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Biomedical subjects

M Hoehn

Publications and source records attributed to M Hoehn.

27 records · Page 2Linked to original sources
PubMed2000

Penumbral tissue alkalosis in focal cerebral ischemia: relationship to energy metabolism, blood flow, and steady potential.

The effect of focal ischemia on tissue pH was studied at various times up to 6 hours after permanent middle cerebral artery occlusion in rats. Tissue pH was imaged by using umbelliferone fluorescence and correlated with cerebral blood flow, ATP content, and recordings of the steady potential. Circumscribed foci of allalosis (pH 7.32+/-0.11) were detected with increasing frequency in penumbral regions having near-to-normal ATP concentrations and cerebral blood flow values between 20% and 40% of control. Both the infarct core, defined by ATP loss and cerebral blood flow values of less than 20% of control, and the inner peri-infarct rim were consistently acidic (pH 6.03+/-0.36 and 6.53+/-0.24, respectively). Treatment with the glutamate antagonist dizocilpine (MK-801) suppressed negative shifts of the steady potential and reduced significantly the occurrence of alkalosis observed in 90% of untreated but only in 44% of treated animals. Penumbral alkalosis appeared to be a time-dependent event occurring 30 to 60 minutes after the passage of peri-infarct depolarizations. The diversity of penumbral pH changes reflects the local disturbance of pH regulation and, possibly, the differential fate of penumbral subareas.

Acidosis↗
PubMed1999

Thrombolysis of cerebral clot embolism in rat: effect of treatment delay.

Rats submitted to focal cerebral ischemia by middle cerebral artery clot embolism were treated with recombinant tissue plasminogen activator (rt-PA) at increasing delays (1.5, 3 and 4.5 h) after the onset of ischemia. Treatment efficacy was evaluated by NMR imaging of the apparent diffusion coefficient of water (ADC). In untreated animals the size of the ADC-detectable lesion gradually increased after clot embolism, expanding over 8 h to 174 +/- 17% of the volume visible at 30 min. Thrombolysis initiated 1.5 h after embolism did not reverse the ischemic lesion but reduced its growth to 113 +/- 19% (p < 0.05). Lesion size increased to 135 +/- 14% after 3 h (NS) and to 214 +/- 35% after 4.5 h delay (NS). Thrombolysis with rt-PA attenuates infarct expansion but does not reverse ischemic injury.

Animals↗
PubMed1999

Diffusion- and perfusion-weighted MR imaging of transient focal cerebral ischaemia in mice.

Temporary focal ischaemia was induced in wild-type C57Black/6 mice by thread occlusion of the middle cerebral artery (MCA). Recirculation was started after 60 min and maintained for 24 h, after which the mouse brain was frozen in situ. Development of the cerebral infarct was monitored by diffusion-, perfusion- and T(2)-weighted magnetic resonance imaging (MRI) during ischaemia, during the early reperfusion period of 90 min, and at 24 h after reperfusion. Ischaemia caused a marked reduction of the perfusion signal intensity and of the apparent diffusion coefficient (ADC) of tissue water in the ipsilateral MCA territory. In sham-operated control animals ADC remained unchanged. Hemispheric lesion volume after 1 h MCA occlusion was 53 +/- 6% (n = 6), as defined by an ADC decrease of more than 20%. Recirculation reduced hemispheric lesion volume to only 27 +/- 13%, while there was a trend towards secondary lesion growth at 24 h. Post-ischaemic recovery of perfusion was slow, heterogeneous and incomplete. A region-of-interest analysis showed only partial and transient recovery of the ADC, particularly in the dorsolateral cortex and lateral caudate putamen, which may be explained by inadequate reperfusion in these regions. Detailed MRI studies of cerebral ischaemia and reperfusion may now also be performed in the transgenic mice.

Animals↗
PubMed1999

Gradient echo time dependence and quantitative parameter maps for somatosensory activation in rats at 7 T.

The dependence of functional magnetic resonance imaging (MRI) contrast on the gradient echo time TE in T2*-weighted blood oxygenation level-dependent (BOLD) fast low-angle shot (FLASH) imaging has been studied at 7 T for electrical forepaw stimulation in alpha-chloralose anesthetized rats. The observed variation of both the activation signal intensity and spatial pattern with echo time TE, resulting from the regional heterogeneity of T2*, was assessed by the calculation of quantitative T2* and quantitative STE = 0 maps, the latter representing the back-extrapolated signal intensity for TE = 0. The subsequently determined T2* and STE = 0 activation maps allowed a pixelwise separation of true BOLD from inflow contributions to forepaw stimulation-induced signal change in the somatosensory cortex of rat brain. For functional activation experiments performed with one single echo time the prior measurement of a quantitative T2* map is recommended as minimum further information to judge the intensity and the regional pattern of the resulting activation maps.

Afferent Pathways↗
PubMed1999

Quantitative T*(2) and T'(2) maps during reversible focal cerebral ischemia in rats: separation of blood oxygenation from nonsusceptibility-based contributions.

Quantitative imaging contrast is evaluated which allows the selective measurement of the blood oxygenation state during cerebral ischemia within a multiparametric imaging study on rats. In a first step, the ambiguities arising in T*(2)-weighted images due to T*(2) heterogeneity are eliminated by calculating T*(2) maps. Then, 1/T'(2) maps are calculated according to 1/T'(2) = 1/T*(2) - 1/T(2) to eliminate nonsusceptibility-induced changes of 1/T*(2) after the induction of stroke. This is of particular importance in the presence of vasogenic edema. The changes Delta(1/T'(2)) after the onset of ischemia selectively quantify the variations of the deoxyhemoglobin content during the development of the infarct. The presented results are not available from conventionally recorded parameters of a stroke study and, together with perfusion-weighted images, form a powerful combination to analyze the oxygen consumption and the metabolism of the tissue. Magn Reson Med 42:1027-1032, 1999.

Animals↗
PubMed1999

Rapid monitoring of diffusion, DC potential, and blood oxygenation changes during global ischemia. Effects of hypoglycemia, hyperglycemia, and TTX.

BACKGROUND AND PURPOSE: The increasing interest in diffusion-weighted MRI (MRI) for diagnosis and monitoring of acute stroke in humans calls for a sound understanding of the underlying mechanisms of this image contrast in acute cerebral ischemia. The present study aimed to show that a rapid decrease in brain-water apparent diffusion coefficient (ADC) occurs coincident with anoxic depolarization and that this change is delayed by hyperglycemia and sodium channel blockade but accelerated by hypoglycemia. METHODS: Rats were divided into groups: normoglycemic, hypoglycemic, and hyperglycemic, and those given local tetrodotoxin (TTX) application. Cardiac arrest was effected by intravenous KCl injection during serial high-speed diffusion and blood oxygenation-sensitive gradient-recalled echo MRI. Brain DC potential was recorded simultaneously. Serial ADC maps were calculated from the diffusion-weighted data and fitted to a model function to measure the delay between cardiac arrest and rapid ADC decrease. RESULTS: The time of anoxic depolarization indicated by DC change agreed well with the rapid drop in ADC in all groups; both were accelerated with hypoglycemia and delayed by hyperglycemia. A more gradual ADC decline occurred before anoxic depolarization, which was more pronounced in hyperglycemic animals and less pronounced in hypoglycemic animals. Rapid drop in ADC was also delayed by local TTX application. Changes in gradient-recalled echo image intensity were not significantly different among groups. CONCLUSIONS: While much of the ADC decrease in ischemia occurs during anoxic depolarization, significant but gradual ADC changes occur earlier that may not be due to a massive loss in ion homeostasis.

Animals↗
PubMed1996

Intensive speech treatment for patients with Parkinson's disease: short-and long-term comparison of two techniques.

The purpose of this study was to evaluate the long-term (12 months) effects of two forms of speech treatment on the speech and voice deficits that occur in Parkinson's disease. Thirty-five patients with idiopathic Parkinson's disease were assigned to one of two speech treatment groups: voice and respiration (The Lee Silverman Voice Treatment [LSVT]) or placebo (respiration) treatment. Vocal intensity data from before, immediately after, and at 6 and 12 months after speech treatment revealed statistically significant differences between the treatment groups. Only subjects in the LSVT group improved or maintained vocal intensity above pretreatment levels by 12 months after treatment. The placebo group had statistically significant deterioration of vocal intensity levels from before to 12 months after treatment during conversational monologue. The LSVT group did not deteriorate to levels below pretreatment in vocal intensity over the 12-month period. This study is the first to document the short-and long-term effects of intensive speech treatment (LSVT), which focuses on the voice, for patients with Parkinson's disease compared with a placebo speech treatment group.

Aged↗
PubMed1992

Bilateral fetal grafts for Parkinson's disease: 22 months' results.

Five patients with severe Parkinson's disease underwent bilateral multiple graft implants of nondissociated fetal mesodiencephalic tissues. Graft implantation was performed in China following CT-guided stereotactic placement of a novel delivery system. Follow-up has demonstrated substantially reduced levodopa requirements and clinical improvements of motor, postural functions and reduction of freezing and on-off phenomenon. PET utilizing [18F]-dopa, at 14 months in the first case, suggested graft-induced restoration of dopaminergic transmission in the striatum.

Brain Tissue Transplantation↗