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Biomedical subjects

C McGurk

Publications and source records attributed to C McGurk.

At least 19 recordsLinked to original sources
PubMed2001

Bradykinin infusion in chronic cardiac failure and the effects of captopril.

BACKGROUND: Patients with chronic cardiac failure (CCF) have abnormal vascular responses. Bradykinin (BK) is thought to contribute to the vasodilator effects of ACE inhibitors, but the effect of BK itself in patients with CCF has not been examined. METHODS: We studied the responses to infused BK at 10, 30 and 100 pmol min(-1) in patients with CCF (n=10) and controls (n=10). The slope of the dose-response curve was used for comparisons between the groups. Forearm blood flow (FBF) was measured by venous occlusion plethysmography. RESULTS: Following BK, vasodilatation was observed in both groups as the slopes were positive in all, but the difference between the groups was not significant (P=0.77). The study was repeated with the co-administration of 4 micromol min(-1) of N(G)-monomethyl L-arginine (L-NMMA). The vasodilator response to BK was reduced in both groups, and the effect was somewhat greater in the patient group (P=0.23). The vasodilator response to the endothelium-independent vasodilator sodium nitroprusside was slightly less in the patient group (P=0.08). The patients only then underwent repeat infusion of BK before and after a single oral dose of captopril 12.5 mg or placebo. Following captopril, the vasodilator response to BK was unchanged when compared to placebo (difference between slopes, P=0.53). CONCLUSIONS: BK produces dose-dependent vasodilatation in both patients with CCF and controls; there was no difference in the responses, which were antagonised by L-NMMA and therefore in part NO (endothelium)-dependent. The responses were also unchanged after administration of an ACE inhibitor (captopril).

Aged↗
PubMed2000

Vasoconstriction to endothelin-1 is blunted in non-insulin-dependent diabetes: a dose-response study.

The haemodynamic hypothesis for the pathogenesis of diabetic microangiopathy argues that an initial increase in microvascular blood flow leads to microvascular sclerosis and disturbed autoregulation. Endothelin-1 (ET-1) is an endothelium-derived vasoconstrictor peptide that contributes to basal vascular tone. Impairment of the vasoconstrictor response to ET-1 could result in hyperperfusion and subsequent microvascular damage. The purpose of this study was to determine whether vascular responses to ET-1 are impaired in patients with non-insulin-dependent diabetes mellitus (type 2 diabetes). Ten patients with type 2 diabetes and nine control subjects underwent brachial artery cannulation. Forearm blood flow was measured using strain-gauge venous occlusion plethysmography. ET-1 in three doses of 5, 10, and 20 pmol/min and 0.9% saline placebo was infused in a balanced double-blind randomised manner. Vascular smooth muscle function also was assessed using sodium nitroprusside. Control subjects showed vasoconstriction to ET-1 of 5 (p < 0.05), 10 (p < 0.05), and 20 pmol/min (p < 0.01). In the diabetic group, there was no significant response to ET-1 at 5 pmol/min (p > 0.05); however, significant vasoconstriction developed at 10 and 20 pmol/min (p < 0.01). There was a significant difference in response to ET-1 at 5 pmol/min between the diabetic and control groups (p < 0.05). Responses to sodium nitroprusside were similar in both groups (p > 0.05). Patients with type 2 diabetes have a blunted vasoconstrictor response to ET-1 despite preserved vascular smooth muscle function.

Adult↗
PubMed2000

Vasoconstriction to endogenous endothelin-1 is impaired in patients with type II diabetes mellitus.

Endothelin-1 has potent vasoconstrictor and vasopressor actions contributing to basal vascular tone and maintenance of blood pressure acting predominantly through endothelin-A receptors. Endothelin antagonists may be of value in the treatment of hypertension and heart failure. However, the role of endothelin-1 in the regulation of vascular tone and the potential benefits of endothelin antagonists in non-insulin-dependent diabetes mellitus (Type II diabetes) are less clear. Vasoconstriction to exogenous endothelin-1 is impaired in Type II diabetes. The purpose of this study was to determine whether vasoconstriction to endogenous endothelin-1 acting through the endothelin-A receptor is impaired in Type II diabetes. In ten patients with Type II diabetes and nine controls the endothelin-A receptor antagonist BQ123 was infused intra-arterially at 100 nmol/min for 60 min followed by normal saline for 30 min. Forearm blood flow was measured using venous occlusion plethysmography. Control subjects showed gradual onset of vasodilation in response to BQ123 (P < 0.001). Diabetic subjects, however, showed no significant response (P > 0.05). There was a significant difference between the diabetic and control groups (P < 0.05). Blockade of the endothelin-A receptor is associated with impaired vasodilation in Type II diabetes indicating vasoconstriction to endogenous endothelin-1 mediated by the endothelin-A receptor is impaired.

Adult↗
PubMed1999

Forearm reactive hyperaemia is not mediated by nitric oxide in healthy volunteers.

AIMS: To determine the role of nitric oxide (NO) in forearm reactive hyperaemia in healthy human subjects. METHODS: Ten healthy subjects aged 19-34 years underwent brachial artery cannulation. Forearm circulatory arrest was achieved by means of an upper arm cuff inflated to 200 mmHg for 5 min. The blood flow responses during reactive hyperaemia were measured using venous occlusion plethysmography following a 10 min intra-arterial infusion of 8 micromol min-1 N-monomethyl L-arginine (L-NMMA) and following matching placebo administered in random order. Results were analysed by repeated measures anova and t-tests. RESULTS: L-NMMA resulted in a significant reduction of basal forearm blood flow indicating inhibition of basal NO release (P=0.005). There was no significant difference between the blood flow responses during reactive hyperaemia following L-NMMA and placebo (P=0.97). CONCLUSIONS: Nitric oxide production does not make a significant contribution to the vasodilatation associated with reactive hyperaemia in the human forearm.

Adult↗
PubMed1999

Integrating information literacies into an undergraduate nursing programme.

The development of support for a more research-based approach to care has created the imperative for nursing education to tackle the issue of information literacy. Information literacy means the ability to locate, evaluate and apply information in critical thinking and problem solving. This paper outlines and provides a rationale for a curriculum-integrated information literacy programme, implemented in the pre-registration Bachelor of Nursing course at the University of Wollongong, NSW, Australia. It also describes a multidimensional evaluation process for determining nursing students' growth in cognitive and affective domains. Results of the programme evaluation will be featured in a future paper.

Computer Literacy↗
PubMed1999

Effect of methionine supplementation on endothelial function, plasma homocysteine, and lipid peroxidation.

BACKGROUND: Acetaminophen (paracetamol) poisoning is a major source of morbidity and mortality. It has been proposed that methionine be incorporated into acetaminophen tablets routinely as a protective mechanism. Methionine has been shown to be effective in the treatment of acetaminophen toxicity and a combination preparation of acetaminophen and methionine may prevent toxicity. However, there has been some concern that chronic methionine supplementation may be associated with vascular disease. The aim of the study was to investigate if methionine supplementation causes changes in endothelial function, plasma homocysteine, or lipid peroxidation which may be associated with atherosclerosis. METHODS: Sixteen healthy volunteers were studied. Forearm blood flow in response to local intra-arterial infusion of acetylcholine to assess endothelium-dependent vasodilatation and sodium nitroprusside to assess endothelium-independent vasodilatation was measured by venous occlusion plethysmography. Plasma homocysteine and lipid peroxidation, measured as thiobarbituric acid reactive substances, were measured using high-performance liquid chromatography. Forearm vascular responses, plasma homocysteine concentrations, and thiobarbituric acid reactive substances were measured at baseline and following methionine supplementation. RESULTS: There was no significant difference in endothelial-dependent vascular responses after acute (methionine 250 mg orally, p > 0.05), 1 month of low-dose (methionine 250 mg daily, p > 0.05), or 1 week of high-dose (methionine 100 mg/kg daily, p > 0.05) methionine administration. There was no significant difference in plasma homocysteine concentrations after acute (p > 0.05) or 1 month of low-dose (p > 0.05) methionine administration. However, 1 week of high-dose methionine (100 mg/kg) administration daily significantly increased homocysteine concentrations (p < 0.0015). Thiobarbituric acid reactive substances were unchanged during the period of study (p > 0.05). CONCLUSIONS: Methionine supplementation does not impair endothelial-dependent vascular responses in healthy volunteers. Although high-dose methionine administration causes elevation of plasma homocysteine concentrations, doses similar to those used in combination preparations with acetaminophen do not affect plasma homocysteine concentrations.

Acetylcholine↗
PubMed1998

Abnormal vascular responses in human chronic cardiac failure are both endothelium dependent and endothelium independent.

OBJECTIVE: To study underlying vascular responses in chronic heart failure in patients without ACE inhibitor treatment, and to compare them with age matched controls. DESIGN: Forearm blood flow was studied using venous occlusion plethysmography in patients with chronic heart failure (n = 12) and matched controls (n = 13), after infusion of L-NMMA (a nitric oxide synthase inhibitor), glyceryl trinitrate (an endothelium independent vasodilator), and serotonin (an endothelium dependent vasodilator). RESULTS: L-NMMA produced significant vasoconstriction in normal subjects (forearm blood flow reduced by 24%), but not in patients (6%; difference between groups p < 0.03). The vasodilator responses to glyceryl trinitrate were impaired in patients (p < 0.02). In normal controls, serotonin produced initial dilatation, followed by vasoconstriction at high doses. In patients, no vasodilator responses were observed, only late vasoconstriction (p < 0.03). CONCLUSIONS: The vascular responses of patients are confirmed as being abnormal. The lack of response to L-NMMA suggests that nitric oxide does not contribute to basal vascular tone in patients with chronic heart failure. The responses to glyceryl trinitrate and to serotonin suggest that there is both smooth muscle and endothelial dysfunction in patients with chronic heart failure.

Aged↗
PubMed1997

Forearm endothelium-dependent vascular responses and the potassium-ATP channel.

AIMS: Vasodilation to acetylcholine is mediated at least in part by endothelium-derived hyperpolarising factor (EDHF) which causes membrane hyperpolarisation by activating potassium channels. It is however uncertain which potassium channel mediates this effect. The aim of this study was to determine the role of the potassium-ATP (K(+)-ATP) channel in mediating endothelium-dependent vascular responses to acetylcholine. METHODS: In 10 healthy volunteers acetylcholine, an endothelium-dependent vasodilator, and sodium nitroprusside as a control assessing endothelium-independent vasodilatation were infused into the non-dominant brachial artery. Forearm blood flow (FBF) in response to each dose was measured by strain-gauge venous occlusion plethysmography. The K(+)-ATP channel blocker glipizide (2.5 mg) was then administered orally. After 45 min the infusions with FBF measurements were repeated. RESULTS: Acetylcholine (P < 0.01) and sodium nitroprusside (P < 0.01) both caused an increase in FBF. There was no significant difference in vascular responses to acetylcholine (P > 0.05) or sodium nitroprusside (P > 0.05) following K(+)-ATP channel blockade. CONCLUSIONS: The K(+)-ATP channel does not modulate forearm arteriolar endothelium-dependent responses in healthy volunteers and therefore does not play a role in membrane hyperpolarisation.

Acetylcholine↗
PubMed1997

Sources of inaccuracy in the use of the Hawksley random-zero sphygmomanometer.

OBJECTIVE: To identify possible causes of inaccuracy in the use of the Hawksley random-zero sphygmomanometer and methods that could reduce this. METHODS: Four Hawksley random-zero sphygmomanometers were compared with a standard sphygmomanometer under static conditions. Two methods (standard and rapid) were used to release pressure from the inflated cuff with pressures recorded by independent blinded observers. The rate at which the hand valve released pressure was analysed. The effects of varying filling times and pressures on the size of the final zero correction were investigated. RESULTS: The Hawksley devices all under-recorded pressure compared with that measured by using a standard machine. A rapid means of pressure release approximately halved this error in each case. Pressure release through the hand valve was shown to have a characteristic and prolonged exponential decay. Using low filling times and pressures reduced the observed range of zeros seen, with the production of a correlation between the size of the zero and the inflation pressure used. CONCLUSION: These findings suggest that overestimation of the final zero correction is a common and major source of error in the use of the Hawksley sphygmomanometer. A simple change in the design of the final pressure release would improve the machine's reliability in clinical usage. The machine's zero mechanism is susceptible to unintentional misuse. Such misuse could occur when the machine is used in accordance with current sphygmomanometry guidelines.

Equipment Design↗
PubMed1996

Forearm vascular responses to serotonin are not mediated by products of cyclooxygenase.

The involvement of cyclooxygenase-derived substances in the forearm arteriolar responses to serotonin was determined in 10 healthy male volunteers. Serotonin was infused in five incremental doses (0.003-30 micrograms min-1) for 2 min each into the brachial artery of the non-dominant forearm. Forearm blood flow (FBF) responses to each dose were measured by strain-gauge venous occlusion plethysmography. The cyclooxygenase inhibitor indomethacin (100 mg) was administered orally following the serotonin infusions. After 90 min the serotonin infusions were repeated and FBF responses measured. Serotonin caused a biphasic response with vasodilatation occurring at low doses (0.003-3 micrograms min-1, P < 0.01) and vasoconstriction occurring at the highest dose (P < 0.01). There was no significant difference in vascular response to serotonin following cyclooxygenase inhibition. In conclusion, cyclooxygenase products are not involved in the forearm vascular responses to serotonin in healthy human subjects.

Adult↗