagulant protein, is increased in healthy volunteers and surgical patients after treatment with stanozolol.

On both oral and intramuscular administration, the anabolic steroid stanozolol was found to increase protein C antigen concentrations in circulating blood. In fourteen healthy young volunteers (who received stanozolol orally, dose 10 mg/day) the average increase was 1.5-1.6 times the normal concentrations after 3-6 weeks' treatment and was accompanied by more moderate increases in the other vitamin K-dependent factors II, IX and X to 1.4, 1.4 and 1.2 times their normal concentration respectively. However, there was no change in factor VII. In sixteen elderly surgical patients, intramuscular injection (50 mg) one day prior to surgery induced a moderate increase within 24 hours (to 1.11 times the pretreatment concentration) and seven days after operation (to 1.19 times), and reduced the postoperative fall in protein C. Stanozolol administration seems to be a promising pharmacological method for increasing anticoagulant protein C levels in congenital and acquired deficiencies.

Adult↗
PubMed1984

Effect of stanozolol on delta-aminolaevulinic acid synthase and hepatic monooxygenase activity in man and rat.

Stanozolol is an anabolic steroid which is used in the treatment of aplastic anaemia and has been recently advocated for the prophylaxis of vascular thrombosis. Similar steroid substances stimulate the activity of delta-aminolaevulinic acid synthase (ALA S), the rate limiting enzyme of haem biosynthesis, in rat hepatocytes and chick embryo liver cell cultures and activate acute hepatic porphyria. In the present study stanozolol (10 mg daily for 14 days) has been shown to increase significantly leucocyte ALA S activity in 9 healthy male subjects. There was a concomitant rise in urinary ALA and total porphyrin excretion but no change in antipyrine kinetics or urinary 6 B hydroxycortisol excretion. In a complementary study in male Sprague Dawley rats, stanozolol administered intraperitoneally, produced a dose-dependent increase in hepatic ALA S activity without changing hepatic cytochrome P 450 content. Stanozolol has been clearly shown to elevate ALA S activity, probably directly, and thereby, porphyrin production without affecting hepatic monooxygenase activity. This porphyrinogenic effect may be relevant to the successful treatment of aplastic anaemia with anabolic steroids. Leucocyte ALA S activity may provide a human system for the study of drug porphyrinogenicity in vivo.

5-Aminolevulinate Synthetase↗
PubMed1984

The relationship of plasma and serum viscosity to disease activity and smoking habit in rheumatoid arthritis.

Viscosity measurements of serum and plasma have been suggested as improvements on other indicators of activity in the rheumatic diseases. We compared the clinical assessment of disease activity in 71 patients with rheumatoid arthritis against various laboratory tests including viscosity measurements. The effects of smoking were also studied. While many of the tests showed correlations with each other, none was found to correlate with any of the clinical parameters. Smoking lowered the ESR, but did not affect the plasma viscosity in these patients. Thus viscosity measurements were no improvement in assessing activity in a cross section of patients, though its lack of dependence on smoking habit may be an advantage in sequential studies.

Arthritis, Rheumatoid↗
PubMed1984

The correlation of clinical assessment of synovial fluid with its measured viscosity.

The viscosity of 10 specimens of rheumatoid synovial fluid was assessed using side-room tests as well as being measured in a viscometer. All of the tests, and particularly the 'mucin clot', correlated well with measured viscosity. We conclude that the mucin clot test does indeed reflect viscosity and can demonstrate the presence of inflammatory joint disease.

Arthritis, Rheumatoid↗
PubMed1984

Blood rheology in pre-eclampsia and intrauterine growth retardation: effects of blood pressure reduction with labetalol.

Blood viscosity ( Contraves L S 30) and its determinants were measured in 23 patients with mild/moderate pre-eclampsia, 10 patients with intrauterine growth retardation and 22 control subjects, matched for age and gestation. Both abnormal groups had a significantly increased blood viscosity at high shear rate (94 s-1) associated with increased haematocrit. Fibrinogen levels were also increased, but there were no significant differences between groups in plasma viscosity, low shear viscosity (0.94 s-1) or red cell deformability, measured by a low-shear washed cell system of filtration through 5-micron pore diameter Nuclepore filters. In the pre-eclamptic group, measurements were repeated after 1-2 weeks in nine patients treated with labetalol (a combined alpha and beta adrenergic blocker) and in 10 patients treated with bed rest. Labetalol reduced blood pressure but no change in rheology was seen in either group. Control of blood pressure by labetalol does not adversely affect rheology, in contrast to diuretics which are known to cause haemoconcentration and increased blood viscosity.

Adult↗
PubMed1984

Blood coagulation and platelet function following maximal exercise: effects of beta-adrenoceptor blockade.

Alterations of platelet function and blood coagulation may occur with exercise or beta-adrenoceptor blockade. To determine if beta-blockade could modify exercise-induced changes in haemostatic factors we performed a double-blind study of acute strenuous exercise in normal males with and without beta-blockade. Exercise increased prostacyclin and plasminogen activator levels but there was no evidence of thrombin generation as indicated by unchanged platelet aggregation responses, beta-thromboglobulin and fibrinopeptide A levels. The only alteration in coagulation by beta-blockade was a reduction in the factor VIII:C and VIII:RAg rise after exercise and this modification may be relevant to the protective effect of these drugs in patients with coronary artery disease.

Adrenergic beta-Antagonists↗
PubMed1984

Effect of prostacyclin (epoprostenol) on the aggregation of human platelets in whole blood in vitro.

Prostacyclin (PGI2) is a potent endogenous inhibitor of platelet aggregation. The effect of PGI2 on platelet aggregation and disaggregation in whole human blood was studied at 37 degrees C in vitro. Aggregation or disaggregation was quantified by counting single platelets using the recently developed Ultra Flo 100 Whole Blood Platelet Counter. Aggregation of platelets in whole blood was induced by arachidonic acid (AA, 400 microM), adenosine 5'-diphosphate (ADP, 10 microM), thrombin (0.1 U/ml) and collagen (1 microgram/ml). At peak aggregation, each aggregating agent induced about a 90% fall in the number of single platelets counted. When whole blood was pre-incubated with PGI2 (0.5-8 nM), it dose dependently inhibited aggregation of platelets induced by all four aggregating agents. Platelet aggregates induced by ADP or thrombin could rapidly be disaggregated by PGI2 added to blood at peak aggregation. Disaggregation of collagen-induced platelet aggregation by PGI2 was slow and minimal and it was completely ineffective in disaggregating AA-induced platelet aggregates. Unlike platelet-rich plasma, which is routinely used to study platelet aggregation, the present whole-blood method allows red and white blood cells to exert their influences on platelet function, and is an important step towards a physiological state for evaluating the effects of pharmacological agents on platelets in whole blood in vitro and ex vivo.

Adenosine Diphosphate↗
PubMed1984

Effects of diabetic control and biosynthetic human insulin on blood rheology in established diabetics.

Blood rheology (blood viscosity, haematocrit, plasma viscosity, erythrocyte sedimentation and deformability) was measured in 22 diabetics in a study to compare animal insulins with biosynthetic human insulin. All rheological variables were significantly abnormal in the diabetics when compared with matched normal controls, and were not influenced by the type of insulin injected. However, blood rheology was related to diabetic control, as judged by glycosylated haemoglobin levels; when diabetic control was worst (mean glycosylated haemoglobin 11%), blood viscosity was significantly higher and red cell deformability significantly lower than when control was at its best (mean glycosylated haemoglobin 9.5%). A similar correlation between mean red cell deformability and mean glycosylated haemoglobin was found when individual diabetics were compared (r = 0.66; p less than 0.001). The occurrence of abnormal blood viscosity and red cell deformability during periods of poor diabetic control may contribute to the development of diabetic vascular complications.

Adolescent↗
PubMed1983

The novel effect of a new prostacyclin analogue ZK36374 on the aggregation of human platelets in whole blood.

Platelet aggregation was studied at 37 degrees C in citrated whole human blood, using the Ultra Flo 100 Whole Blood Platelet Counter. Aggregation was measured as a fall in the number of single platelets following addition of an aggregating agent. At peak aggregation, the fall in the number of platelets induced by ADP (10 microM), collagen (1 microgram/ml) or thrombin (0.2 U/ml) was about 90%. When blood was incubated with the prostacyclin-analogue ZK36374, the aggregation responses to ADP, collagen and thrombin were reduced with IC50's = 0.5, 1.5 and 3 nM respectively and the corresponding IC100's were: 1, 3 and 12 nM. When ZK36374 was added at peak aggregation, the number of single platelets increased significantly due to disaggregation of preformed platelet aggregates. It is concluded that the present technique represents a rapid, sensitive and more physiological approach for investigating the effects of pharmacological agents on platelet aggregation.

Adenosine Diphosphate↗
PubMed1983

Immunological abnormalities in haemophilia: are they caused by American factor VIII concentrate?

Scottish patients with haemophilia, most of whom had received no American factor VIII concentrate for over two years, were found to have immunological abnormalities similar to those in their American counterparts--that is, a reduced proportion of T helper cells, an increased proportion of T suppressor cells, and a reduced response to concanavilin A. Factor VIII from both the United States and Scotland severely inhibited the in vitro lymphocyte response to mitogens in patients and controls. The American and Scottish concentrates could not be distinguished in terms of either patient usage or their effect in vitro. These results argue against a disease vector specific to American blood products.

Adult↗
PubMed1983

Plasma fibrinopeptide A and beta-thromboglobulin in patients with chest pain.

Plasma levels of beta-thromboglobulin (BTG) and fibrinopeptide A (FPA), markers of platelet release and thrombin generation respectively, were measured in 48 patients within 3 days of admission to hospital for acute chest pain. Twenty-one patients had a confirmed myocardial infarction (MI); 15 had unstable angina without infarction; and 12 had chest pain due to noncardiac causes. FPA and BTG were also measured in 23 control hospital patients of similar age. Mean plasma BTG levels were not significantly different in the 4 groups. Mean plasma FPA levels were significantly higher in all 3 groups with acute chest pain when compared to the control subjects (p less than 0.01), but there were no significant differences between the 3 groups. Increased FPA levels in patients with acute chest pain are not specific for myocardial infarction, nor for ischaemic chest pain.

Adult↗
PubMed1983

Prognostic value of beta-thromboglobulin in patients with transient cerebral ischaemia.

Plasma levels of beta-thromboglobulin (BTG) and fibrinopeptide A (FPA), markers of platelet alpha-granule release and thrombin generation respectively, were measured in 27 subjects with transient cerebral ischaemic attacks (TIA), 43 age-matched controls, and 32 young controls. BTG and FPA were both higher in elderly controls than in young controls. BTG was higher in TIA subjects than in age-matched controls and higher in the 12 TIA subjects who had further vascular events in the next year than in those who had no further events. FPA was not significantly associated with TIA or with further events. These results support a relationship between platelet activation and TIA and suggest that BTG levels indicate a group at higher risk of further vascular events.

Adult↗
PubMed1983

Blood viscosity and haemostasis in the nephrotic syndrome.

Blood viscosity and its major determinants (haematocrit, plasma viscosity and fibrinogen) as well as several haemostatic variables were measured in 21 patients with the nephrotic syndrome, and 21 controls matched for age, sex, smoking habit and serum creatinine. Blood viscosity was significantly increased in the nephrotic group, measured at a low shear rate (mean increase 41%, p less than 0.01) and at a high shear rate (mean increase 25%, p less than 0.01). Haematocrit was not significantly increased, but plasma viscosity was significantly higher (p less than 0.01), associated with increased plasma macroglobulins especially fibrinogen, which was increased to double the plasma concentration of the control group (p less than 0.01). Nephrotic subjects also had increased plasma levels of alpha 2-macroglobulin, factor VIII activity, factor VIII antigen and beta-thromboglobulin; differences in antithrombin III, fibrin degradation products, plasminogen, and platelet count were not significant. We suggest that increased blood and plasma viscosity may play a role in the vascular complications of the nephrotic syndrome.

Adult↗
PubMed1983

Platelet aggregation studies in whole human blood.

Since the development of the photometric aggregometer, platelet aggregation studies are routinely performed on platelet-rich plasma (PRP). We have studied platelet aggregation in fresh citrated whole human blood using the recently developed Ultra Flo 100 Whole Blood Platelet Counter. Aggregation of platelets in whole blood was induced with adenosine 5'-diphosphate (ADP; 0.25-10 microM), collagen (0.25-1.0 microgram/ml) and thrombin (0.05-0.2U/ml). Platelet aggregation induced by ADP and thrombin was maximum within 1 min, and that of collagen within 3 mins. Aggregation responses to low concentration of ADP and thrombin were rapidly reversible, whereas responses to collagen and high concentrations of ADP and thrombin were virtually irreversible. The aggregation of platelets was indicated by a fall in platelet count; confirmed by scanning electron micrographs which revealed the presence of large aggregates of platelets, and was prevented when blood was treated with EDTA as anticoagulant. The present technique appears to be rapid, sensitive and reliable; and allows direct measurement of platelet aggregation and disaggregation in whole blood in vitro and ex-vivo.

Adenosine Diphosphate↗