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Biomedical subjects

K K Hampton

Publications and source records attributed to K K Hampton.

At least 55 records · Page 3Linked to original sources
PubMed1991

Haemostatic responses and vasopressin release during colonoscopy in man.

1. During major abdominal surgery there are increases in Factor VIII and plasminogen activator activity, associated with elevated plasma concentrations of vasopressin, of a magnitude shown to affect haemostasis. 2. To investigate the mechanisms involved in the haemostatic response to surgery, 12 patients undergoing fibre-optic colonoscopy were studied, of which six had a complete and six had an incomplete examination. 3. Venous blood samples were taken before, during and after the procedure for assay of plasma vasopressin, adrenaline and noradrenaline concentrations, Factor VIII coagulant activity, von Willebrand factor antigen level, euglobulin clot lysis time, tissue-type plasminogen activator activity and tissue-type plasminogen activator inhibition. 4. In the six patients who underwent a complete procedure the median plasma vasopressin concentration rose from 0.6 pg/ml to 153 pg/ml during colonoscopy. Factor VII coagulant activity rose from 0.9 to 2.4 i.u./ml and von Willebrand factor antigen level rose from 139 to 224%. Plasminogen activator activity increased from 20 to 144 units and tissue-type plasminogen activator activity rose from 107 to 1338 m-i.u./ml, whereas tissue-type plasminogen activator inhibition fell from 4.8 to 1.0 i.u./ml. 5. In the six patients in whom a limited procedure was performed, there were no changes in haemostatic function or in plasma vasopressin concentration. Plasma concentrations of adrenaline and noradrenaline did not change in either group. 6. The results indicate that vasopressin regulates the intrinsic coagulation pathway and fibrinolytic system in the absence of adrenaline release.

Adult↗
PubMed1991

Elevation of plasma vasopressin in spontaneous migraine.

Vasopressin is a vasoactive hormone secreted from the posterior pituitary. At low concentration its role is in regulating renal water excretion, but at higher concentrations it has a number of extrarenal actions, including effects on blood flow. To investigate the role of vasopressin in spontaneous migraine, paired samples were collected from 14 subjects (a) during an acute attack of spontaneous migraine, and (b) when symptom-free for at least seven days. During an attack, vasopressin was consistently raised (median (range) 3.5 (1.2-9.6) pg/ml v 0.5 (0.5-1.1) pg/ml, p less than 0.001). The highest vasopressin concentration occurred in the only patient who vomited. The results suggest vasopressin rises during an attack of spontaneous migraine, and this may, in part, be related to emesis. In the majority, vasopressin levels only rose sufficiently to have some renal antidiuretic effect, although in some these levels could have been sufficient to cause alteration in peripheral blood flow. Release of vasopressin may be responsible for the facial pallor and antidiuresis observed in migraine.

Adult↗
PubMed1991

Potential thrombogenicity of heat-treated prothrombin complex concentrates in Haemophilia B.

We have studied the potential thrombogenicity of two different heat-treated prothrombin complex concentrates (PCC) in patients with Haemophilia B. Seven patients were studied on nine separate occasions. Four of the patients had chronic hepatitis C (HCV) associated liver disease and three were HIV-antibody positive. The PCCs were Profilnine (Alpha Therapeutics, Thetford, UK) and 9A (Bio-Products Laboratory, Elstree, UK) and the dose administered ranged from 35 to 60 U/kg. Blood samples were taken on ten separate occasions; twice before the infusion and at 15, 40, 60, 75 and 120 min and 4, 8 and 24 h after the infusion of PCC. Investigations included prothrombin time, kaolin cephalin clotting time, thrombin time, fibrin(ogen) degradation products, factor VIII, factor IX, antithrombin III and fibrinopeptide A (FPA). Fibrinopeptide A rises were seen following two of six infusions of 9A and one of three infusions of Profilnine. On all three occasions the rise in FPA was transient, returning to baseline levels within 120 min. Plasma beta-thromboglobulin (BTG) was assayed in three patients and in one patient, the rise in FPA was followed by an increase in BTG. No other changes were observed and there were no clinical features of disseminated intravascular coagulation. Our results indicate that even with normal clinical doses of PCC, intravascular thrombin generation can occur in patients with Haemophilia B. However, this effect is inconsistent both with respect to PCC batch and patient, but may occur in the absence of HIV infection and HCV liver disease.

Blood Coagulation↗
PubMed1991

Vasopressin and haemostatic responses to inguinal hernia repair under local anaesthesia.

Major abdominal surgery is accompanied by intra-operative increases in factor VIII (FVIII), plasminogen activator activity (PAA) and fibrinopeptide A (FPA). Vasopressin (aVP) released during surgery mediates some of the effects but the mechanisms involved in this response are unclear. To investigate the role of the operative procedure, 20 subjects were studied during inguinal hernia operation under local anaesthesia. Venous blood samples were taken for FVIII coagulant activity (FVIII:C), euglobulin clot lysis time (ECLT), FPA, crosslinked FDPs (XL-FDP) and a VP. In six patients, aVP rose from (median) 0.5 to 38.3 pg/ml at bowel manipulation and fell to 4.1 pg/ml post-operatively. PAA rose from 33 units to 377 and 316 units (P less than 0.01), FVIII:C from 1.58 to 2.4 IU/ml (P less than 0.01) and FPA from 5.0 to 6.8 and 11.0 pmol/ml intra-operatively (P less than 0.002). XL-FDP rose from a median value of 34 ng/ml pre-operatively to 230 ng/ml post-operatively. In 14 patients plasma aVP levels remained constant and both FVIII:C and PAA remained unchanged. FPA rose from 2.6 pmol/ml to 5.9 pmol/ml intra-operatively (P less than 0.05) and XL-FDP fell from 110 to 60 ng/ml. Between groups, the changes were significantly different for FVIII:C (P less than 0.05) and PAA (P less than 0.03) with no differences in blood pressure, pulse or symptoms. These results support the hypothesis that aVP secretion during surgery mediates increases in FVIII and PAA. FPA tended to be higher in the aVP secreting group which indicates that aVP mediated activation of coagulation results in a hypercoagulable state.

Adult↗
PubMed1991

Contrasting fibrinolytic responses in type 1 (insulin-dependent) and type 2 (non-insulin-dependent) diabetes.

To study fibrinolysis in relation to microvascular diabetic complications, 20 control subjects were compared with 50 Type 1 (insulin-dependent) diabetic patients of similar age, 20 with no complications, 17 with laser-treated retinopathy, and 13 with neuropathy and retinopathy. None were smokers, hypertensive or had macrovascular disease. Pre- and post-venous occlusion blood samples for tests of fibrinolysis were taken. Median (interquartile range) basal tissue plasminogen activator (t-PA) activity was lower in control subjects (100 (less than 100-100) IU l-1) than diabetic patients (uncomplicated 145 (100-280) IU l-1, p = 0.015; retinopathy 180 (100-228) IU l-1, p = 0.037; neuropathy 210 (125-310) IU l-1, p = 0.004, respectively). Basal t-PA inhibition (PAl-1 activity) was higher in control subjects (5.9 (4.5-9.5) kIU l-1) than diabetic patients (uncomplicated 4.0 (3.3-5.0) kIU l-1, p = 0.001; retinopathy 4.5 (3.1-6.3) kIU l-1, p = 0.058; neuropathy 4.0 (3.0-5.4) kIU l-1, p = 0.015, respectively). Post-venous occlusion t-PA antigen was higher in control subjects (10.2 (7.3-15.1) micrograms l-1) than neuropathic patients (5.5 (4.9-7.3) micrograms l-1, p = 0.004). Other tests showed a consistent, but non-significant, trend towards increased basal fibrinolysis in the Type 1 diabetic patients. The results indicate that Type 1 diabetic patients have enhanced basal fibrinolysis. The diminished response to venous occlusion in neuropathic patients is consistent with an endothelial cell defect.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Coagulation, fibrinolytic and platelet function in patients on long-term therapy with aspirin 300 mg or 1,200 mg daily compared with placebo.

Aspirin has been shown to be beneficial in the prophylaxis of arterial thromboembolic disease. The rationale for its use as an antithrombotic drug lies in its inhibition of thromboxane A2-dependent platelet function. However, the effect of aspirin on coagulation and fibrinolysis during chronic therapy has not been studied. We have measured a range of haemostatic and platelet functions in 49 patients with transient ischaemic attacks randomly allocated to aspirin 300 mg a day, aspirin 1,200 mg a day or placebo. All had been taking their allocated treatment for between 9 months and 4 years prior to investigation. Bleeding time was prolonged, serum thromboxane diminished and platelet aggregation to arachidonic acid but not ADP was abolished by both 300 mg and 1,200 mg aspirin, in a non-dose dependent fashion. Serum salicylate increased with the dose of aspirin ingested. No effect was seen with either dose of aspirin on urinary thromboxane and 6-keto-PGF1 alpha excretion, or on coagulation. Patients taking 1,200 mg aspirin a day had a lower haemoglobin and packed cell volume, lower resting fibrinopeptide A concentration and lower basal plasminogen activator activity than those on placebo. Response to venous occlusion was normal in all groups. The results suggest 300 mg and 1,200 mg aspirin have an equivalent platelet inhibitory effect but 1,200 mg aspirin causes greater gastro-intestinal blood loss.

Aged↗
PubMed1990

The effect of modified electroconvulsive therapy on vasopressin release and haemostasis in man.

Plasma concentrations of plasminogen activator activity (PAA) and factor VIII are partly controlled by circulating adrenaline and vasopressin. Acute rises in PAA and factor VIII occur during electroconvulsive therapy (ECT). To investigate the relationships between vasopressin (aVP), adrenaline and changes in PAA and factor VIII during ECT, 8 female and 2 male patients, median age 57 years (range 39-75) undergoing modified ECT had venous blood samples taken before and at 2 min, 15 min, 60 min and 24 h after cessation of seizure activity. AVP rose from 0.5 before ECT to 35.5 pg/ml at 2 min (P less than 0.005) and fell thereafter. PAA (10(6)/ECLT2) increased from 22 to 69 units (P less than 0.005) over the same time and fell to 13 units at 24 h (P less than 0.02). Tissue plasminogen activator activity (tPA) rose from 162 before to 1447 mIU/ml at 2 min. (P less than 0.005) and its inhibition activity fell from 8 to 3.75 IU/ml (P less than 0.005) over the same time and rose to 10.4 IU/ml after 24 h (P less than 0.02). There were no changes in adrenaline, noradrenaline, factor VIIIc, vWF or fibrinopeptides A and B beta 15-42. AVP correlated with tPA (rs = 0.64, P = 0.0022) and PAA (rs = 0.61, P = 0.004). These results support the hypothesis that aVP has a role in the regulation of fibrinolytic activity mediated by an increase in tPA. The absence of a factor VIII response may indicate that adrenaline is more important in the regulation of factor VIIIc and vWF.

Adult↗
PubMed1990

Microproteinuria in type 2 diabetes mellitus from diagnosis.

Glomerular and tubular microproteinuria precede the development of overt nephropathy in Type 1 diabetes mellitus. However, in Type 2 diabetes urinary protein excretion and its relationship to diabetic nephropathy has not been clearly characterized. Twenty consecutive, newly diagnosed patients with Type 2 diabetes, whose urine was Albustix-negative and sterile on culture, were studied. Two timed overnight urine samples were collected at diagnosis, and after 2 months and 2 years, and excretion rates of albumin, alpha-1-microglobulin and N-acetyl-beta-D-glucosaminidase were calculated. HbA1c fell from 12.1 +/- 2.4% at diagnosis to 9.5 +/- 1.5% at 2 months and 9.6 +/- 2.2% at 2 years. Albumin excretion rate fell marginally from 6.5 (2.1-242.5) micrograms min-1 at diagnosis to 5.5 (1.7-274.0) micrograms min-1 at 2 months (p less than 0.05) rising again to 6.1 (1.9-201.7) micrograms min-1 at 2 years. alpha-1-Microglobulin excretion rate fell from 13.5 (3.6-59.9) micrograms min-1 at diagnosis to 8.4 (2.9-16.1) micrograms min-1 at 2 months and 8.8 (1.8-54.1) micrograms min-1 at 2 years (both p less than 0.05). Albumin excretion rate was found to correlate significantly with creatinine clearance at diagnosis (rs = 0.61, p less than 0.005), though not subsequently. In contrast, excretion rates of alpha-1-microglobulin and N-acetyl-beta-D-glucosaminidase correlated with HbA1c (rs = 0.68 and 0.66, respectively, p less than 0.005 at diagnosis and rs = 0.57 and 0.53, p less than 0.05 subsequently in both cases).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylglucosaminidase↗
PubMed1990

Therapeutic defibrinogenation by ancrod: effect on limb blood flow in peripheral vascular disease.

Reduction of blood viscosity by venesection may improve peripheral blood flow but similar haemorheological changes have not been conclusively demonstrated following reduction of plasma viscosity by defibrinogenation. Ancrod is a defibrinogenating enzyme from the venom of the Malayan pit viper. We studied six male patients with severe intermittent claudication before, during and after treatment with ancrod for 48 h. Ancrod was given by initial infusion of 2 U/kg over 6 h and four subsequent bolus i.v. injections of 2 U/kg. Skin blood flow in feet and toes were measured repeatedly by laser Doppler velocimetry and calf blood flow by electronic plethysmography both before and after 2 min arterial occlusion. Plasma fibrinogen [median (range)] fell from 2.3(1.4-3.9) to 0.1(0.1-0.3) g/l and plasma viscosity from 1.81(1.61-1.90) to 1.49(1.45-1.72) cp. Dorsal foot and toe skin blood (resting or post-ischaemic) flows were not changed significantly by ancrod. Resting calf blood flow fell significantly after 49 h treatment with ancrod (P less than 0.04). Brachial and ankle blood pressures remained unchanged and haematocrit was not changed. Thus, treatment with ancrod for 48 h did not improve peripheral blood flow in patients with peripheral vascular disease. The fall observed in calf blood flow could be related to increased circulating fibrin/fibrinogen high-molecular-weight complexes and degradation products.

Adult↗
PubMed1990

Pelvic haemophilic pseudotumour occurring in a patient with mild haemophilia: a brief report.

Haemophilic pseudotumour is a rare but well-recognized complication of moderate and severe haemophilia, particularly in patients who have developed a factor VIII inhibitor. It has only been reported in haemophiliacs with factor VIII or IX levels less than 5%. We report a patient with mild haemophilia (factor VIII 11%, factor IX 78%) who developed a pelvic pseudotumour that was successfully treated with a novel surgical technique and who has no evidence of recurrence five years after operation.

Fistula↗
PubMed1989

Resistance to ischaemic conduction failure in chronic hypoxaemia and diabetes.

Median nerve function was studied in twelve diabetic subjects, six subjects with chronic hypoxaemia and ten control subjects. Resistance to ischaemic conduction failure (RICF), a characteristic electrophysiological feature of diabetic neuropathy, was assessed by measuring the decline in median nerve action potential amplitude at minute intervals for up to 20 minutes while the arm was rendered ischaemic. Initial nerve conduction velocity and action potential amplitude was similar in all three groups. Following the onset of ischaemia the time to a 50% reduction in action potential amplitude was prolonged in both diabetic subjects and hypoxaemic subjects compared with controls. After 20 minutes of ischaemia no control subject had persisting nerve function, while function remained in 5 (80%) of hypoxaemic subjects and 10 (83%) of diabetic subjects. The time to a 50% reduction in action potential amplitude during ischaemia correlated with the blood oxygen saturation among the hypoxic subjects and haemoglobin Alc among diabetic subjects. These results are consistent with the hypothesis that hypoxia has a role in the pathogenesis of resistance to ischaemic conduction failure in diabetes.

Adult↗
PubMed1988

Plasma vasopressin levels in induced migraine attacks.

Vasopressin (aVP) at low concentrations functions as an antidiuretic hormone and has vasoconstrictive effects. To investigate the possible role of aVP in the pathogenesis of migraine, six patients with a history of induced migraine were given 100 g chocolate, and blood samples for plasma aVP were taken before ingestion and every hour for 4 h. In one patient who presented with severe headache and nausea the base-line plasma aVP concentration was 15.2 pg/ml; it fell to 3.2 pg/ml at 2 h before rising to 10 pg/ml at 3 h and 4 h as the symptoms worsened. In the five patients with moderate or no headache plasma aVP concentrations remained in the normal range (less than 3 pg/ml) throughout. The results suggest that aVP does not have a role in the aetiology of migraine. The possibility exists that during severe attacks of nausea there is release of aVP, which may be responsible for the facial pallor, antidiuresis, and coagulation abnormalities occasionally observed in migraine.

Adult↗