Biomedical subjects

A P Gibson

Publications and source records attributed to A P Gibson.

11 recordsLinked to original sources

PubMed2006

Three dimensional optical imaging of blood volume and oxygenation in the neonatal brain.

Optical methods provide a means of monitoring cerebral oxygenation in newborn infants at risk of brain injury. A 32-channel optical imaging system has been developed with the aim of reconstructing three-dimensional images of regional blood volume and oxygenation. Full image data sets were acquired from 14 out of 24 infants studied; successful images have been reconstructed in 8 of these infants. Regional variations in cerebral blood volume and tissue oxygen saturation are present in healthy preterm infants. In an infant with a large unilateral intraventricular haemorrhage, a corresponding region of low oxygen saturation was detected. These results suggest that optical tomography may provide an appropriate technique for investigating regional cerebral haemodynamics and oxygenation at the cotside.

Blood Volume↗

PubMed2005

Three-dimensional whole-head optical tomography of passive motor evoked responses in the neonate.

Optical tomography has been used to reconstruct three-dimensional images of the entire neonatal head during motor evoked responses. Data were successfully acquired during passive movement of each arm on four out of six infants examined, from which eight sets of bilateral images of hemodynamic parameters were reconstructed. Six out of the eight images showed the largest change in total hemoglobin in the region of the contralateral motor cortex. The mean distance between the peak response in the image and the estimated position of the contralateral motor cortex was 10.8 mm. These results suggest that optical tomography may provide an appropriate technique for non-invasive cot-side imaging of brain function.

Algorithms↗

PubMed2005

Recent advances in diffuse optical imaging.

We review the current state-of-the-art of diffuse optical imaging, which is an emerging technique for functional imaging of biological tissue. It involves generating images using measurements of visible or near-infrared light scattered across large (greater than several centimetres) thicknesses of tissue. We discuss recent advances in experimental methods and instrumentation, and examine new theoretical techniques applied to modelling and image reconstruction. We review recent work on in vivo applications including imaging the breast and brain, and examine future challenges.

Diffusion↗

PubMed2003

A method for generating patient-specific finite element meshes for head modelling.

Finite element modelling of fields within the body, whether electrical or optical, requires knowledge of the geometry of the object being examined. It can be clinically impractical to obtain accurate surface information for individual patients, although a limited set of measurements such as the locations of sensors attached to the body, can be acquired more readily. In this paper, we describe how a generic surface taken from an adult head is warped to fit points measured on a neonatal head surface to provide a new, individual surface from which a finite element mesh was generated. Simulations show that data generated from this mesh and from the original neonatal head surface are similar to within experimental errors. However, data generated from a mesh of the best fit sphere were significantly different from data generated from the original neonatal head surface.

Adult↗

PubMed2001

Endothelial dysfunction induced by oxidized low-density lipoproteins in isolated mouse aorta: a comparison with apolipoprotein-E deficient mice.

We characterized the acute effects of oxidized low-density lipoproteins (oxidized-LDL) on vascular reactivity in isolated aorta from wild-type C57BL/6J mice, and compared these with the chronic alterations in vascular function observed in apolipoprotein-E gene knockout [ApoE(-/-)] mice fed a high-fat diet, which results in hyperlipidemia and atherosclerosis. In the abdominal (but not thoracic) aorta, oxidized-LDL (100 microg/ml) reduced relaxations induced by acetylcholine (10(-9) M-10(-5) M), which are mediated entirely by nitric oxide (NO). The relaxations induced by the NO donor S-nitroso-N-acetylpenicillamine (SNAP, 10(-8) M-10(-4) M), the cyclic GMP analogue 8-bromo cyclic GMP (100 microM) and the nonspecific vasodilator papaverine (100 microM) were not changed by oxidized-LDL. Native LDL had no effect on vasorelaxations. The attenuation of endothelium-dependent relaxations caused by oxidized-LDL mimicked the endothelial dysfunction found in ApoE(-/-) mice. These results are consistent with the suggestion that oxidized-LDL has an important role in the pathogenesis of endothelial NO dysfunction associated with hyperlipidemia and atherosclerosis in these mice.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed1991

Evidence against the involvement of vasoactive intestinal peptide in ovine parotid secretion and blood flow.

1. The proposition that stimulation of the secretomotor nerve to the ovine parotid gland might involve co-release of vasoactive intestinal peptide (VIP) was tested by studying responses to infusion of VIP directly into the gland's arterial blood supply and by assay of VIP in parotid venous blood. 2. In unstimulated glands, an arterial blood concentration of 1.5 - 2.5 X 10(-9) mol/L VIP did not evoke fluid secretion but it increased K+ and phosphate secretion and glandular blood flow. The same blood concentration of VIP potentiated the stimulation of salivary flow rate caused by intraarterial infusion of bethanechol but nerve stimulation was not potentiated. VIP increased glandular blood flow in both conditions of stimulation. 3. Atropine blocked neurally stimulated salivary secretion but an increase in glandular blood flow was still detectable. There was therefore no evidence for a non-cholinergic neural mechanism for salivary secretion. 4. Furthermore, VIP concentrations in glandular venous blood were not increased by nerve stimulation. 5. The results indicate that exogenous VIP can affect the flow and composition of ovine parotid secretion but was not involved in the response to secretomotor nerve stimulation.

Animals↗

PubMed1990

Opening the blood-brain barrier to zinc.

Sheep with guide tubes implanted over the brain lateral ventricles, in order to facilitate episodic sampling of cerebrospinal fluid (CSF), were used to determine the effects of increasing cranial blood osmolality or electroconvulsive shock (ECS) on the permeability of the blood-brain barrier (BBB) to zinc. Zinc acetate solution (1 mg Zn/ml) was infused intravenously (i.v.) at 1.0 ml/min for 30 min and then continuously at 0.125 ml/min. This infusion increased plasma total zinc concentration (pZn) approximately 10-fold without altering CSF zinc concentration (CSFZn). After 1.5-3.5 h, 4 M NaCl was infused at 5-10 ml/min for 10 min into one carotid artery with the other carotid artery occluded, or the animals were anaesthetized and given an ECS (140 V, 2 s). Paired samples of blood and CSF were collected before and after these treatments. Results were: (i) CSFZn was approximately one tenth of pZn; (ii) zinc administered i.v. was almost completely excluded from the CSF; (iii) increased cranial blood osmolality or ECS increased CSFZn in all experiments, but the time course and extent of the rise were variable. CSFZn reached the concentrations of zinc in normal sheep plasma in some experiments; (iv) CSFZn subsequently fell towards the low values of zinc in normal CSF; (v) the animals suffered no evident ill-effects from either procedure. The procedures may, therefore, be used for reversible opening of the BBB to particles such as zinc in conscious or anaesthetized sheep with no troublesome sequelae.

Animals↗

PubMed1988

Renal effects of atrial natriuretic factor (99-126) in conscious sodium-replete sheep.

1. The effect of renal arterial infusion of synthetic human atrial natriuretic factor (ANF (99-126] on renal function in the conscious euvolaemic sheep was characterized. ANF (99-126) was infused for 2 h at 5 and 50 micrograms/h into the renal artery of crossbred Merino ewes with chronically indwelling cannulae inserted in the renal artery. The effect on absolute and fractional excretion of Na, K, Ca, Cl and HCO3, glomerular filtration rate (GFR), effective renal plasma flow (ERPF) and free water clearance (CH2O) were measured. 2. Infusion at 50 micrograms/h produced a fourfold increase in Na and Cl excretion. Ca excretion increased eightfold, while K and HCO3 increased by small amounts. At the lower dose only Na, Cl and Ca excretion increased significantly. The changes in absolute excretion of each ion were closely mirrored by changes in fractional excretion. CH2O became more negative at both levels of infusion. Small changes in GFR were measured at both rates of infusion. No changes in ERPF or renin secretion were observed. 3. ANF (99-126) infusion at 50 micrograms/h for 1 h increased the excretion of Li, such that more than 70% of the change in Na excretion was associated with the changes in Li clearance. Changes in GFR accounted for less than 10% of change in Na excretion. 4. Following either long-term (50 micrograms/h for 6 h) or repeated short-term (20 micrograms/h for 30 min) infusions of ANF (99-126), the response of Na excretion was not sustained. The mechanisms of the tachyphylaxis remains undetermined. 5. ANF (99-126) is a powerful stimulus to the absolute and fractional excretion of Na, K, Ca, Cl and HCO3. The mechanism of action is not known, but appears to be related to changes in tubular function and/or a change in glomerulotubular balance.

Animals↗

PubMed1987

Vasopressin release in sheep following various degrees of rehydration.

Restriction of the water intake of sheep to 0.5 1/day for 7-9 days increases plasma arginine vasopressin (pAVP), and voluntary rehydration causes a rapid fall in pAVP with no change in plasma osmolality. The extent of that inhibition of AVP release was assessed by comparing the decline of pAVP after drinking with pAVP disappearance curves obtained in the same sheep after stopping a constant infusion of AVP at 0.5 micrograms/h, which increased pAVP to the dehydration level. The fall in pAVP after drinking was almost identical with the disappearance curve showing that AVP release was almost completely inhibited during the 2-3 min taken for the sheep to drink 3-5 liters to satiate themselves. The response seemed, therefore, to be cued before the intake reached the satiating volume. When dehydrated sheep drank only 0.5 or 1.0 liter, in 30 s or less, pAVP again fell rapidly but only to a minimum approximately 15 min after drinking. The pAVP was unaltered in dehydrated sheep presented with water but denied access to it. Thus satiation was not necessary for rapid inhibition of AVP release after drinking, but satiation was necessary for this inhibition to be maintained. The initial inhibition was associated with falls in hematocrit and plasma total protein but not plasma osmolality. This isosmolar dilution occurred even in sheep that saw but were denied access to the water and suggests a shift of fluid from the extravascular space.

Animals↗

PubMed1985

Acute reduction of plasma vasopressin levels by rehydration in sheep.

Sheep were depleted of water by restricting water intake to 500 ml/day for 7-9 days and were then rehydrated by three treatments: voluntary intake of water, administration of water by tube into the stomach, or voluntary intake of 0.9% NaCl solution (saline). The volumes of fluids drunk within 2-3 min, or administered by tube, were approximately equal to the animal's weight loss. Plasma vasopressin rose from 4.4 +/- 0.6 to 16.8 +/- 1.0 pg/ml during water restriction. After drinking water plasma vasopressin fell from 19.0 +/- 1.9 to 7.5 +/- 0.4 pg/ml (P less than 0.001) in 15 min and gradually fell to 3.2 +/- 0.4 pg/ml over 6 h. Plasma osmolality fell from 302.4 +/- 0.9 to 301.0 +/- 1.1 mosmol/kg (NS) 15 min after water drinking and then gradually fell to subnormal levels. Sheep given water by stomach tube showed a similar decline in plasma osmolality, but the fall in plasma vasopressin was attenuated. The fall in plasma vasopressin in the first 30 min after drinking saline was almost identical with the fall after drinking water, but plasma osmolality was unaltered. Plasma vasopressin fell so rapidly after drinking water or saline as to suggest that the act of drinking caused almost complete inhibition of vasopressin release without a change in plasma osmolality. The results are consistent with earlier evidence that oropharyngeal receptors initiate the inhibition of vasopressin release after drinking.

Animals↗

PubMed1977

Plasma renin activity and blood corticosteroids in the Australian lungfish Neoceratodus forsteri.

Plasma renin activity (PRA) and blood aldosterone and deoxycorticosterone levels were measured in Australian lungfish. Plasma renin activity was depressed after intravenous infusions of iso-osmotic (0-6%) NaCl but not after hypo-osmotic (0-3%) infusions. The presence of PRA in this fish is consistent with prior reports of renal renin activity in other sarcopterygian fishes. The results of the infusion experiments suggest that a fall in plasma osmolality or electrolyte concentrations may oppose the reduction in renin release in response to volume expansion. Aldosterone and deoxycorticosterone were identified in the blood of Neoceratodus. The concentrations of both appeared higher in females than in males. Infusions of [5-valine]-angiotensin II amide for 2-4 h at rates known to increase blood pressure in this species did not alter blood aldosterone concentrations. This negative finding may suggest that the renin/angiotensin system is not involved in aldosterone regulation in Neoceratodus or that angiotensin receptors involved in regulation of steroidogenesis have a greater specificity for endogenous angiotensin than do vascular receptors.

Aldosterone↗