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1.
The activity of the medial olivocochlear (MOC) efferent system in mustached bats, Pteronotus p. parnellii, was studied by monitoring changes in the mechanical properties of the cochlea. The changing properties were expressed by the decay time (DT) of cochlear microphonic potentials produced by transient-induced ringing (Henson et al., 1995). Tape-recorded roost noise (biosonar and communication sounds) produced sudden, marked decreases in DT when presented to the contralateral ear of animals adapted to the quiet. When the animals were first removed from their roosts the DT was relatively short (1.2-1.5 ms) but this gradually lengthened by about 0.5-1.0 ms as they rested in a quiet chamber. The time required to reach a stable, quiet-adapted state after noise exposure varied with SPL and exposure time; in many experiments recovery was in the range of 90-120 min. When quiet-adapted bats were isolated and allowed to fly and echolocate for 20 min, the DTs measured within a few minutes after the end of the flight were also short and only slowly returned to longer preflight values. The administration of a single dose of gentamicin, which blocks MOC effects, greatly reduced the amount of suppression (damping) observed after periods of noise and echolocation sound exposure. We conclude that tonic MOC activity is induced by the natural vocalizations and roost noise and this activity probably regulates and protects the highly resonant cochlear partition.  相似文献   

2.
Reactive oxygen species (ROS) generation may play a role in ototoxicity, however, the specific effects of ROS generation upon cochlear function are unstudied. Therefore, guinea pig cochleas were instilled with artificial perilymph (AP), H2O2, or confirmed generating systems for the superoxide anion (O2-) or the hydroxyl radical (OH.), or with an ROS system plus its respective scavenger -catalase (CAT), superoxide dismutase (SOD) or deferoxamine (DEF). O2- generating system instillation led to significantly greater mean high frequency compound action potential (CAP) threshold shifts at 10 and 120 min post infusion than seen in AP control or SOD/O2- groups. H2O2 group CAP threshold shifts were significantly greater than control and CAT/H2O2 group values at 10 (16-30 kHz), and 120 min (above 12 kHz). OH generating system instillation led to significantly greater CAP threshold shifts at 10 (12-30 kHz) and 120 min (above 6 kHz) than seen in control or DEF/OH groups. No significant CAP differences were found between controls and scavenger/ROS groups. Mean 1.0 microV cochlear microphonic isopotential curve shift values did not systematically differ among groups. The rapid degradation of high frequency CAP threshold sensitivity seen here may provide insight into the portion of cochlear dysfunction which is ROS-mediated following noise, radiation or chemical exposures.  相似文献   

3.
Lidocaine was applied to the round window (RW) in order to localize its site of action in the cochlea. Cochlear microphonic (CM), summating potential (SP), and compound action potential (CAP) input/output functions were measured to a 16 kHz tone burst to assess the functional changes of the cochlea. In separate experiments, the effect of lidocaine on the whole cell current of isolated outer hair cells (OHC) was studied. A dose of 2 microliters of 40 mM lidocaine in saline solution, when applied to the RW, caused a small change in all measured variables, indicating a passage of the drug through the RW membrane to sites of action. However, 160 mM of lidocaine further decreased CM, SP, and CAP by a total of 40% from the control. A partial recovery occurred for CM during the 30 min follow-up period. CAP and SP continued to decline. In isolated OHCs, lidocaine decreased the whole cell current in a dose-dependent fashion. The KD for lidocaine effect on OHCs was 7 mM. Our in vivo results indicate that lidocaine affects OHCs and reduces CM, causing a subsequent reduction in SP and CAP. The increased effect of lidocaine on CAP and SP, while CM is recovering, suggests an additional specific effect of lidocaine on the cochlear nerve and/or on inner hair cells. Considering that lidocaine alters OHC current (in isolated hair cells) and that lidocaine does not affect endocochlear potential [Laurikainen et al. Acta Otolaryngol (Stockh) 1991: 112: 800-9], the observed CM changes are most likely due to an in vivo effect on OHCs. Thus, the early effect of lidocaine on the cochlea appears to be due to a significant change in organ of Corti function, rather than to direct anesthesia of the cochlear nerve. Later, an independent effect of the drug may occur on neural tissues in the inner ear.  相似文献   

4.
The role of the inner hair cells (IHCs) in generating the cochlear summating potentials (SP) was assessed by measuring SP, cochlear nerve action potentials (CAP), cochlear microphonics (CM) and 2f1-f2 distortion product otoacoustic emissions (DPOAEs) in 15 chinchillas with either acute chemical de-afferentation, accomplished by applying kainic acid to the round window, or surgical de-afferentation and basal IHC loss, which developed within two months after sectioning the auditory nerve. In the auditory nerve sectioned ears, type I ganglion cells disappeared whereas most, if not all, type II ganglion cells were still present. Histological analysis of surface preparations and sections through the modiolus verified the de-afferentation in both models and showed a large IHC loss at the base of the cochlea in the ears with the auditory nerve sectioned while other structures of the cochlea remained intact. Unoperated (left) ears of 9 animals served as controls. CM and DPOAEs were normal in all ears whereas the CAP was substantially depressed in de-afferented ears. Comparisons among the SP input-output functions suggest that (1) the IHCs are the major generator of SP recorded from the round window in chinchilla, in particular at low to moderate stimulus levels, (2) the SP recorded from the round window largely reflects the responses from hair cells at the base of the cochlea, and (3) kainic acid results in an increase of SP amplitude to high-level stimuli whereas the SP to low- to moderate-level stimuli remains in the normal range.  相似文献   

5.
Making an ideal animal model of cochlear microcirculatory disorders is an important method in studying inner ear microcirculation. After intravenous injection of Rose bengal (30 mg/kg), the lateral wall of the cochlea of guinea pigs was illuminated with green light (wavelength: 550 +/- 20 nm). The Rose bengal photoactivatedly produces oxygen radicals and oxygen singlets, which subsequently damage the endotheliocytes to cause adhesion and aggregation of platelets in the small vessels. After the photo-illumination, cochlea blood flow reduced sharply, and CAP amplitude decreased in 10 min and disappeared completely in about 20-40 min. With prolongation of time, stria vascularis, Corti's organ and spiral ganglion cells showed further disintegration due to ischemia, which resembled the histopathological changes of the cochlea with microcirculatory disorders. Therefore, this animal model may be considered an ideal one for studying the mechanisms of hearing loss that was caused by microcirculatory disorders and also for evaluating the effects of drugs on microcirculation of damaged cochlea.  相似文献   

6.
It is well documented that damage to the chick cochlea caused by acoustic overstimulation or ototoxic drugs is reversible. Second-order auditory neurons in nucleus magnocellularis (NM) are sensitive to changes in input from the cochlea. However, few experiments studying changes in NM during cochlear hair cell loss and regeneration have been reported. Chicks were given a single systemic dose of gentamicin, which results in maximal hair cell loss in the base of the cochlea after 5 days. Many new hair cells are present by 9 days. These new hair cells are mature but not completely recovered in organization by 70 days. We counted neurons in Nissl-stained sections of the brainstem within specific tonotopic regions of NM, comparing absolute cell number between gentamicin- and saline-treated animals at both short and long survival times. Our data suggest that neuronal number in rostral NM parallels hair cell number in the base of the cochlea. That is, after a single dose of gentamicin, we see a loss of both cochlear hair cells and NM neurons early, followed by a recovery of both cochlear hair cells and NM neurons later. These results suggest that neurons, like cochlear hair cells, can recover following gentamicin-induced damage.  相似文献   

7.
We studied the post-resuscitation syndrome in 42 healthy dogs after normothermic ventricular fibrillation cardiac arrest (no blood flow) of 7.5, 10, or 12.5 min duration, reversed by standard external cardiopulmonary resuscitation (CPR) (< or = 10 min) and followed by controlled ventilation to 20 h and intensive care to 72 h. We reported previously, in the same dogs, no difference in resuscitability, mortality, or neurologic outcome between the three insult groups. There was no pulmonary dysfunction, but post-arrest cardiovascular failure, of greater severity in the 12.5 min arrest group. This report concerns renal, hematologic, hepatic and bacteriologic changes. Renal function recovered within 1 h after arrest, without permanent dysfunction. Clotting derangements at 1-24 h postarrest reflect transient disseminated intravascular coagulation with hypocoagulability, more severe after longer arrests, which resolved by 24 h after arrest. Hepatic dysfunction was transient but more severe in the animals that did not recover consciousness and correlated with neurologic dysfunction, but not with brain histologic damage. Bacteremia was present in all animals postarrest. We conclude that in the previously healthy organism after cardiac arrest of 7.5-12.5 min no flow, visceral and hematologic changes, although transient, can retard neurologic recovery.  相似文献   

8.
Biochemical and pharmacological evidence supports a role for nitric oxide (NO) in the cochlea. In the present experiments, we tested sodium nitroprusside (SNP), an NO donor, applied by intracochlear perfusions on sound-evoked responses of the cochlea (CM, cochlear microphonic; SP, summating potential; EP, endocochlear potential; CAP, compound action potential) and in vitro on outer hair cell (OHC) voltage-induced length changes and current responses. In vivo application of SNP in increasing concentrations (10, 33, 100, 330 and 1000 microM) reduced all sound-evoked responses starting at about 300 microM. The responses continued to decline after a postdrug wash. At 1 mM SNP decreased EP slowly (approximately 80 min) whereas at 10 mM it reduced EP more rapidly (approximately 20 min). Ferricyanide (1 mM) and S-nitroso-N-acetylpenicillamine (SNAP; 1 mM) had no effect on sound-evoked cochlear potentials. Ferricyanide (1 mM and 10 mM) and ferrocyanide (10 mM) had no effect on EP. In vitro, SNP (10 mM) significantly reduced both OHC voltage-induced length changes and whole-cell outward currents. Results suggest that SNP, possibly acting by released NO, influences cochlear function through effects at the stria vascularis and at the OHCs.  相似文献   

9.
Surface preparations showed that the "jerker" mutant mouse has a normal total number of cochlear hair cells when young but that these progressively degenerate with increasing age. However, no gross 8th nerve action potentials or cochlear microphonics could be detected at the round window in 12–20 day old mutants, although many hair cells still appeared to be intact at these ages. Light microscopy of surface preparations is apparently a poor indicator of the functional state of hair cells, at least in genetically determined inner-ear defects. The endocochlear potential (EP) was significantly higher in the mutants than in controls during the maturation of the cochlea. During anoxia induced in adults, EP fell to a significantly less negative value in mutants than in controls. This abnormality in the anoxia potential probably reflects an organ of Corti abnormality. (30 ref) (PsycINFO Database Record (c) 2010 APA, all rights reserved)  相似文献   

10.
Although brain ischemia has been extensively studied using diffusion-weighted magnetic resonance imaging, most studies performed so far have not had adequate time resolution to follow the temporal changes in the water apparent diffusion coefficient (ADC) in hyperacute ischemia. Using diffusion echo planar imaging, we obtained ADC maps (calculated from measurements made with 8 b-values) with a time resolution of 43 s in a feline model of global brain ischemia and reperfusion. Different protocols were performed: 10-min hypoperfusion, 10- and 22-min ischemia followed by reperfusion, and cardiac arrest. ADC values were obtained from white matter of the internal capsule and from the thalamus. Cortical gray matter measurements were not deemed reliable due to the close proximity of CSF in the cortical sulci. Following occlusion, the ADC declined in the thalamus to < 2 SD of its normal baseline value within 1.5-2.5 min. This decay was exponential with a time constant (tau +/- SD) of 6.0 +/- 2.6 min; no further decrease in the ADC was observed 10 min following ischemia. Following reperfusion, in animals that showed ADC recovery, the ADC began increasing immediately, returning to its preischemic value in approximately 15 min. No significant ADC changes were observed during hypoperfusion. Following cardiac arrest, the decay of ADC was more rapid in the thalamus (tau = 2.6 +/- 0.6 min) than in white matter (tau = 6.6 +/- 1.8 min). We observed that the ADC at 40 min after cardiac arrest was similar to the ADC at 10 min after ischemia. Given that all animals subjected to 10-min ischemic episodes showed ADC recovery with reperfusion, doubt is cast on whether it is possible to define a threshold value of the ADC below which brain tissue is irreversibly damaged. Finally, despite variability in the time constants of the ADC decay induced by ischemia, the ADC values at 10 min were very similar in all the animals. This suggests that when blood flow is diminished sufficiently to induce an ADC reduction, differences in perfusion affect the rapidity of the decrease but not the final asymptotic value reached.  相似文献   

11.
After exposure to a loud, non-traumatic low-frequency tone, auditory thresholds are elevated. Thresholds recover to normal in a non-monotonic manner, decreasing rapidly at first before increasing again, until they finally decrease monotonically towards normal. Although the transient elevation of thresholds after the initial improvement was originally called a 'bounce' by Hirsh and Ward (1952), Kemp (1986) suggests that the initial rapid recovery is the oddity: under some conditions a low-frequency tone can produce hypersensitivity in otoacoustic emissions, psychophysical thresholds, and perceived loudness (Kemp's 'bounce') without a later elevation of threshold (Hirsh and Ward's 'bounce'). Kemp also suggested that the transient hypersensitivity was caused by changes in the sensitivity of the active process within the cochlea. We have investigated the origin of this transient hypersensitivity (Kemp's bounce) in guinea pigs, recording cochlear potentials (CM, CAP, SP and EP) and otoacoustic emissions (DPOAEs at f2-f1, 2f1-f2, 2f2-2f1 and 3f1-2f2). Our results indicate that the bounce does not require neural activity, but is probably produced by non-neural cochlear mechanisms, possibly a transient decrease in the permeability of the organ of Corti which produces a small but significant change in standing current through outer hair cells. At least part of these changes, which are reduced as the stimulation frequency increases, and absent above 2 kHz, seem due to a small and transient movement of the cochlear partition towards scala tympani, probably due to a transient osmotic imbalance.  相似文献   

12.
Dorsal column axons of the rat spinal cord are partially protected from anoxic injury following blockade of voltage-sensitive Na+ channels and the Na+/--Ca2+ exchanger. To examine the potential contribution of voltage-gated Ca2+ channels to anoxic injury of spinal cord axons, we studied axonal conduction in rat dorsal columns in vitro following a 60-min period of anoxia. Glass microelectrodes were used to record field potentials from the dorsal columns following distal local surface stimulation. Perfusion solutions containing blockers of voltage-gated Ca2+ channels were introduced 60 min prior to onset of anoxia and continued until 10 min after reoxygenation. Pharmacological blocking agents which are relatively selective for L- (verapamil, diltiazem, nifedipine) and N- (omega-conotoxin GVIA) type calcium channels were significantly protective against anoxia-induced loss of conduction, as was non-specific block using divalent cations. Other Ca2+ channel blockers (neomycin and omega-conotoxin MVIIC) that affect multiple Ca2+ channel types were also neuroprotective. Ni2+, which preferentially blocks R-type Ca2+ channels more than T-type channels, was also protective in a dose-dependent manner. These data suggest that the influx of Ca2+, through L-, N- and possibly R-type voltage-gated Ca2+ channels, participates in the pathophysiology of the Ca2+-mediated injury of spinal cord axons that is triggered by anoxia.  相似文献   

13.
Coronary thrombosis was induced in 14 miniature pigs by means of direct current. The induction electrode was introduced via the common carotid artery into the coronary artery. The intensity of current (1 mA) and the duration of current flow (60 min) were kept constant in all the experimental animals. 6 miniature pigs survived the period of observation (48 h). In all instances, an injury to the intima was the morphopathological location factor. With the exception of one animal, which died after an induction time of 60 min, coronary thrombosis was stated in all the miniature pigs. The experimental arrangement which produces closed-thorax coronary thrombosis is suited for cardiosurgical, physiopathological and pharmacological experiments, especially because the anatomy and the degree of development of the porcine heart are most similar to those of the human heart.  相似文献   

14.
Exposure to turbulence, an environmental stimulus, produces behavioral adaptation in the Aplysia siphon-withdrawal response (SWR). The authors show that the duration and spatial extent of turbulence influence adaptation recovery. In terms of duration, recovery in whole animals and reduced preparations (tail, siphon, and CNS) was more rapid after longer exposures to turbulence (10 min) than after briefer exposures (10 s-5 min). In terms of spatial extent, recovery in reduced preparations was more rapid after diffuse turbulence (tail and siphon together) compared with focal turbulence (siphon alone). Furthermore, spatial extent and duration interact: Duration regulates recovery only when turbulence is diffuse. Results suggest that SWR adaptation reflects a composite of cellular processes, including short-term synaptic enhancement in L30 inhibitory interneurons. (PsycINFO Database Record (c) 2010 APA, all rights reserved)  相似文献   

15.
Some cochlear implant patients achieve better speech recognition with pulsatile electrical stimulation presented at high rates. The present study aimed to explore, in an animal model of cochlear implants, how the excitability of the cochlear nerve is affected by pulsatile electrical stimulation delivered at high rates, of up to 1,000-2,000 pulses per second (pps). Adult rats (n=23) were implanted with two or three stimulating electrodes in the left cochlea. In four of these rats, the left cochlea was deafened by local perfusion with 1 per cent or 4 per cent neomycin solutions prior to implantation. Pulsatile stimuli consisted of 20 micros electrical pulses, delivered in trains of 200 ms duration, separated by a pause of 200 ms. The pulse rates ranged from 100 to 2,000 pps (intra-train pulse rate). Electrically evoked compound action potentials (ECAPs) of the cochlear nerve were recorded either intracochlearly or from epidural electrodes (extra-cochlearly). With increasing pulse rates, the average ECAP amplitude decreased, whereas the average ECAP latency and its variability (SD) increased. For rates above 300 pps, the amplitude of the ECAP to the individual successive pulses delivered in the train progressively decreased during the initial part of the train, corresponding to a short-term adaptation of the cochlear nerve. This effect progressively increased for pulse rates ranging from 300 to 2,000 pps. In addition, there was a phenomenon of long-term adaptation, as indicated by a decrease in the amplitude of the ECAP to the first pulse of the train, indicating that the pause of 200 ms between each train was not long enough for full recovery of the cochlear nerve. This long-term adaptation was progressively more pronounced for increasing pulse rates. To characterize further the recovery in excitability of the cochlear nerve, forward masking experiments were conducted, showing a decrease of the ECAP amplitude when the interval between the first pulse (masker) and the second pulse (probe) was shorter than 2 ms. This ECAP decrease was slow for intervals between 2 and 1 ms and then abrupt for shorter intervals. The observations described above were similar for extra- and intra-cochlear recordings and were little, if at all, affected by treatment of the cochlea with neomycin.  相似文献   

16.
Effects of azelnidipine, a dihydropyridine derivative, on stunned myocardium were examined in anesthetized open-chest dogs. The left anterior descending (LAD) coronary artery was ligated for 20 min and then released for 60 min. Dimethyl sulfoxide (DMSO), the solvent of azelnidipine, or azelnidipine (0.03, 0.1 or 0.3 mg/kg) was injected i.v. 20 min before ligation. Segment shortening was determined by sonomicrometry. The levels of high-energy phosphate were measured in 60-min reperfused hearts. Azelnidipine at 0.1 and 0.3 mg/kg significantly decreased diastolic blood pressure and increased % segment shortening. The increase in % segment shortening due to azelnidipine appeared to be abolished by propranolol and atropine pretreatment. Ischemia significantly decreased % segment shortening in all groups. The % segment shortening that had been decreased by ischemia recovered during reperfusion, but did not reach its preischemic level in each group. In the 0.1 and 0.3 mg/kg of azelnidipine-treated dogs, a significant enhancement of % segment shortening recovery during reperfusion was observed, as compared with that in the DMSO-treated dogs. Azelnidipine did not affect the high-energy phosphate levels in 60-min reperfused hearts. In conclusion, azelnidipine improved the contractile dysfunction in stunned myocardium, without any preservation of high-energy phosphate.  相似文献   

17.
We have compared the duration of motor block produced by four local anaesthetics administered into a chronically implanted subarachnoid catheter in rabbits. Each group (n = 6) received four different doses of amethocaine, bupivacaine, lignocaine or procaine, and the duration of the resulting motor block was assessed. Dose-response curves were plotted for each drug. As a measure of activity of the anaesthetics, we used the dose of each drug required to produce block of 60-min duration (D60 min) and the correlation between D60 min and different drug properties was examined. An inverse linear correlation (r = 0.995; P < 0.01) was observed between log D60 min and the log of the partition coefficient of the local anaesthetics. No correlation was found between the effect and degree of protein binding, pKa or molecular weight. These results suggest that, in spinal anaesthesia, the partition coefficient could be used as a predictor of the duration of anaesthetic action.  相似文献   

18.
We studied the effect of halothane on regional myocardial function during acute ischemia and reperfusion in an open-chest pig model. Anesthesia was induced with thiopental and fentanyl and maintained with an intravenous (IV) infusion of pentobarbital and fentanyl. Regional myocardial function was studied with microsonometers placed in the subendocardium supplied by the left anterior descending coronary (LAD) and circumflex coronary artery (LX). Systolic function was evaluated with reference to the end-systolic pressure-length relationship (ESPLR) and regional systolic shortening. Diastolic dysfunction was studied with postsystolic shortening (PSS). Ischemia was induced with 15 min of total occlusion of the LAD artery, and thereafter reperfusion was allowed for 120 min. Five groups were studied: one group received only pentobarbital and fentanyl (n = 10); the other groups received halothane 0.2% (n = 5), 0.4% (n = 7), 0.6% (n = 5), and 0.8% (n = 5). The pentobarbital and fentanyl infusion was adjusted in the halothane groups in an effort to maintain arterial blood pressure and heart rate within specified limits (when possible). Results indicate that regional dysfunction during acute ischemia was equal among all the groups. However, on reperfusion, halothane significantly reduced the incidence of ventricular arrhythmias. Halothane (0.6% and 0.8%) was associated with less regional postischemic systolic dysfunction during reperfusion when compared to the other groups. Hearts subjected to 0.6% and 0.8% halothane also were less stiff at the end of systole (i.e., the extrapolated ventricular volume at zero ventricular pressure was less) after 120 min reperfusion compared to animals receiving less halothane. However, diastolic dysfunction was equal among the groups during reperfusion. We conclude that, in this model, administration of halothane is associated with improved recovery of regional systolic function and potentially beneficial pressure-length relations at the end of systole after acute severe myocardial ischemia and reperfusion. Furthermore, administration of halothane was associated with fewer reperfusion arrhythmias compared to animals not receiving halothane.  相似文献   

19.
The flow threshold for alterations of the in vitro [3H]cyclic AMP (cAMP) binding, an indicator of the total amount of particulate cAMP-dependent protein kinase, was evaluated in the gerbil brain after 30 min, 2 h, and 6 h of unilateral common carotid artery occlusion, respectively. The autoradiographic method developed in our laboratory enabled us to measure the [3H]cAMP binding and local CBF in each region of the same brain. The ischemic flow thresholds for reduction of the cAMP binding in the hippocampus CA1 were 18, 34, and 49 ml 100 g-1 min-1 after 30-min, 2-h, and 6-h ischemia, respectively. These values were higher than those in other regions such as the hippocampus CA, and temporal cerebral cortex in each duration of ischemia. These findings indicate that (a) the ischemic flow threshold for perturbation of the cAMP system may be higher in the hippocampus CA1 than in other brain regions, suggesting that the hippocampus CA1 could be especially vulnerable to acute ischemic stress; and (b) the level of the aforementioned threshold may increase progressively during the time course of ischemia in particular regions such as the hippocampus CA1 and CA3, suggesting that the duration of ischemia exerts a definite influence on the viability of the ischemic neuronal cells in these regions.  相似文献   

20.
Renal function can be severely impaired through injuries sustained after both short and prolonged periods of complete ischemia. The magnitude of renal dysfunction resulting from these conditions and their reversibility depend on the duration of anoxia. In this study, we used a Sprague-Dawley rat model (5 to 7 rats in each group) to study the pathogenesis of short-term ischemia (30, 60, and 120 min)/reperfusion (2, 4, 24 h, 1 wk, and 3 wk) injury of the kidney under warm (room temperature) or cold (4 degrees C) conditions. Ischemia was induced by clamping the renal artery. Changes in kidney weight, histopathology, concentrations of serum thromboxane and leukotriene, and tissue malonyldialdehyde (MDA) concentration, numbers of apoptotic bodies, and p53 expression in the kidney were compared with those of sham-operated rats. The results showed that the immediate increase in kidney weight due to inflammatory swelling was associated with simultaneous elevation of serum thromboxane and leukotriene levels. The changes in mediator levels were closely related to the duration of ischemia and temperature. Histologic structures were preserved better when renal artery clamping was done at 4 degrees C. MDA peroxidation products from the ischemic tissue prominently increased 1 week following ischemia; this paralleled a secondary increase in leukotriene levels. Flow cytometric detection of p53 oncoprotein showed a marked increase at 1 week following ischemia, which was accompanied by the development of apoptotic bodies in ischemic tissues. These changes were also closely related to the ischemic time and temperature during ischemia. This animal model may be useful for future studies of the prevention of ischemia/reperfusion injury of the kidney and for selection of effective antioxidants.  相似文献   

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