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Biomedical subjects

R G Woolfson

Publications and source records attributed to R G Woolfson.

At least 37 records · Page 2Linked to original sources
PubMed1994

Functional characteristics of small placental arteries.

OBJECTIVES: The aim of this study was to investigate characteristics of placental arteries capable of influencing vasomotor tone in the fetoplacental vascular bed. Contractile characteristics and endothelium-dependent and endothelium-independent relaxation were examined. STUDY DESIGN: By means of a small vessel myograph arteries of mean normalized internal diameter 353.22 +/- 13.14 microns were studied under isometric conditions. Contractile function was assessed with a variety of agonists, including angiotensin II, endothelin-1, the thromboxane mimetic U46619, prostaglandin E2, and prostaglandin F2 alpha. The effect of physiologic and supraphysiologic PO2 on vascular function was also examined. Relaxation was assessed in response to known endothelium-dependent vasodilators, including acetylcholine, bradykinin, histamine, and A23187 and to sodium nitroprusside (endothelium independent). The effect of indomethacin and the nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester on contractile function was also evaluated. RESULTS: Sensitivity to sodium nitroprusside was reduced by a high PO2. U46619 was the most potent constrictor agonist studied. The response of precontracted arteries to known endothelium-dependent vasodilators was minimal, other than for histamine, which led to modest relaxation. The constrictor response to U46619 was increased in the presence of NG-nitro-L-arginine methyl ester. CONCLUSIONS: Oxygen tension may be an important determinant of relaxation in small placental arteries. Receptor-mediated release of endothelium-derived relaxing factor is not a major mechanism in the fetoplacental circulation.

Arteries↗
PubMed1994

Acute hypernatraemia during bicarbonate-buffered haemodialysis.

Five patients on maintenance haemodialysis were exposed to varying degrees of hypernatric dialysate, leading to acute hypernatraemia (plasma sodium concentrations 158 mmol/l to 179 mmol/l). With the exception of one patient, who developed pulmonary oedema, symptoms were minimal and in each case hypernatraemia was corrected without residual complications. The hypernatric dialysate resulted from a granular and less soluble batch of sodium bicarbonate powder. The extra effort required to dissolve the powder caused CO2 to be shaken out of solution, producing sodium carbonate and raising the pH. Mixing calcium from the 'acid' concentrate with excess carbonate in the 'bicarbonate' concentrate led to rapid precipitation of calcium carbonate on the conductivity monitoring cells. Dialysate conductivity was incorrectly sensed as low by the coated conductivity cells, so that an increasing amount of 'acid' concentrate, with its accompanying electrolytes, was delivered to the patient. When the granular powder was ground to a fine powder, passed through a 125 microns sieve and gently dissolved, the machine operated normally. We recommend that sodium bicarbonate powder is supplied with a sieve size no greater than 125 microns, kept dry to prevent the formation of large crystals, and dissolved gently.

Acute Disease↗
PubMed1994

Scintigraphic evidence of abnormal ureteric peristalsis following urological surgery.

OBJECTIVE: To investigate the effect of urological surgery on ureteric peristaltic activity. SUBJECTS AND METHODS: Ureteric peristalsis was assessed in a sample urological population (n = 29 patients) and the findings compared with a control population (n = 14 patients). RESULTS: The incidence of disordered peristalsis was significantly increased (P < 0.05) following urological surgery and, in particular, the incidence of retrograde peristalsis was very significantly increased (P < 0.01) following ureteric division and re-anastomosis. CONCLUSION: The results of this study are consistent with a central role for myogenic activity in the conduction of ureteric peristalsis in man.

Humans↗
PubMed1993

Inhibition of nitric oxide limits infarct size in the in situ rabbit heart.

Recent data has suggested a dual role for nitric oxide (NO) so that it can both attenuate myocardial injury during ischaemia and reperfusion as well as mediate reperfusion injury. In this study in the in situ rabbit heart, we have shown that pretreatment with intravenous NG-nitro-L-arginine methyl ester (L-NAME, an inhibitor of NO synthesis) significantly reduced infarct size following sustained coronary artery occlusion and reperfusion. L-NAME was also noted to increase myocardial lactate concentration. This study provides further evidence that protection against ischaemia-reperfusion injury can be derived from manipulation of the microcirculation.

Analysis of Variance↗
PubMed1993

Abnormal endothelial cell function of resistance arteries from women with preeclampsia.

OBJECTIVE: There is substantial indirect evidence that the vascular endothelium may be dysfunctional in preeclampsia and that reduced production of endothelial-derived vasodilators may account for the increased vascular resistance and enhanced pressor sensitivity characteristic of this disorder. In this study we directly investigated endothelial function by examining acetylcholine-mediated relaxation in small arteries dissected from the subcutaneous fat layer examined at the time of cesarean section. STUDY DESIGN: By means of a small vessel myograph we measured tension in resistance arteries of normal pregnant women (n = 12) and women with preeclampsia (n = 12) and assessed the contributions of vasodilatory prostanoids and endothelium-derived relaxing factor to endothelium-dependent relaxation, as elicited by acetylcholine, 1 nmol/L to 10 mumol/L, after precontraction with 3 mumol/L norepinephrine. RESULTS: Endothelium-dependent relaxation was impaired in arteries of women with preeclampsia compared with arteries from normotensive pregnant women. Endothelium-independent relaxation as assessed by sodium nitroprusside was not altered in the arteries from preeclamptic women. CONCLUSIONS: This study provides direct evidence of abnormal endothelial function in preeclampsia. No deficiency in endothelium-independent relaxation could be detected.

Acetylcholine↗
PubMed1993

Effects of sodium-transport inhibition in human resistance arteries.

It is hypothesized that endogenous inhibitors of active sodium transport may lead to an increase in peripheral vascular resistance. From studies in animal conduit arteries there is substantial evidence that cardiac glycosides may increase tension. A number of studies from our laboratory demonstrate that inhibition of active sodium transport may also increase tension in human resistance arteries, and that reduced Ca efflux via Na/Ca exchange could be a contributory mechanism. Further experiments also have suggested that endogenous inhibitors of sodium transport could lead to an increase in peripheral vascular resistance by reducing endothelium-dependent relaxation.

Arginine↗
PubMed1993

Ureteric peristalsis studies in loin pain and haematuria syndrome: another diagnostic disappointment.

Although not a cause of progressive renal damage, loin pain and haematuria syndrome is nevertheless associated with significant morbidity. The management of pain often presents a formidable problem to urologists, physicians and general practitioners. An earlier study noted hold-up of urine in the renal pelvis and implicated this in the pathogenesis of pain. In this study we have failed to demonstrate an excess incidence of disordered urinary peristalsis in loin pain and haematuria syndrome.

Back Pain↗
PubMed1993

Renal scintigraphy in acute scleroderma: report of three cases.

Scintigraphic findings in acute renal failure secondary to scleroderma are reported. In three patients, we have demonstrated severe reduction of renal perfusion with little or no parenchymal uptake of tracer and absent excretion. These findings are compatible with the known histological process of occlusive vasculopathy, and such scintigraphic findings at presentation may reflect a poor prognosis for renal recovery.

Acute Kidney Injury↗
PubMed1992

Effect of bufalin and pregnanes on vasoreactivity of human resistance arteries.

Endogenous Na/K ATPase inhibitory activity has been implicated in salt and water homeostasis in mammals and amphibians. Recent interest has focused on endogenous cardiac glycosides, some progesterone derivatives (pregnanes) and the amphibian bufodienolides. This study has examined the effects of non-planar and planar pregnanes and the bufodienolide bufalin on vasoreactivity of human resistance arteries. Bufalin and a non-planar pregnane caused concentration-dependent potentiation of the tone of submaximally pre-contracted arteries and inhibited endothelium-dependent relaxation, whereas a planar pregnane affected neither response. The relative potency of the compounds studied suggest the results do not simply reflect degrees of Na/K ATPase inhibition. The active compounds may be important in the regulation of vascular tone.

Acetylcholine↗
PubMed1991

Low-concentration ouabain does not inhibit noradrenaline-induced contraction of human resistance arteries.

1. Using a Mulvany-Halpern myograph to measure changes in isometric tension, we have investigated the effect of ouabain on noradrenaline-induced contraction of human subcutaneous resistance arteries. 2. Low concentrations of ouabain (10 nmol/l or less) were shown not to alter vascular smooth muscle contractility or sensitivity to noradrenaline. 3. In contrast, higher concentrations of ouabain (100 nmol/l or more) were found to depress vascular smooth muscle contractility and to reduce the sensitivity of the noradrenaline concentration-response relationship. 4. These findings may have implications regarding the presence of an endogenous inhibitor of the sodium pump in essential hypertension and in pregnancy-associated hypertension.

Arteries↗
PubMed1991

Effect of ouabain on endothelium-dependent relaxation of human resistance arteries.

Inhibition of active sodium transport by ouabain was found to cause concentration- and time-dependent impairment of acetylcholine-induced relaxation in human resistance arteries with a significant effect at 100 pM. The reduced acetylcholine response was attributable to inhibition of the NG-monomethyl L-arginine-sensitive but not the indomethacin-sensitive component of relaxation. Relaxation by sodium nitroprusside was not affected by ouabain, suggesting that inhibition of sodium transport, directly or indirectly, must affect synthesis or release of endothelium-derived relaxing factor rather than its effector pathway. These results do not support the existence of an additional endothelium-derived relaxing factor other than endothelium-derived relaxing factor, which is dependent on sodium pump activity. The finding that inhibition of sodium transport has a profound effect on vascular relaxation may have implications in the pathogenesis of certain forms of hypertension.

Acetylcholine↗