M. Ward

Publications61
h-index18
Citations1,046
Highly Influential Citations35
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Optimization of Respiratory Muscle Relaxation during Mechanical Ventilation
TLDR
It is concluded that inspiratory muscle activity can be substantial during MV, particularly during AMV at low trigger sensitivity and flow, and in the assist mode (AMV), where Wp approached 65% of the total inspiratory work.
Hypoxia induces a functionally significant and translationally efficient neuronal NO synthase mRNA variant.
TLDR
A novel human nN OS promoter is revealed that confers the ability to rapidly upregulate nNOS expression in response to hypoxia with a functionally significant effect on vascular smooth muscle contraction.
Impaired reactivity of rat aorta to phenylephrine and KCl after prolonged hypoxia: role of the endothelium.
  • G. Auer, M. Ward
  • Biology, Medicine
    Journal of applied physiology
  • 1 August 1998
TLDR
In aortic rings from control rats, endothelial removal enhanced contraction, whereas, in rings from rats exposed to hypoxia, removal of the endothelium was associated with a decrease in maximum tension, which did not alter the EC50 for either agent.
Regulation of Proliferation and Membrane Potential by Chloride Currents in Rat Pulmonary Artery Smooth Muscle Cells
TLDR
Findings are consistent with the conclusion that ICls regulate proliferation of PASMCs and suggest that selective ICl inhibition may be useful in treating pulmonary hypertension.
Enhanced Translation of Heme Oxygenase-2 Preserves Human Endothelial Cell Viability during Hypoxia*
TLDR
Inhibition of HO-2 expression by small interference RNA increased oxidative stress, exacerbated mitochondrial membrane depolarization, and enhanced caspase activation and apoptotic cell death in cells incubated under hypoxic but not normoxic conditions, indicating that HO- 2 is important in maintaining endothelial viability and may preserve local regulation of vascular tone, thrombosis, and inflammatory responses during reductions in systemic oxygen delivery.
Dilation of rat diaphragmatic arterioles by flow and hypoxia: roles of nitric oxide and prostaglandins.
  • M. Ward
  • Biology
    Journal of applied physiology
  • 1 May 1999
TLDR
In rat diaphragmatic arterioles, the response to ACh is dependent on endothelial nitric oxide release, whereas theresponse to hypoxia is mediated by endothelium-derived prostaglandins, and flow-dilation requires that both Nitric oxide and cyclooxygenase pathways be intact.
Regulation of cerebellar nitric oxide production in response to prolonged in vivo hypoxia
TLDR
It is proposed that cofactor availability for NO production may also increase during hypoxia because of upregulation of GTP cyclohydrolase I expression, which is essential for the recycling of L‐citrulline to L‐arginine.
Downregulation of endothelial nitric oxide synthase in rat aorta after prolonged hypoxia in vivo.
TLDR
Ipaired endothelial NO release may handicap the vascular responses that defend vital organ function during hypoxia, and this study results suggest that endothelial nitric oxide synthase expression in the systemic circulation is affected.
Regulation of baseline vascular resistance in the canine diaphragm by nitric oxide
TLDR
Basal NO release plays a role in the regulation of baseline diaphragmatic vascular resistance and l‐Arginine analogues tested potently and specifically inhibited this process.
Interaction between endothelial heme oxygenase-2 and endothelin-1 in altered aortic reactivity after hypoxia in rats.
TLDR
In rings from normoxic rats, the HO inhibitor tin protoporphyrin IX (SnPP IX, 10 microM) did not alter the response to phenylephrine or ET-1 and maximum tension generated in response to these agonists was higher in endothelium-intact but not -denuded rings in the presence of SnPP IX.
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