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C H Sotak

Publications and source records attributed to C H Sotak.

At least 19 recordsLinked to original sources
PubMed2005

Spatial characterization of T1 and T2 relaxation times and the water apparent diffusion coefficient in rabbit Achilles tendon subjected to tensile loading.

Tendons exhibit viscoelastic mechanical behavior under tensile loading. The elasticity arises from the collagen chains that form fibrils, while the viscous response arises from the interaction of the water with the solid matrix. Therefore, an understanding of the behavior of water in response to the application of a load is crucial to the understanding of the origin of the viscous response. Three-dimensional MRI mapping of rabbit Achilles tendons was performed at 2.0 T to characterize the response of T(1) and T(2) relaxation times and the apparent diffusion coefficient (ADC) of water to tensile loading. The ADC was measured in directions both parallel (ADC( parallel)) and perpendicular (ADC( perpendicular)) to the long axis of the tendon. At a short diffusion time (5.8 ms) MR parameter maps showed the existence of two regions, here termed "core" and "rim", that exhibited statistically significant differences in T(1), T(2), and ADC( perpendicular) under the baseline loading condition. MR parameter maps were also generated at a second loading condition of approximately 1 MPa. At a diffusion time of 5.8 ms, there was a statistically significant increase in the rim region for both ADC( perpendicular) (57.5%) and ADC( parallel) (20.5%) upon tensile loading. The changes in core ADC(( perpendicular), ( parallel)), as well as the relaxation parameters in both core and rim regions, were not statistically significant. The effect of diffusion time on the ADC(( perpendicular), ( parallel)) values was investigated by creating maps at three additional diffusion times (50.0, 125.0, 250.0 ms) using a diffusion-weighted, stimulated-echo (DW-STE) pulse sequence. At longer diffusion times, ADC(( perpendicular), ( parallel)) values increased rather than approaching a constant value. This observation was attributed to T(1) spin-editing during the DW-STE pulse sequence, which resulted in the loss of short-T(1) components (with correspondingly lower ADCs) at longer diffusion times (corroborating the results from earlier spectroscopic work). The T(1) spin-editing effect was observed both in the core and in the rim regions of the tendon and hence was not solely due to the redistribution of water from the core to the rim upon loading. A measure reflective of the regional change in proton density was noted to be consistent with tensile-load-induced water transport from the central to the peripheral tendon region.

Achilles Tendon↗
PubMed2004

Application of porous-media theory to the investigation of water ADC changes in rabbit Achilles tendon caused by tensile loading.

The water apparent diffusion coefficient (ADC) in rabbit Achilles tendon is anisotropic, diffusion-time dependent, and changes as a function of tensile load. Water ADC changes of tendon under mechanical load are thought to be due to the extrusion of water from the more restricted tendon core to a relatively unrestricted bulk phase at the periphery (rim) of the tendon. Tensile loading may influence water ADC values by changing the spatial separation of restricting barriers (e.g., increasing the tendon fibril packing density). To explore this issue, we have applied porous-media theory to the investigation of water ADC changes in rabbit Achilles tendon under two different mechanical loading conditions (a baseline condition with a minimal tensile stress and a second in which the tensile stress was approximately 1 MPa). Diffusion sensitivity was applied in directions parallel and perpendicular to the long axis of the tendon. The short diffusion-time behavior of the resulting time-dependent ADC curves was used to indirectly infer information regarding the average surface area to volume ratio of the space available for molecular diffusion. From these values, we estimated a 40% reduction in volume available for diffusion in the perpendicular direction after tensile loading, but only a 10% reduction in the parallel direction. These differences are consistent with the known geometry of the tendon microstructure and suggest an increase in fibril packing density upon loading. The long diffusion-time behavior of the time-dependent ADC curves was used to indirectly infer the tortuosity of the diffusion pathways through the interstitial space. The tortuosity in the direction perpendicular to the tendon long axis was approximately 2.5 times greater than that in the parallel direction. Stimulated-echo measurement of the ADC values at longer diffusion times resulted in T1 spin editing of water with shorter T1 values (and correspondingly lower ADC values). The resulting increase in water ADC with increasing diffusion time was attributed to multiple components arising from the (overlapping) distribution of T1 values in the core and rim regions of the tendon.

Achilles Tendon↗
PubMed2004

Measurement of the spatial redistribution of water in rabbit Achilles tendon in response to static tensile loading.

The redistribution of water in response to static tensile loading was investigated in rabbit Achilles tendons in vitro. The distribution of water was measured along a radially oriented line, using a one-dimensional proton-density map created from fits to diffusion-weighted magnetic resonance (MR) data. Water movements were measured during application of tensile loads of 5N (N=7) and 10N (N=6). Water distribution along the line was measured before loading and up to 42 min after load application. Static loading with either 5 or 10N loads caused a steady increase in proton density in the outside edge (rim) of the tendon. The 10N load lowered the proton density in the core of the tendon, but did so in a single step that was observed when the load was applied. The 5N load caused no change in proton density in the core region. The immediate redistribution from the core was statistically significant for the 10N load, but not the 5N load application. Statistically significant within-group proton-density increases were observed in the rim after 42 min postload for all tendons irrespective of load condition. The rate of proton-density postload increase at the rim region did not depend upon load. The rate for the 5N load case was 0.010 +/- 0.002 min(-1) and 0.007 +/- 0.002 min(-1) in the 10N case. Thus, while generally consistent with an extrusion model, the data show other features that argue for a more complex model.

Achilles Tendon↗
PubMed2001

Regional variations in the apparent diffusion coefficient and the intracellular distribution of water in rat brain during acute focal ischemia.

BACKGROUND AND PURPOSE: The apparent diffusion coefficient of water (ADC) rapidly drops in ischemic tissue after cerebral artery occlusion. This acute drop is thought to be caused by the loss of extracellular fluid and the gain of intracellular fluid. To test the latter possibility, changes in ADC and the size of several cellular compartments were assessed in 3 regions of rat brain at the end of 90 minutes of focal cerebral ischemia. METHODS: One middle cerebral artery was permanently occluded in 8 Sprague-Dawley rats; sham occlusions were performed in 2 other rats. ADC maps were generated 90 minutes later, and the brains were immediately perfusion fixed. Three regions of interest (ROIs) were defined on the basis of ADC range. Various neuronal, astrocytic, and capillary compartments in each ROI were quantified with light and electron microscopy. RESULTS: At the end of 90 minutes of ischemia, mean ADC was normal in the cortex of sham-operated rats and the contralateral cortex of ischemic rats (ROI-a), 25% lower in the ipsilateral frontoparietal cortex (ROI-b), and 45% lower in the ischemic lateral caudoputamen (ROI-c). At this time, the frequency of swollen astrocytic cell bodies and volume of swollen dendrites and astrocytic processes in neuropil were ROI-a<ROI-b<ROI-c. In ROI-b and ROI-c, 40% and 60% of the neurons, respectively, were shrunken; the shrunken neurons were approximately 25% smaller in ROI-c than in ROI-b. In these areas, many capillary endothelial cells, pericytes, and perivascular foot processes were swollen. CONCLUSIONS: The initial lowering of ADC during focal ischemia probably is the result of not only the acute loss of extracellular fluid and concomitant swelling of various cellular compartments but also concurrent neuronal shrinkage.

Acute Disease↗
PubMed2000

Broad-spectrum cation channel inhibition by LOE 908 MS reduces infarct volume in vivo and postmortem in focal cerebral ischemia in the rat.

Cation channels conduct calcium, sodium and potassium, cations that are likely deleterious in the evolution of focal ischemic injury. We studied the effects of a novel, broad-spectrum inhibitor of several cation channels, LOE 908 MS, on acute ischemic lesion development with diffusion-weighted magnetic resonance imaging (DWI) and on cerebral perfusion with perfusion imaging (PI) in vivo and on cerebral infarct size using 2,3,5-triphenyltetrazolium chloride (TTC) staining postmortem. A total of 18 male Sprague-Dawley rats underwent 90 min of middle cerebral artery occlusion (MCAO) and were randomly and blindly assigned to either LOE 908 MS or vehicle starting 30 min after inducing focal ischemia and continuing for 4 h. Whole-brain DWI and multislice PI were done before initiation of treatment and repeated frequently for the next 3.5 h. DWI-derived lesion volume at 4 h showed a significant difference in favor of the drug treated group (P=0.03), whereas PI-derived perfusion deficit volumes did not significantly differ between the groups. The postmortem infarct volume at 24 h was significantly attenuated in the treated group in comparison to controls (P=0.0001) and neurological score was significantly better in the treated group (P<0.02). Blocking several distinct cation channels with LOE 908 MS significantly reduced infarct size and improved neurological outcome without observable adverse effects in this focal ischemia model.

Acetamides↗
PubMed2000

Temporal evolution of ischemic injury evaluated with diffusion-, perfusion-, and T2-weighted MRI.

OBJECTIVE: Ischemic lesions seen on diffusion-weighted imaging (DWI) are reversible if reperfusion is performed within minutes after the onset of ischemia. This study was designed to determine whether acute reversibility of DWI abnormalities is transient following brief temporary focal brain ischemia and to characterize the temporal evolution of in vivo ischemic lesions. METHODS: Eight rats were subjected to 30 minutes of temporary middle cerebral artery occlusion and underwent diffusion-, perfusion-, and T2-weighted MRI during occlusion; immediately after reperfusion; 30, 60, and 90 minutes after reperfusion; and 12, 24, 48, and 72 hours after reperfusion. Average apparent diffusion coefficient (ADCav) values and the cerebral blood flow index (CBFi) ratio were calculated in both the lateral caudoputamen and overlying cortex at each time point. The size of the in vivo ischemic abnormalities was calculated from the ADCav and the T2 maps. Postmortem triphenyltetrazolium chloride (TTC) staining was used to verify ischemic injury. RESULTS: Both the CBFi ratio and ADCav values declined significantly in the two regions during occlusion. The CBFi ratio recovered immediately after reperfusion and remained unchanged over 72 hours. However, ADCav values returned to normal at 60 to 90 minutes and secondarily decreased at 12 hours after reperfusion as compared with those in the contralateral hemisphere. The extent of the in vivo ischemic lesions maximized at 48 hours and was highly correlated with TTC-derived lesion size. CONCLUSIONS: Acute recovery of initial ADCav-defined lesions after reperfusion is transient, and secondary ADCav-defined lesions develop in a slow and delayed fashion.

Animals↗
PubMed2000

Multispectral analysis of the temporal evolution of cerebral ischemia in the rat brain.

A major difficulty in staging and predicting ischemic brain injury by magnetic resonance (MR) imaging is the time-varying nature of the MR parameters within the ischemic lesion. A new multispectral (MS) approach is described to characterize cerebral ischemia in a time-independent fashion. MS analysis of five MR parameters (mean diffusivity, diffusion anisotropy, T2, proton density, and perfusion) was employed to characterize the progression of ischemic lesion in the rat brain following 60 minutes of transient focal ischemia. k-Means (KM) and fuzzy c-means (FCM) classification methods were employed to define the acute and subacute ischemic lesion. KM produced an estimate of lesion volume that was highly correlated with postmortem infarct volume, independent of the age of the lesion. Overall classification rates for KM exceeded FCM at acute and subacute time points as follows: KM, 90.5%, 94.4%, and 95. 9%; FCM, 82.4%, 90.6%, and 82.6% (for 45 minutes, 180 minutes, and 24-120 hours post MCAO groups). MS analysis also offers a formal method of combining diffusion and perfusion parameters to provide an estimate of the ischemic penumbra (KM classification rate = 70.3%). J. Magn. Reson. Imaging 2000;12:842-858.

Acute Disease↗
PubMed2000

Acute changes in MRI diffusion, perfusion, T(1), and T(2) in a rat model of oligemia produced by partial occlusion of the middle cerebral artery.

Oligemic regions, in which the cerebral blood flow is reduced without impaired energy metabolism, have the potential to evolve toward infarction and remain a target for therapy. The aim of this study was to investigate this oligemic region using various MRI parameters in a rat model of focal oligemia. This model has been designed specifically for remote-controlled occlusion from outside an MRI scanner. Wistar rats underwent remote partial MCAO using an undersize 0.2 mm nylon monofilament with a bullet-shaped tip. Cerebral blood flow (CBF(ASL)), using an arterial spin labeling technique, the apparent diffusion coefficient of water (ADC), and the relaxation times T(1) and T(2) were acquired using an 8.5 T vertical magnet. Following occlusion there was a decrease in CBF(ASL) to 35 +/- 5% of baseline throughout the middle cerebral artery territory. During the entire period of the study there were no observed changes in the ADC. On occlusion, T(2) rapidly decreased in both cortex and basal ganglia and then normalized to the preocclusion values. T(1) values rapidly increased (within approximately 7 min) on occlusion. In conclusion, this study demonstrates the feasibility of partially occluding the middle cerebral artery to produce a large area of oligemia within the MRI scanner. In this region of oligemic flow we detect a rapid increase in T(1) and decrease in T(2). These changes occur before the onset of vasogenic edema. We attribute the acute change in T(2) to increased amounts of deoxyhemoglobin; the mechanisms underlying the change in T(1) require further investigation.

Animals↗
PubMed2000

Changes in ADC caused by tensile loading of rabbit achilles tendon: evidence for water transport.

Water diffusion measurements were performed on rabbit Achilles tendons during static tensile loading and tendons in an unloaded state. The apparent diffusion coefficient (ADC) was measured along two directions: parallel and perpendicular to the long axis of the tendon. Tendons were studied after being prepared in two ways: (a) after being stored frozen in phosphate-buffered saline (PBS) and (b) freshly isolated. Statistically significant directional anisotropy was observed in the ADC in all tendons. The ADC was significantly greater in the direction parallel to the long axis of the tendon than in the perpendicular direction. The anisotropy is attributed to the greater restrictions seen by the water molecules in the perpendicular direction and is consistent with the known geometry of the tendon. Storage in PBS caused tendons to swell. This increased the ADC measured along both directions and reduced the anisotropy. The existence of anisotropy in the ADC was not related to the orientation of the specimen in the magnet. The ADC increased along both directions following the application of a 5-N tensile load; the increase was greatest along the perpendicular axis of the tendon. In order to determine whether load-related changes in the ADC reflected changes in interfibrilar spacing, we used electron microscopy to measure load-related changes in fibril spacing. Load-related changes in fiber spacing could not account for the observed changes in the ADC. The increase in ADC caused by loading was attributed to the extrusion of tendon water into a bulk phase along the outside surface of the tendon. In PBS-stored samples, enough fluid was extruded that it could be visualized. The transient response of the ADC to a 5-N tensile load was also studied. The absolute ADC in both directions increased with loading and recovered to baseline upon unloading. The transient changes in ADC, for both loading and unloading, had a mean time constant of approximately 15 min. The magnitude of the load-induced transient ADC changes was comparable to that seen in the static-loading experiments.

Achilles Tendon↗
PubMed2000

Broad-spectrum cation channel inhibition by LOE 908 MS reduces infarct volume in vivo and postmortem in focal cerebral ischemia in the rat.

Cation channels conduct calcium, sodium, and potassium, cations that are likely deleterious in the evolution of focal ischemic injury. Diffusion-weighted magnetic resonance imaging (DWI) is a powerful tool for evaluation of acute cerebral ischemia. We studied the effects of a novel, broad-spectrum inhibitor of several cation channels, LOE 908 MS, on acute ischemic lesion development with DWI and on cerebral infarct size using 2,3,5-triphenyltetrazolium chloride (TTC) staining postmortem. Eighteen male Sprague-Dawley rats underwent middle cerebral artery occlusion (MCAO) and were randomly and blindly assigned to either LOE 908 MS (1 mg/kg bolus 30 min after MCAO and continuous i.v. infusion of 10 mg/kg for 4 h thereafter) or vehicle. Whole-brain DWI was done before initiation of treatment and repeated every 30 min for the next 3.5 h. The animals were reperfused in the magnetic resonance imaging (MRI) scanner 90 min after MCAO. At 24 h, the animals were killed, and the brains were cut into six 2-mm-thick slices and stained with 2% TTC. Percent hemispheric lesion volume (%HLV) was calculated for each animal. Physiological parameters, body weight, and premature mortality (3 in the placebo group and 1 in the treated group) did not differ between the groups. No hypotension, abnormal behavior, or other adverse effects were seen. Pretreatment, the DWI-derived %HLV did not differ between the groups (19.8 +/- 6.2 in the control group and 17.9 +/- 7.9 in the treated group), whereas at 4 h after MCAO, it was significantly smaller in the treated group (21.8 +/- 15.4 vs 40.4 +/- 15.5, p = 0.03). Postmortem, TTC-derived %HLV was significantly attenuated in the LOE 908 MS group (21.3 +/- 11.9 vs 50.1 +/- 10.7, p = 0.0001) and the neurological scores at 24 h were significantly better among the treated rats (2.1 +/- 1.5 vs 4.0 +/- 1.0, p < 0.02). LOE 908 MS significantly improved neurological outcome and reduced infarct size without observable effects in rats as demonstrated in vivo by DWI and confirmed postmortem by TTC staining. Blocking several distinct cation channels by LOE 908 MS showed significant neuroprotection.

Acetamides↗
PubMed2000

Inapparent hemodynamic insufficiency exacerbates ischemic damage in a rat microembolic stroke model.

BACKGROUND AND PURPOSE: Patients with severe carotid artery stenosis may have more severe ischemic damage after embolic stroke than patients without this abnormality. Unilateral proximal carotid occlusion (UCO) alone typically does not induce infarction in normotensive rats. The aim of this study was to investigate whether UCO increases infarct size after microembolic, experimental stroke. METHODS: Microembolic infarction was induced in 2 groups of Sprague-Dawley rats by injecting 2000 microspheres (50-micrometer diameter) intracranially from the external carotid artery. The common carotid artery (CCA) was either ligated just after the injection (CCA occlusion group, n=8) or left intact (CCA open group, n=8). In the control group (n=4), vehicle without microspheres was injected and the CCA was ligated. Twenty-four hours later, the brains were removed and infarct volumes measured. Perfusion-weighted imaging was used to evaluate the cerebral circulation before and after CCA occlusion with and without microsphere injection in a separate group of animals (n=16). RESULTS: All animals in the microemboli groups survived and had only a slight hemiparesis 24 hours after occlusion. No neurological deficits were observed in the control group. Infarct volumes were 145+/-57 mm(3) in the CCA occlusion group and 45+/-26 mm(3) in the CCA open group (P <0.01). There were no infarctions detected in the control group. Perfusion-weighted imaging showed that cerebral blood flow decreased after the CCA occlusion in both experiments with and without the microsphere injection. CONCLUSIONS: UCO alone does not induce ischemic damage, but it worsens ischemic lesion size after multiple microemboli. This is probably due to the slight cerebral perfusion insufficiency caused by UCO. These results suggest that patients with cerebral hemodynamic insufficiency, such as those with severe carotid stenosis, may have increased ischemic damage after microembolic events.

Animals↗
PubMed2000

Transient and permanent resolution of ischemic lesions on diffusion-weighted imaging after brief periods of focal ischemia in rats : correlation with histopathology.

BACKGROUND AND PURPOSE: The early ischemic lesions demonstrated by diffusion-weighted imaging (DWI) are potentially reversible. The purposes of this study were to determine whether resolution of initial DWI lesions is transient or permanent after different brief periods of focal brain ischemia and to evaluate histological outcomes. METHODS: Sixteen rats were subjected to 10 minutes (n=7) or 30 minutes (n=7) of temporary middle cerebral artery occlusion or sham operation (n=2). DWI, perfusion-weighted imaging (PWI), and T(2)-weighted imaging (T(2)WI) were performed during occlusion; immediately after reperfusion; and at 0.5, 1.0, 1.5, 12, 24, 48, and 72 hours after reperfusion. After the last MRI study, the brains were fixed, sectioned, stained with hematoxylin and eosin, and evaluated for neuronal necrosis. RESULTS: No MRI or histological abnormalities were observed in the sham-operated rats. In both the 10-minute and 30-minute groups, the perfusion deficits and DWI hyperintensities that occurred during occlusion disappeared shortly after reperfusion. The DWI, PWI, and T(2)WI results remained normal thereafter in the 10-minute group, whereas secondary DWI hyperintensity and T(2)WI abnormalities developed at the 12-hour observation point in the 30-minute group. Histological examinations demonstrated neuronal necrosis in both groups, but the number of necrotic neurons was significantly higher in the 30-minute group (95+/-4%) than in the 10-minute group (17+/-10%, P<0.0001). CONCLUSIONS: Transient or permanent resolution of initial DWI lesions depends on the duration of ischemia. Transient resolution of DWI lesions is associated with widespread neuronal necrosis; moreover, permanent resolution of DWI lesions does not necessarily indicate complete salvage of brain tissue from ischemic injury.

Animals↗
PubMed2000

Secondary decline in apparent diffusion coefficient and neurological outcomes after a short period of focal brain ischemia in rats.

This study was designed to characterize the initial and secondary changes of the apparent diffusion coefficient (ADC) of water with high temporal resolution measurements of ADC values and to correlate ADC changes with functional outcomes. Fourteen rats underwent 30 minutes of temporary middle cerebral artery occlusion (MCAO). Diffusion-, perfusion-, and T2-weighted imaging was performed during MCAO and every 30 minutes for a total of 12 hours after reperfusion (n = 6). Neurological outcomes were evaluated during MCAO, every 30 minutes for a total of 6 hours and at 24 hours after reperfusion (n = 8). The decreased cerebral blood flow during MCAO returned to normal after reperfusion and remained unchanged thereafter. The decreased ADC values during occlusion completely recovered at 1 hour after reperfusion. The renormalized ADC values started to decrease secondarily at 2.5 hours, accompanied by a delayed increase in T2 values. The ADC-defined secondary lesion grew over time and was 52% of the ADC-defined initial lesion at 12 hours. Histological evaluation demonstrated neuronal damage in the regions of secondary ADC decline. Complete resolution of neurological deficits was seen in 1 rat at 1 hour and in 6 rats between 2.5 and 6 hours after reperfusion; no secondary neurological deficits were observed at 24 hours. These data suggest that (1) a secondary ADC reduction occurs as early as 2.5 hours after reperfusion, evolves in a slow fashion, and is associated with neuronal injury; and (2) renormalization and secondary decline in ADC are not associated with neurological recovery and worsening, respectively.

Animals↗
PubMed1999

Neuroprotective effects of a novel broad-spectrum cation channel blocker, LOE 908 MS, on experimental focal ischemia: a multispectral study.

Thirty-four rats undergoing 90 minutes of temporary middle cerebral artery occlusion were randomly and blindly assigned to vehicle or (RS)-(3,4-dihydro-6, 7-dimethoxyisoquinoline-1-gamma1)-2-phenyl-N,N-di-2-(2, 3, 4-trimethoxyphenyl)ethyl acetamide (LOE 908 MS; 0.5 mg/kg) i.v. bolus at 30 minutes after arterial occlusion followed by a 5 mg/kg/hr i.v. infusion for 3.8 hours (n =17/group). Perfusion-, diffusion- and T(2)-weighted magnetic resonance imaging was performed before treatment and repeatedly after treatment. Multispectral analysis was used to define ischemic abnormalities. The size of the ischemic abnormalities, including the ischemic core and penumbra, was not different between the two groups before treatment. However, a significant difference in ischemic lesion size was detected beginning 1.5 hours after treatment. The size of the ischemic core was significantly smaller in the treatment group, while the size of the ischemic penumbra was similar in the two groups at 85 minutes after arterial occlusion. Postmortem infarct size at 24 hours was significantly smaller in the drug-treated group than in the placebo group. These results demonstrate that LOE 908 MS can reduce ischemic lesion size, which is probably attributable to inhibition of expansion of the ischemic core. J. Magn. Reson. Imaging 1999;10:138-145.

Acetamides↗
PubMed1999

Comparison of evoked cortical activity in conscious and propofol-anesthetized rats using functional MRI.

Changes in cortical activity during foot shock were assessed under conscious and propofol-anesthetized conditions using functional magnetic resonance imaging (fMRI). Increases in signal intensity were observed in the contralateral somatosensory cortex in response to electrical shock of the hindpaw under both conditions. These increases in cortical signal ranged from 6% to 26% while awake and from 1% to 6% under propofol anesthesia. In each of the six animals studied, the largest increase in blood oxygenation level-dependent (BOLD)-based signal intensity was observed during consciousness. In three of six animals, propofol anesthesia depressed signal intensity by as much as 10-fold, showing that the level of cortical activity during foot shock is dampened by anesthesia. These results indicate it would be advantageous to use fully conscious animals to maximize BOLD-based MRI signal in certain behavioral studies using MR spectrometers with modest field strengths (1.0-2.0 T).

Anesthesia, General↗
PubMed1999

Early changes in water diffusion, perfusion, T1, and T2 during focal cerebral ischemia in the rat studied at 8.5 T.

The time evolution of water diffusion, perfusion, T1, and T2 is investigated at high magnetic field (8.5 T) following permanent middle cerebral artery occlusion in the rat. Cerebral blood flow maps were obtained using arterial spin tagging. Although the quantitative perfusion measurements in ischemic tissue still pose difficulties, the combined perfusion and diffusion data nevertheless distinguish between a "moderately affected area," with reduced perfusion but normal diffusion; and a "severely affected area," in which both perfusion and diffusion are significantly reduced. Two novel magnetic resonance imaging observations are reported, namely, a decrease in T2 and an increase in T1, both within the first few minutes of ischemia. The rapid initial decrease in T2 is believed to be associated with an increase in deoxyhemoglobin levels, while the initial increase in T1 may be related to several factors, such as flow effects, an alteration in tissue oxygenation, and changes in water environment.

Animals↗
PubMed1999

Reversal of acute apparent diffusion coefficient abnormalities and delayed neuronal death following transient focal cerebral ischemia in rats.

Twenty-two rats were subjected to 8, 15, 30, or 60 minutes of temporary middle cerebral artery occlusion (n = 5 per group) or sham occlusion (n = 2) in the magnetic resonance imaging unit. Diffusion-, perfusion-, and T2-weighted imaging were acquired before and during occlusion, and after reperfusion. A coregistration method was used to correlate the acute changes of the average apparent diffusion coefficient (ADCav) with the histology after 72 hours at the same topographic sites. The initially reduced ADCav values recovered completely in both the lateral caudoputamen and upper frontoparietal cortex in the 8-, 15-, and 30-minute groups, partially in the cortex, and not at all in the caudoputamen in the 60-minute group. The histology showed that the caudoputamen was either normal or had mild neuronal injury in the 8-minute group and invariably had some degree of neuronal death in the 15-, 30-, and 60-minute groups, whereas the cortex was either normal or had varying degrees of neuronal injury in all groups. No histological abnormalities were seen in the sham-operated rats. Our data suggest that acute ADCav reversal does not always predict tissue recovery from ischemic injury and that temporary focal ischemia for even 8-minute duration can cause delayed neuronal death that is more severe in the caudoputamen where the initial ADCav decline was greater than in the cortex.

Animals↗