The effect of surgery and severe injury on blood vessels

Golding, Elke M.; Bryan, Robert M.; Golding, R.M.

doi:10.1088/0967-3334/23/4/302

Cited by 4 publications

(3 citation statements)

References 6 publications

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“…Understanding the mechanical properties of arteries is important for modeling, interpretation of in vivo and in vitro physiological experiments, regulation of blood pressure, vasomotorics, pulse propagation, and other applications (Alastruey et al 2011, Balaguera et al 2010, García et al 2011, Golding and Golding 2001, Golding et al 2002, Leguy et al 2010, Watton et al 2009.…”

Section: Introductionmentioning

confidence: 99%

The contribution of vascular smooth muscle, elastin and collagen on the passive mechanics of porcine carotid arteries

et al. 2012

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The main components responsible for the mechanical behavior of the arterial wall are collagen, elastin, and smooth muscle cells (SMCs) in the medial layer. We determined the structural and mechanical changes in porcine carotid arteries after administration of Triton® X-100, elastase, and collagenase using the inflation-deflation test. The arteries were intraluminarly pressurized from 0 to 200 mmHg, and the outer diameter of the artery was measured. The pressure-strain elastic modulus was determined based on the pressure/diameter ratio. The intima-media thickness, wall thickness, thickness of the tunica adventitia layer, and the area fractions of SMCs, elastin, and collagen within the arterial wall (A(A)(SMC/elastin/collagen, wall)) were measured using stereological methods. The relative changes in the relevant components of the treated samples were as follows: the decrease in A(A)(SMC, wall) after administration of Triton® X-100 was 11% ± 7%, the decrease in A(A)(elastin, wall) after administration of elastase was 40% ± 22%, and the decrease in A(A)(collagen, wall) after the application of collagenase was 51% ± 22%. The Triton® X-100 treatment led to a decrease in the SMC content that was associated with enlargement of the arterial wall (outer diameter) for pressures up to 120 mmHg, and with mechanical stiffening of the arterial wall at higher pressures. Elastase led to a decrease in the elastin content that was associated with enlargement of the arterial wall, but not with stiffening or softening. Collagenase led to a decrease in collagen content that was associated with a change in the stiffness of the arterial wall, although the exact contribution of mechanical loading and the duration of treatment (enlargement) could not be quantified.

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Section: Introductionmentioning

confidence: 99%

The contribution of vascular smooth muscle, elastin and collagen on the passive mechanics of porcine carotid arteries

et al. 2012

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“…Ott et al (12) demonstrated that such regulation also occurs in response to a range of physiological conditions. Golding and Johnson (13) recently presented evidence for such regulation during exposure of plants to drought.…”

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confidence: 99%

Thiol Regulation of the Thylakoid Electron Transport ChainA Missing Link in the Regulation of Photosynthesis?

Johnson

2003

Biochemistry

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Avoidance of over-reduction of the chloroplast ferredoxin pool is of paramount importance for plants in avoiding oxidative stress. The redox state of this pool can be controlled through regulation of the thylakoid electron transport chain. A model is presented for regulation of this chain via a thiol reduction mechanism, possibly involving a thioredoxin. It is shown in isolated thylakoids that electron transport is inhibited by the thiol reducing agent dithiothreitol. The kinetics of this reduction are rapid and readily reversible. The midpoint redox potential is -365 mV at pH 7.7, with a pH dependency of about -90 mV/pH. At physiological pH values, this places the potential of the species titrated between that of ferredoxin and NADPH and thus in the right potential range to be regulating the redox poise of the ferredoxin pool. This is also close to the potential of NADPH-malate dehydrogenase, an enzyme known to be regulated by thioredoxin. Regulation of electron transport by thioredoxin provides a mechanistic link between the regulation of photosynthesis and gene expression by sugars and the redox regulation of gene expression mediated through the plastoquinone pool.

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“…This could importantly limit its efficacy in severely contused brain regions, where the vasculature might be unresponsive. The responsivity of isolated cerebral vessels in rat is directly related to injury severity (Golding et al, 2002). Fluid percussion injury has been shown to blunt both G-protein-mediated vasodilatation and agonistmediated elevations in cyclic nucleotides (Armstead, 1998(Armstead, , 2003, both of which could be relevant to the attenuation of 2-CA-mediated effects on CBF at the higher injury level.…”

Section: Limitationsmentioning

confidence: 99%

Characterization of the Effects of Adenosine Receptor Agonists on Cerebral Blood Flow in Uninjured and Traumatically Injured Rat Brain using Continuous Arterial Spin-Labeled Magnetic Resonance Imaging

Kochanek

Hendrich

Jackson

et al. 2005

J Cereb Blood Flow Metab

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Hypoperfusion after traumatic brain injury may exacerbate damage. Adenosine, a vasodilator, regulates cerebral blood flow (CBF). Treatment with adenosine receptor agonists has shown benefit in experimental CNS trauma; however, their effects on CBF after injury remain undefined. We used magnetic resonance imaging to assess CBF in uninjured rats both early and at 24 h after intrahippocampal administration of either the nonselective adenosine receptor agonist 2-chloroadenosine (2-CA, 12 nmol) or the A 2A -receptor agonist 2-p-(2-carboxyethyl)-phenethylamino-5 0 -N-ethylcarbox-amidoadenosine (CGS 21680, 6 nmol). We also assessed the effects of these agents on cerebral metabolic rate for glucose (CMRglu). We then assessed the effect of 2-CA on CBF at 3.5 to 5 h after controlled cortical impact (CCI). Injection of 2-CA into uninjured rat brain produced marked increases in CBF in ipsilateral hippocampus and cortex versus vehicle (Po0.05); CBF increases persisted even at 24 h. Measurement of hippocampal levels of 2-CA showed persistent increases to 24 h. CGS 21680 produced even more marked global increases in CBF than seen with 2-CA (2-6-fold versus vehicle, Po0.05 in 10/12 regions of interest (ROIs)). Neither agonist altered CMRglu versus vehicle. After CCI, 2-CA increased CBF in ipsilateral hippocampal and hemispheric ROIs (Po0.05 versus vehicle), but the response was attenuated at severe injury levels. We report marked increases in CBF after injection of adenosine receptor agonists into uninjured rat brain despite unaltered CMRglu. 2-Chloroadenosine produced enduring increases in CBF in uninjured brain and attenuated posttraumatic hypoperfusion. Future studies of adenosine-related therapies in CNS injury should address the role of CBF.

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The effect of surgery and severe injury on blood vessels

Cited by 4 publications

References 6 publications

The contribution of vascular smooth muscle, elastin and collagen on the passive mechanics of porcine carotid arteries

The contribution of vascular smooth muscle, elastin and collagen on the passive mechanics of porcine carotid arteries

Thiol Regulation of the Thylakoid Electron Transport ChainA Missing Link in the Regulation of Photosynthesis?

Characterization of the Effects of Adenosine Receptor Agonists on Cerebral Blood Flow in Uninjured and Traumatically Injured Rat Brain using Continuous Arterial Spin-Labeled Magnetic Resonance Imaging

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