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Biomedical subjects

R A Hutton

Publications and source records attributed to R A Hutton.

At least 55 records · Page 3Linked to original sources
PubMed1985

The effect of non-specific beta-blockade on metabolic and haemostatic variables during hypoglycaemia.

Several haemostatic and metabolic variables were monitored during insulin stress tests (ISTs), which were preceded by placebo, nadolol or propranolol ingestion for 10 days. Nadolol administration blocked the rise in plasma factor VIII: RAg concentrations, but no significant changes were observed in platelet aggregation/thromboxane A2 release. Propranolol administration reduced the significance, but not the magnitude, of the plasma factor VIII:Rag rise and also marginally inhibited platelet aggregation/TXA2 release. Both nadolol and propranolol inhibited the hypokalaemia of hypoglycaemia and retarded the recovery of plasma glucose concentrations, probably by inhibiting lipolysis (as indicated by serum nonesterified fatty acid concentrations). Both nadolol and propranolol often masked and delayed the onset of the symptoms of hypoglycaemia. Beta-blockers may exert beneficial effects by modifying haemostatic variables and by preventing hypokalaemia during stressful situations, such as hypoglycaemia or myocardial infarction, both in diabetics and in non-diabetics. However, any benefit must be balanced against the risk of masking, and possibly increasing the incidence of, hypoglycaemia in diabetics.

Adenosine Diphosphate↗
PubMed1985

Platelet size and shape in hereditary giant platelet syndromes on blood smear and in suspension: evidence for two types of abnormalities.

Platelet size on blood smear is compared with platelet size and shape in suspension (i.e., whole blood and citrated platelet-rich plasma [PRP]) for normal donors and 16 patients with hereditary "giant" platelet syndromes (HGPS), including Bernard-Soulier syndrome (BSS) (seven patients), Montreal platelet syndrome (MPS) (three patients), May-Hegglin anomaly (one patient) and Rafael platelet defect (one patient). In whole blood platelet shape is normal for HGPS, but in PRP for 10 of 16 patients with HGPS there is a decrease in the proportion of smooth, discoid-shaped platelets (discocytes [D]). The platelets of all patients with HGPS had abnormally large mean volume (VT) and increased size on peripheral blood smear. Furthermore, 12 of 16 patients with HGPS, including six of seven donors with BSS, had abnormally large discocytes. The measured size of HGPS shape-changed platelets was compared with the size predicted from the size of the D by assuming that the relationship between the size of shape-changed platelets and D was the same as observed for normal donors. In this manner it was shown that for all donors with BSS and MPS, the shape-changed platelets are disproportionately larger than the D. In contrast, in the remaining patients with HGPS the size of the shape-changed platelets was consistent with the size predicted from the D. Examination of VT for MPS as a function of time after addition of 10 mumol/L adenosine diphosphate to PRP revealed an abnormal time course, thereby pointing to an abnormality in the mechanisms that regulate platelet size during shape change. With the lone exceptions of BSS and MPS, the size of platelets on blood smear was well correlated with the total platelet plasma membrane surface area as measured by the osmotic spherocyte method. Our observations point to two distinct abnormalities in platelet size in HGPS: a disproportion between the size of D and "shape-changed" platelets, which may be related to an abnormal shape change and which is observed only for MPS and BSS, and an abnormal increase in platelet size on blood smear, which appears to reflect the increased amount of platelet plasma membrane in other HGPS platelets.

Adenosine Diphosphate↗
PubMed1984

Assessment of platelet function in patients with Raynaud's syndrome.

Platelet function was studied in 11 patients with Raynaud's syndrome and 11 healthy controls. Platelets obtained from patients with Raynaud's syndrome were significantly more responsive to adrenaline, produced more thromboxane A2, and were resistant to prostaglandin inhibitors (prostacyclin and prostaglandin E1) of platelet aggregation. Platelets from control subjects and patients with Raynaud's syndrome were more resistant to prostaglandin inhibitors when reactions were carried out at 27 degrees C rather than at 37 degrees C. Patients with Raynaud's syndrome also had significantly increased plasma concentrations of beta-thromboglobulin, fibrinogen, and circulating platelet aggregates. In an attempt to elicit local platelet responses, the forearms of control subjects and patients with Raynaud's syndrome were cooled in water tanks and platelet function tests performed before and after cooling. No significant difference in the results was observed. The potential role of platelets in the pathogenesis of Raynaud's syndrome is discussed.

Adult↗
PubMed1983

The effect of intravenous epoprostenol (prostacyclin, PGI2) on cerebral blood flow and cardiac output in man.

Epoprostenol (prostacyclin, PGI2) was given intravenously to seven healthy volunteers in a dose of 4 ng kg-1 min-1 over a 30 min period. Diastolic blood pressure fell but there was no change in cardiac output. The mean PGI2 concentration at the end of the infusion was 0.43 ng/ml (1.1 nM) and a significant inhibition of ADP-induced platelet aggregation occurred. Although obvious facial flushing occurred in all subjects and some subjects complained of headache, cerebral blood flow tended to fall. The results do not support the hypothesis that PGI2 acts as a physiological vasodilator involved in the homeostasis of normal cerebral blood flow.

Adolescent↗
PubMed1983

Changes in the blood platelets of alcoholics during alcohol withdrawal.

The effects of alcohol withdrawal on platelet count and platelet function was studied sequentially in a group of alcoholics. Baseline values for platelet count, platelet adenine nucleotides and plasma beta-thromboglobulin (beta TG) level were within the normal range but platelet aggregability (especially with ADP and adrenaline) and circulating platelet aggregates were decreased for the group as a whole. After alcohol withdrawal there was a pronounced increase in all parameters measured which reached statistical significance in many cases and persisted for two to four weeks. The potential implications and possible mechanisms for these changes are discussed.

Adenosine Diphosphate↗
PubMed1982

Morphological and functional disturbances of platelets induced by cryopreservation.

In vitro morphological and functional studies were carried out on platelets which had been cryopreserved in the presence of 5% dimethyl sulphoxide (DMSO). Overall loss of platelets was around 50%. Those which survived freezing and reconstitution showed marked morphological deterioration, increase of procoagulant activity (PF3a) and a decrease in their aggregability and adenine nucleotide content. We conclude that if transfused, cryopreserved platelets are likely to be less effective than fresh platelets and may activate coagulation in vivo and that they should only be used when suitable fresh platelets are not available.

Blood Platelets↗
PubMed1981

Depressed responsiveness to adrenaline in platelets from apparently normal human donors: a familial trait.

Decreased responsiveness to adrenaline has been observed in five apparently normal unrelated human donors. In four of the donors this trait is inherited. Three of the donors, as well as their affected relatives, also exhibited depressed responsiveness to collagen and vasopressin but normal responsiveness to ADP and thrombin. The other two affected donors exhibit normal responsiveness to most other agonists. Normal responsiveness can be restored in all instances either by incubating the platelet-rich plasma at 20 degrees C or by addition of a low concentration of the divalent cation ionophore, A-23187. All affected platelets which have been examined have ATP and ADP contents, cholesterol to phospholipid ratios, and phospholipid class compositions within the normal range. Both the resting level of cyclic-3'5'-AMP and the ability of adrenaline to prevent elevation of cyclic-3',5'-AMP levels by prostaglandin E1 are normal. Mixing experiments demonstrate the absence of a circulating inhibitor of platelet function and suggest that the defect resides in the platelets. We conclude that the depressed responsiveness of human platelets to adrenaline may result from a defect in Ca2+ mobilization to the cytosol.

Adenosine Diphosphate↗
PubMed1981

Platelet hyperaggregability during alcohol withdrawal.

Platelet function was assessed before and one week after acute alcohol withdrawal in eighteen male alcoholics. Compared to normal male controls, the platelets of the alcoholics were slightly hypoaggregable on admission but became hyperaggregable one week after commencement of alcohol withdrawal therapy. The changes were most noticeable in those patients who were alcoholaemic on admission and when using ADP or adrenaline as aggregating agents. There was no consistent change in platelet counts or in platelet adenine nucleotide levels, both of which were normal.

Alcoholism↗
PubMed1981

Platelet lipid composition and platelet aggregation in human liver disease.

Abnormal plasma lipoproteins in patients with liver disease are associated with an increase in erythrocyte cholesterol concentration and a raised erythrocyte cholesterol/phospholipid molar ratio. We hypothesized that their platelets would also have an increased cholesterol/phospholipid ratio and that this might affect aggregation in vitro. Platelet aggregates by adrenaline and ADP was measured in 34 patients with a variety of liver diseases and in 20 normal subjects and the values were related to platelet lipid composition. The platelet cholesterol/phospholipid ratio was 13% higher in the patients and correlated closely with erythrocyte cholesterol/phospholipid ratio. Platelet aggregation was reduced in most of the patients and inversely correlated with the cholesterol/phospholipid ratio. Cross-incubation and hemostasis studies indicated that there were no inhibitory factors present in the plasma; the defect was in the platelets. In contrast, other workers have shown that cholesterol-rich platelets, either from patients with Type IIa hyperlipoproteinemia or prepared in vitro, aggregate more readily than normal platelets. However, the phospholipid and fatty acid compositions of our patient platelets were also abnormal: the lecithin/sphingomyelin ratio was increased and was inversely correlated with aggregation; the proportion of arachidonic acid was decreased and positively correlated with the aggregation. In our patients with liver diseases the effects of the altered phospholipid and fatty acid composition presumably overrode those of the increased cholesterol content so that instead of enhanced aggregation, only reduced or normal aggregation was seen. We conclude that the reduced platelet aggregation seen in liver disease may reflect a decrease in arachidonic acid availability for prostaglandin and/or thromboxane production.

Blood Platelets↗
PubMed1980

Prostacyclin-like activity in the female rat thoracic aorta and the inferior vena cava after ethinyloestradiol and norethisterone.

1. Female rats were injected with ethinyloestradiol, norethisterone or both compounds for 30 days. Prostacyclin-like activity was measured in the thoracic aorta and inferior vena cava. 2. In the thoracic aorta of rats injected with ethinyloestradiol and ethinyloestradiol/norethisterone, prostacyclin-like activity was significantly increased. Norethisterone alone had no effect. 3. In the inferior vena cava of rats injected with ethinyloestradiol, norethisterone or both compounds, prostacyclin-like activity was not significantly altered. The amount of prostacyclin generated by the inferior vena cava was much lower than that by the aorta. 4. Experimentally induced changes in the vessel wall after the administration of contraceptive steroids must be due to factors other than diminished prostacyclin production.

Animals↗