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Biomedical subjects

John R Cockcroft

Publications and source records attributed to John R Cockcroft.

42 records · Page 3Linked to original sources
PubMed2002

Inhibition of basal nitric oxide synthesis increases aortic augmentation index and pulse wave velocity in vivo.

AIMS: To investigate the role of basal nitric oxide (NO) production in regulating large artery stiffness in vivo. METHODS: Incremental doses of the NO synthase inhibitor L-N(G)-monomethyl arginine (LNMMA: 0.1, 0.3, 1.0 and 3.0 mg kg-1 min-1) or placebo were infused in eight healthy men. Arterial stiffness was assessed noninvasively by pulse wave analysis. RESULTS: Compared with placebo, infusion of LNMMA led to a dose-dependent increase in mean arterial pressure, peripheral vascular resistance, and aortic and systemic arterial stiffness. There was an accompanying reduction in heart rate and cardiac index. The highest dose of LNMMA resulted in an increase of 25% in AIx (95% confidence limits; 12, 38) and of 16 mmHg in mean arterial pressure (9, 23) compared with infusion of saline. CONCLUSIONS: These data indicate functional regulation of large artery stiffness in vivo by NO, and may provide new therapeutic strategies for cardiovascular risk reduction.

Adult↗
PubMed2002

Pulse-wave analysis: clinical evaluation of a noninvasive, widely applicable method for assessing endothelial function.

Current methods for assessing vasomotor endothelial function are impractical for use in large studies. We tested the hypothesis that pulse-wave analysis (PWA) combined with provocative pharmacological testing might provide an alternative method. Radial artery waveforms were recorded and augmentation index (AIx) was calculated from derived aortic waveforms. Thirteen subjects received sublingual nitroglycerin (NTG), inhaled albuterol, or placebo. Twelve subjects received NTG, albuterol, and placebo separately during an infusion of N(G)-monomethyl-L-arginine (LNMMA) or norepinephrine. Twenty-seven hypercholesterolemic subjects and 27 controls received NTG followed by albuterol. Endothelial function was assessed by PWA and forearm blood flow in 27 subjects. Albuterol and NTG both significantly and repeatably reduced AIx (P<0.001). Only the response to albuterol was inhibited by LNMMA (-9.8+/-5.5% vs -4.7+/-2.7%; P=0.02). Baseline AIx was higher in the hypercholesterolemic subjects, who exhibited a reduced response to albuterol (P=0.02) but not to NTG when compared with matched controls. The responses to albuterol and acetylcholine were correlated (r=0.5, P=0.02). Consistent with an endothelium-dependent effect, the response to albuterol was substantially inhibited by LNMMA. Importantly, the response to albuterol was reduced in subjects with hypercholesterolemia and was correlated to that of intra-arterial acetylcholine. This methodology provides a simple, repeatable, noninvasive means of assessing endothelial function in vivo.

Acetylcholine↗