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Biomedical subjects

R B Duckrow

Publications and source records attributed to R B Duckrow.

35 records · Page 2Linked to original sources
PubMed1991

Regional cerebral blood flow during spreading cortical depression in conscious rats.

Spreading cortical depression (SCD) of EEG activity was induced in one cerebral hemisphere of conscious restrained rats by direct current stimulation of the lateral frontal cortex. Regional CBF was measured using [14C]iodoantipyrine and brain dissection. An early phase of increased CBF was not measured in conscious rats, but an early relative hyperperfusion was measured if the resting CBF was first reduced by treatment with pentobarbital or indomethacin. A long-lasting reduction in CBF was measured in conscious rats following the passage of SCD. This flow reduction resolved after 3 h. In conscious rats, CBF decreased in the striatum and thalamus ipsilateral to the SCD, paralleling the CBF changes occurring in the cortex. The CBF change in these deep structures was abolished by pentobarbital. An early transient increase in regional CBF was measured in the cerebral cortex contralateral to the hemisphere involved with SCD in conscious rats. This early contralateral hyperperfusion was also abolished by pentobarbital or indomethacin but not by atropine or propranolol. The vascular response to SCD in conscious rats differs from that which occurs in anesthetized rats.

Animals↗
PubMed1990

Brain mitochondrial redox state, tissue haemodynamic and extracellular ion responses to four-vessel occlusion and spreading depression in the rat.

Fibre-optic surface fluorometer reflectrometry was used to monitor the NADH (nicotine adenine dinucleotide) redox state from rat brain during three- or four-vessel occlusion. To compare the completeness of the electrocauterization of the vertebral arteries and the effectiveness of the anterior cerebral arteries, two light guides were implanted above the cerebral hemispheres. The NADH level was measured and correlated with the changes in the intensity of the reflected light at the excitation wavelength (366 nm) and to the ECoG (electrocorticogram). In the present study, we used ten rats in which unilateral and bilateral carotid occlusion were performed. In a second group of rats we tested the effects of four-vessel occlusion on the metabolic and extracellular K+ and Ca2+ activities as compared with those recorded under spreading depression conditions. These experiments were done by using the multiprobe assembly (MPA) approach. The results could be summarized as follows: (1) in the four-vessel occlusion model, the level of cerebral ischaemia could be estimated quantitatively, in real-time, by monitoring the NADH redox state; (2) unilateral carotid occlusion (after vertebral coagulation) led to a variable level of ipsilateral ischaemia, depending upon the blood flow compensation between the two hemispheres; (3) fibre-optic fluorometry enabled the correlation of NADH redox state with other physiological parameters as well as during after-brain ischaemia; (4) using the MPA in rats exposed to four-vessel occlusion as well as spreading depression, we identified the differences between the two pathological states, although there were some similarities in the ion homeostasis responses.

Animals↗
PubMed1990

Effect of hemodilution on regional cerebral blood flow during chronic hyperglycemia in rats.

Regional cerebral blood flow decreases during chronic hyperglycemia, a condition frequently associated with elevated hematocrit. To test the hypothesis that an elevated hematocrit is responsible for the reduced regional cerebral blood flow during chronic hyperglycemia, I used isovolemic hemodilution to normalize the hematocrit in seven normoglycemic and seven streptozotocin-treated (hyperglycemic) rats. Regional cerebral blood flow was measured in 28 awake, restrained rats (14 normoglycemic and 14 hyperglycemic) using [14C]iodoantipyrine and dissection of 17 brain regions. Hemodilution lowered the hematocrit by 6 units (13%) and increased the average cerebral blood flow by 14%. Chronic hyperglycemia did not elevate the hematocrit, but it decreased the average cerebral blood flow by 12% and that in nine nontelencephalic brain regions by 17%. This effect was independent of changes in hematocrit caused by hemodilution. The reduced regional cerebral blood flow during chronic hyperglycemia is not caused by elevated hematocrit.

Animals↗
PubMed1988

Regional cerebral blood flow and glucose utilization during hyperinsulinemia.

Regional cerebral blood flow and glucose utilization were measured in awake-restrained rats during euglycemic hyperinsulinemia and were found to be normal. This indicates that elevated plasma insulin does not alter cerebral blood flow and cannot explain decreases in cerebral blood flow measured during acute hyperglycemia.

Animals↗
PubMed1988

Glucose transfer into rat brain during acute and chronic hyperglycemia.

Chronic hyperglycemia has been reported to decrease the maximum velocity of glucose transport across the blood-brain barrier by 30 to 40%. However, available measurements of brain glucose content during chronic hyperglycemia are consistent with an unaltered transport system. Because of this discrepancy the brain capillary permeability-surface area product (PA) was measured in awake-restrained rats during acute and chronic hyperglycemia. Acute hyperglycemia was produced by intraperitoneal injection of glucose, and chronic hyperglycemia was produced by treatment with streptozotocin. PA was measured using an intravenous tracer method. PA decreased during hyperglycemia, consistent with saturation kinetics for transfer. However, PA was similar in acutely and chronically hyperglycemic rats. These data suggest that down-regulation of facilitated glucose transport into the brain does not occur during chronic hyperglycemia.

Acute Disease↗
PubMed1987

Regional cerebral glucose utilization during hyperglycemia.

Previous data indicate that regional cerebral blood flow (rCBF) decreases during acute and chronic hyperglycemia. To test the hypothesis that the decrease in rCBF is secondary to a decrease in cerebral metabolic rate, the rate of regional cerebral glucose utilization (rCMRgl) was measured in awake-restrained rats during acute and chronic hyperglycemia. Acute hyperglycemia was produced by intraperitoneal injection of glucose, and chronic hyperglycemia was produced by treatment with streptozotocin. The rCMRgl was measured over a 10-min period using [6-14C]glucose. Glucose utilization was normal during acute hyperglycemia but decreased by 13% following 3 weeks of chronic hyperglycemia. The absence of a decrease in rCMRgl measured during acute hyperglycemia indicates that decreased rCBF cannot be explained by a change in the metabolic rate of the brain. The decrease in rCMRgl measured during chronic hyperglycemia does not necessarily indicate the presence of a drop in the metabolic rate of the brain because ketone bodies are available as an alternate fuel for oxidative metabolism. Therefore, it is unlikely that the decrease in rCMRgl measured during chronic hyperglycemia accounts for decreased rCBF.

Animals↗
PubMed1985

Regional cerebral blood flow decreases during hyperglycemia.

The presence of hyperglycemia before brain ischemia increases stroke-related morbidity and mortality in experimental animals and humans. However, little is known of the effect of hyperglycemia on regional cerebral blood flow (rCBF). Acute hyperglycemia was induced in awake but restrained rats by intraperitoneal injection of 50% D-glucose. Regional flow was determined using [14C]iodoantipyrine and quantitative autoradiography. Elevation of plasma glucose from 11 to 39 mM was associated with a 24% reduction in rCBF when compared with controls that received normal saline. Intraperitoneal D-mannitol produced an elevation of plasma osmolality equivalent to that observed with glucose. However, rCBF was only reduced by 10%. Hyperglycemia appears to produce a global decrease in rCBF in awake rats that cannot be completely explained by the attendant increase in plasma osmolality. If a similar influence is present during brain ischemia, hyperglycemia could extend areas of critical flow limitation.

Animals↗
PubMed1985

Effect of bilirubin on brainstem auditory evoked potentials in the asphyxiated rat.

We measured brainstem auditory evoked responses (BAER) in four groups of paralyzed, ventilated, adult rats. Group A (n = 2) received intravenous albumin; group B (n = 5) received bilirubin in albumin; group C (n = 7) was asphyxiated and then received albumin; and group D (n = 19) was asphyxiated and received bilirubin in albumin. When compared with control values, no changes in BAER occurred in groups A or B and only slight changes were found in group C. In group D, seven rats died and seven suffered a marked secondary deterioration of the BAER following recovery, a phenomenon that did not occur in group C (p = 0.02). Bilirubin toxicity appears to be responsible for the changes in BAER but prior asphyxia was necessary for this effect to occur. Because the changes that occurred in group D involved all four major waves, it is not possible to separate out a toxic effect of bilirubin, localized to the auditory nerve and the auditory pathway, from a generalized systemic effect which could cause attenuation of the entire response. The BAER may be useful, however, as a noninvasive means of identifying bilirubin toxicity in the newborn.

Animals↗
PubMed1984

A simplified method for computerized densitometry of complex shapes in 2-deoxyglucose autoradiographs.

A simple, computerized densitometer is described which can be used to measure densities of photographic prints by means of a fiber-optic reflectance densitometric probe coupled to the movable cursor of a digitizing tablet. The cursor, with its attached probe, is moved by hand along a scan trajectory determined by the operator. In its configuration for use with 2-deoxyglucose autoradiographs, the histological section from which the autoradiograph was derived provides architectonic landmarks for guiding the path of the scan. The X, Y and density values taken along a scan line are sequentially stored in the computer memory. Algorithms are presented for plotting densities along unfolded scan lines within layers of structures with complicated shapes, for normalizing non-linearities introduced during photographic processing, for standardizing the data sets with reference to the density of average gray matter in different animals, for calculating total integrated density within defined boundaries along the scan line, for generating averages of multiple scans, and for stacking sequential scans to form pseudo-3-dimensional plots. This system allows densitometric measures to be made from autoradiographs in anatomically defined regions, thereby permitting precise correlation between isotope concentration and histological structure.

Animals↗
PubMed1983

Regional optic nerve blood flow and its autoregulation.

An autoradiographic method (14C-iodoantipyrine autoradiography) was used to measure regional optic nerve blood flow (ONBF) under basal conditions in 11 adult female cats. Flow was measured in six regions of the optic nerve: (1) prelaminar, (2) laminar, (3) 1 mm post-laminar, (4) 4 mm post-laminar, (5) 6 mm post-laminar, and (6) intracranial optic nerve and chiasm. A gradient of flow rates was found with relatively high flow in the prelaminar, laminar, and 1-mm post-laminar optic nerve, and significantly lower flow in the 4- and 6-mm post-laminar nerve and in the intracranial optic nerve and chiasm. Blood flow in the 4- and 6-mm post-laminar nerve and in the intracranial nerve and chiasm was comparable to previously reported values for cerebral white matter in the cat. With alteration of mean arterial blood pressure (MABP), optic nerve blood flow demonstrated autoregulatory compensation in all areas.

Animals↗
PubMed1981

Oxidative metabolic activity of cerebral cortex after fluid-percussion head injury in the cat.

To assess the metabolic and vascular effects of head trauma, fluid-percussion pressure waves were transmitted to the brains of anesthetized, paralyzed, and artificially ventilated cats. Changes in the redox state of cytochrome a,a3, and relative local blood volume were measured in situ by dual-wavelength reflection spectrophotometry of the cortical surface viewed through an acrylic cranial window implanted within the closed skull. Initial fluid-percussion impacts of 0.5 to 2.8 atm peak pressure produced consistent transient oxidation of cytochrome a,a3 and increases of cortical blood volume. These changes occurred despite the presence of transient posttraumatic hypotension i some cases. Also, impact-induced alterations of vascular tone occurred, independent of the presence or absence of transient hypertension in the posttraumatic period. These data demonstrate that hypoxia does not play a role in the immediate posttraumatic period in cerebral cortex, and are consistent with the idea that after injury there is increased cortical energy conservation. These data also support the concept that head trauma alters the relationship of metabolism and cerebral circulation in the period immediately after injury.

Animals↗
PubMed1981

Cerebral compensation for chronic noradrenergic denervation induced by locus ceruleus lesion: recovery of receptor binding, isoproterenol-induced adenylate cyclase activity, and oxidative metabolism.

The long term effects of specific noradrenergic denervation of rat cerebral cortex were considered in parallel studies of in vitro noradrenergic receptor binding and isoproterenol-induced adenosine 3':5'-monophosphate (cycle AMP) generation and of in vivo oxidative metabolism. Noradrenergic denervation was achieved by the local, unilateral injection of 6-hydroxydopamine into the locus ceruleus. Cerebral noradrenaline remained depleted throughout the 8-week duration of the study. Ligand-binding assays showed increased beta-adrenergic receptors 2 weeks after locus ceruleus lesion with recovery occurring by 4 weeks. There were no changes in alpha 1-adrenergic receptors. Isoproterenol-induced cyclic AMP generation increased at 2 weeks after lesion but recovered at 8 weeks. Dual wavelength reflection spectrophotometric measurements of cytochrome oxidase reduction/oxidation and local blood volume shifts, provoked in situ by direct cortical stimulation, also demonstrated abnormalities at 2 weeks with recovery by 4 weeks after lesion. Thus, in vivo and in vitro changes after locus ceruleus lesion are reversible and the time course of these changes is related temporally. These data suggest that cerebral cortex has adaptive capabilities which are activated to compensate for prolonged noradrenaline depletion. We also speculate that there may be a causal relationship between the in vitro and in vivo parameters studied.

Adenylyl Cyclases↗
PubMedDate not supplied

Disparate recovery of resting and stimulated oxidative metabolism following transient ischemia.

To assess the residual effects of transient cerebral ischemia on mitochondrial oxidative metabolic function, changes in the reduction/oxidation state of cytochrome a,a3 and relative local blood volume were measured in situ from the exposed cerebral surface of rat brain before and after 10 minutes of carotid artery ligation. During the ischemic interval, cytochrome a,a3 became reduced and electrocortical activity was abolished. During the first 20 minutes of reperfusion cytochrome a,a3 was hyperoxidized beyond baseline with eventual recovery to the original steady state. Electrocortical activity returned more slowly. Increased energy demand induced by electrical stimulation of the cortex produced transient oxidation of cytochrome a,a3. The amplitude of this oxidative response was decreased during the first 30 minutes of reperfusion. During the first 2 hours of reperfusion the time required for re-reduction of the oxidative response was lengthened despite the recovery of baseline mitochondrial redox state. These data demonstrate residual metabolic dysfunction after transient ischemia not apparent under "resting" conditions but evident when the system is required to perform additional "work." We speculate this metabolic dysfunction could be due to relative substrate limitation.

Animals↗
PubMedDate not supplied

Regional cerebral blood flow decreases during chronic and acute hyperglycemia.

The presence of hyperglycemia prior to stroke or cardiac arrest can increase neuronal damage caused by brain ischemia. Acute hyperglycemia shows this effect in animal models of stroke. However, chronic hyperglycemia and chronic hyperglycemia with additional acute elevation of blood glucose are more common premorbid states for stroke patients. The effect of chronic hyperglycemia on regional cerebral blood flow (rCBF) is unclear but blood flow changes may play a role in this ischemic cell damage. We measured rCBF in awake restrained rats that had chronic hyperglycemia induced by treatment with streptozotocin. This was compared to that measured in rats made acutely hyperglycemic by injecting glucose into the peritoneal space. rCBF was measured in 17 brain regions using [14C]iodoantipyrine. During chronic hyperglycemia, when plasma glucose was 29 microns/ml, rCBF was decreased and a regional distribution of this effect was noted; 9 hindbrain regions showed a mean flow decrease of 14% while forebrain regions demonstrated less flow reduction. Acute elevation of plasma glucose during normoglycemia or superimposed on chronic hyperglycemia produced flow reductions of 7% for each 10 microns/ml increment in plasma glucose up to 60 microns/ml. Both chronic and acute hyperglycemia are associated with decreased rCBF and the mechanism for this effect does not appear to adapt to chronic hyperglycemia.

Acute Disease↗