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Biomedical subjects

R G Woolfson

Publications and source records attributed to R G Woolfson.

42 records · Page 3Linked to original sources
PubMed1991

Ouabain and responses to endothelium-dependent vasodilators in the human forearm.

Ouabain inhibits endothelium-dependent vascular relaxation in vitro, but has not been studied in this regard in vivo. We have therefore measured blood flow responses to carbachol, bradykinin and sodium nitroprusside (endothelium-dependent and endothelium-independent vasodilators) infused into the brachial artery with and without co-infusion of ouabain (2 micrograms min-1). Six healthy male volunteers were each studied on two occasions. Ouabain reduced basal forearm blood flow, by 18.0 +/- 4.1% (mean +/- s.e. mean, 2P less than 0.05), but had no significant effect on responses to any of the three vasodilators. These results indicate that effects of ouabain on endothelium-dependent relaxation in vitro must be interpreted with caution.

Adult↗
PubMed1990

Effect of NG-monomethyl-L-arginine on endothelium-dependent relaxation of human subcutaneous resistance arteries.

1. Using a myograph to measure isometric tension, we have looked at the action of NG-monomethyl-L-arginine on the endothelium-dependent relaxation of human subcutaneous resistance arteries. 2. NG-Monomethyl-L-arginine, the novel inhibitor of endothelium-derived relaxing factor synthesis, caused concentration-dependent but only partial inhibition of maximal relaxation induced by acetylcholine in human subcutaneous resistance arteries. 3. The inhibitory action of NG-monomethyl-L-arginine on acetylcholine-induced maximal relaxation was partially reversed by incubation of the arteries in equimolar concentrations of L-arginine and NG-monomethyl-L-arginine. Subsequent incubation in L-arginine led to further reversal, but this was no greater than with incubation in physiological saline. 4. A component of acetylcholine-induced relaxation was sensitive to indomethacin, suggesting that this response is mediated by prostanoids as well as by endothelium-derived relaxing factor. 5. NG-Monomethyl-L-arginine did not increase the tension of resting human subcutaneous resistance arteries. NG-Monomethyl-L-arginine did enhance the contractile response to noradrenaline, possibly due to inhibition of release of endothelium-derived relaxing factor resulting from stimulation of alpha 2-adrenoreceptors on the endothelial cells.

Acetylcholine↗
PubMed1990

Effects of ouabain and low sodium on contractility of human resistance arteries.

Earlier work with rat arteries has resulted in a widely held assumption that resistance artery smooth muscle will not contract on exposure to a reduced transplasmalemmal sodium gradient. In view of the well-recognized low sensitivity of rat tissue to cardiac glycosides, we have investigated the effects of altering the transplasmalemmal sodium gradient on vascular smooth muscle tone by using human resistance arteries. Incubation of arteries in low sodium or in ouabain to inhibit active sodium efflux for 1 hour increased the contractile response to caffeine stimulation; this finding indicated enhanced calcium buffering by the sarcoplasmic reticulum. Prolonged incubation in ouabain in the presence of phentolamine or diltiazem resulted in a concentration-dependent increase in the tone of resting human resistance arteries. Reduction of the transplasmalemmal sodium gradient by incubation in low sodium buffer effected an increase in tone similar to that obtained in the presence of ouabain. These results suggest that alteration of the transplasmalemmal sodium gradient may increase the vascular smooth muscle tone of human resistance arteries by altering intracellular calcium handling. This is a new finding in human resistance arteries and may involve inhibition and, indeed, reversal of sodium-dependent calcium efflux. A concentration-dependent potentiation of tone was found after the addition of ouabain to submaximally activated arteries. Sodium-calcium exchange may also play a pivotal role in this mechanism.

Arteries↗
PubMedDate not supplied

Low dose dopamine infusion reduces renal tubular injury following cardiopulmonary bypass surgery.

BACKGROUND: The use of dopamine to protect the kidneys against hypoperfusion injury remains controversial with little clinical evidence of benefit and increasing concerns regarding safety. In this double-blind, prospective, randomised study, we investigated the effect of dopamine infusion (2.5 microg/kg/min) on glomerular filtration rate (GFR) and tubular injury in patients undergoing routine cardiopulmonary bypass (CPB). METHODS: Forty eight patients were randomly assigned to receive intravenous dopamine or saline from induction of anaesthesia until 48 hours post-operatively. There were no differences in mean age, bypass time or pre-op creatinine in the 36 patients (33 men) who completed the study. 51Cr-EDTA GFR (ml/min/1.73 m2) was measured pre-operatively and on day 5 only. Urinary markers of tubular injury (albumin, N-acetyl glucosaminidase, NAG; retinol binding protein, RBP) were measured pre-operatively, and on days 1, 2 and 5. RESULTS: GFR was preserved equally in both groups. All patients demonstrated significant tubular injury but urinary levels of NAG and RBP were lower in the dopamine group (41%, p=0.057 and 41%, p=0.007, respectively) on the first post-operative day. CONCLUSION: We conclude that low dose dopamine infusion may reduce renal tubular injury following CPB in patients with normal or near normal baseline renal function.

Acute Kidney Injury↗
PubMedDate not supplied

Evaluation of therapy for cast nephropathy: failure of colchicine to alter urinary Tamm Horsfall glycoprotein excretion in normal subjects.

Tamm Horsfall glycoprotein (THG) is a major constituent of renal tubular casts including the light chain casts of myeloma. Animal studies suggest that the anti-inflammatory agent colchicine reduces urinary THG excretion and prevents light chain cast formation. Six normal male subjects were given therapeutic doses of colchicine (0.5 mg twice daily for 6 days) and excretion of THG, albumin, creatinine and N-acetyl glucosaminidase (NAG) was determined. Colchicine therapy had no effect on the urinary excretion of THG, albumin or NAG or on renal function as assessed by creatinine clearance. This suggests that colchicine will not be a useful therapeutic adjunct to the treatment of light-chain nephropathy.

Acetylglucosaminidase↗