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PubMed1995

Multivariate analysis of factors influencing the functional recovery after finger replantation or revascularization.

A multivariate statistical analysis was utilized to study the influence of the four preoperative (age, mechanism of injury, level of injury, and type of amputation) and one postoperative (rehabilitation) variables on the functional recovery of the replanted or revascularized finger. Statistically significant differences are summarized as follows. The young age group have a better functional recovery due to better sensory recovery than the old age group. The crush injury group have a better functional recovery, with better scores in motion and patient satisfaction, than the avulsion injury group. The middle phalangeal injury group have a better functional recovery, with better score in motion and sensation than the proximal phalangeal injury group. There is no statistically significant difference in functional recovery between the revascularized and replanted fingers, but there is a significantly better sensory recovery in the revascularized finger. The rehabilitation group has a better functional recovery, with better score in motion, subjective symptoms, and patient satisfaction, than the nonrehabilitation group.

Adult↗

PubMed1999

Patterns of movement and orientation during caching and recovery by Clark's nutcrackers, Nucifraga columbiana.

Clark's nutcrackers regularly store large numbers of pine seeds and remember the locations of the cached seeds. Although they are very accurate, they do make some errors during recovery. In an attempt to determine whether any behaviours during caching predicted the occurrence of errors during recovery, we videotaped Clark's nutcrackers while they cached and recovered seeds under laboratory conditions. We used the videotapes to develop complete, quantitative descriptions of caching and recovery behaviour, with an emphasis on body orientation and directions of movement. During caching, the birds showed the greatest change in their orientation and direction following cache creation. During cache recovery, in contrast, body orientation changed most following successful recovery of a seed. When orientation while making a cache was compared with orientation when recovering the same cache, orientations were similar more often than would be expected by chance. However, this consistency of direction was not related to the accuracy of cache recovery, indicating that such consistency is not necessary for accurate cache recovery. The location in which the birds chose to place their caches was the only variable that predicted the location of probes during recovery. Copyright 1999 The Association for the Study of Animal Behaviour.

Journal Article↗

PubMed1999

Intranigral transplants of GABA-rich striatal tissue induce behavioral recovery in the rat Parkinson model and promote the effects obtained by intrastriatal dopaminergic transplants.

Intrastriatal transplantation of fetal ventral mesencephalon (VM) is currently explored as a potential clinical therapy in Parkinson's disease (PD). Although providing substantial benefit for the patient, behavioral recovery so far obtained with intrastriatal VM grafts is not complete. Using the 6-hydroxydopamine lesion model of PD, we show here that near-complete restoration of the striatal dopamine (DA) innervation can be achieved by multiple intrastriatal microtransplants of fetal DA cells; nevertheless, complete recovery in complex sensorimotor behaviors was not obtained in these animals. In line with the current model of basal ganglia function, this suggests that the lesion-induced overactivity of the basal ganglia output structures, i.e., the substantia nigra (SN) and the entopeduncular nucleus, may not be completely reversed by intrastriatal VM grafts. In the present study, we have transplanted fetal VM tissue or fetal striatal tissue, as a source of DA and GABA neurons, respectively, into the SN of DA-depleted rats. Intranigral VM grafts induced behavioral recovery in some sensorimotor behaviors (forelimb akinesia and balance tests), but the effect did not exceed the recovery observed after intrastriatal VM grafts. Intranigral grafts of striatal tissue induced a pattern of functional recovery which was distinctly different from that observed after intranigral VM grafts, and recovery in coordinated forelimb use in the paw-reaching test was even more pronounced than after intrastriatal transplantation of VM cells. Combined transplantation of DA neurons into the striatum and GABA-rich striatal neurons into the SN induced additive effects of behavioral recovery observed in the forelimb akinesia test. We propose that intranigral striatal transplants, by a GABA-mediated inhibitory action, can reduce the overactivity of the host SN projection neurons and can induce significant recovery in complex motor behavior in the rat PD model and that such grafts may be used to increase the overall functional efficacy of intrastriatal VM grafts.

Animals↗

PubMed1991

Neuroplasticity following traumatic brain injury: a study of GABAergic terminal loss and recovery in the cat dorsal lateral vestibular nucleus.

Terminal loss and recovery were assessed in the cat dorsal lateral vestibular nucleus (dLVN) following diffuse axonal damage caused by experimental traumatic brain injury. Using sterile technique, anesthetized adult cats received a moderate fluid-percussion traumatic brain injury. After predetermined survival periods of 7-368 days, the animals were perfused and the dLVN prepared for the immunocytochemical visualization of GABAergic puncta/terminals at the light (LM) and electron (EM) microscopic levels. In controls, the Deiters' neuronal somata within the dLVN were encompassed by numerous GABA-immunoreactive puncta/terminals. Within 7 days of injury, axonal damage was seen scattered throughout the dLVN, and associated with this, some neuronal somata demonstrated a dramatic loss of perisomatic GABA-immunoreactive puncta, while other somata appeared unchanged. Ultrastructural examination demonstrated that the loss of immunoreactive puncta observed with LM was directly correlated with the presence of degenerating GABAergic terminals. Overall, these neuronal somata showed a reduction of perisomatic puncta/terminals to values approximately 25% of controls. Over a thirty day posttraumatic course, this pattern of scattered perisomatic puncta/terminal loss persisted, with some puncta/terminal return by 60 days postinjury. During the next six months, a recovery of the immunoreactive puncta/terminals was observed in relation to the deafferented somata, with perisomatic terminal numbers now reaching 75% of control values. Over the 7 to 12 month postinjury period, recovery continued, with virtually complete recovery observed in the later phases of this period. Importantly, throughout this recovery period, there was a consistent correlation between the light and electron microscopic findings. The observed diffuse pattern of terminal loss, followed a prolonged adaptive recovery process, suggests that traumatic injury with its attendant diffuse axonal injury and related diffuse deafferentation creates a unique environment for rather complete and adaptive synaptic recovery. As diffuse axonal injury is a common feature of human traumatic brain injury, we believe that these studies, performed in cat, help explain some of the initial morbidity as well as some of the partial recovery seen in head-injured man.

Animals↗

PubMed1988

Spared-root deafferentation of a cat's hindlimb: hierarchical regulation of pathways mediating recovery of motor behavior.

Previous studies showed that after complete hindlimb deafferentation in cats, the ipsilateral descending pathways mediated recovery of overground, goal-directed locomotion and accurate placement of the deafferented limb. In the present study deafferentations sparing one dorsal root (L6) were performed to see if the descending systems would still be responsible for the recovery. The partially deafferented hindlimb is initially impaired in postural reflexes and accurate placement during locomotion but considerable recovery occurs. A similar pattern of severe impairment and subsequent recovery is observed in cats in which the only lesion is L1 hemisection. When a hemisection is added 6 months later to chronic spared-root deafferentation the recovery (from the latter lesion) is temporarily reversed but the animals recover again in a fashion similar to that after hemisection alone. Since there is no recovery of overground locomotion when hemisection is added to complete deafferentation but there is when deafferentation is incomplete, the descending pathways apparently are not responsible for maintaining the recovery when one dorsal root is spared as they are when all are cut. The results suggest that a competitive or hierarchical control over residual systems may regulate recovery of motor function.

Animals↗

PubMed1981

Abnormal recovery of DNA replication in ultraviolet-irradiated cell cultures of Drosophila melanogaster which are defective in DNA repair.

Cell cultures prepared from embryos of a control stock of Drosophila melanogaster respond to ultraviolet light with a decline and subsequent recovery both of thymidine incorporation and in the ability to synthesize nascent DNA in long segments. Recovery of one or both capacities is absent or diminished in irradiated cells from ten nonallelic mutants that are defective in DNA repair and from four of five nonallelic mutagen-sensitive mutants that exhibit normal repair capabilities. Recovery of thymidine incorporation is not observed in nine of ten DNA repair-defective mutants. On the other hand, partial or complete recovery of incorporation is observed in all but one repair-proficient mutagen-sensitive mutant. Irradiated cells from two mutants that display no excision capacity exhibit a gradual arrest of thymidine incorporation within 20 h after the initial decline. This arrest of incorporation is not observed in mutants exhibiting only partial defects in excision repair. Recovery of the ability to synthesize nascent DNA in long segments is normal in cells from the two mutants that display no excision capacity, indicating that recovery does not depend upon the excision of pyrimidine dimers from cellular DNA. Recovery of that ability is not observed, however, in cells from one partially excision-defective mutant, two of three postreplication repair-defective mutants, two of four mutants defective in both excision and postreplication repair, and one of five repair-proficient mutagen-sensitive mutants. These results indicate that recovery of normal DNA replication in irradiated Drosophila cells depends upon the activity of several functions.

Animals↗

PubMed1987

The role of the monkey sensory cortex in the recovery from cerebellar injury.

The aim of the study was to investigate the contribution of the primary sensory cortex in the compensation of cerebellar deficits during self-paced movements. For this purpose, monkeys were trained on motor tasks which required goal-reaching and independent finger movements. The intermediate and lateral deep cerebellar nuclei and the sensory cortex were lesioned in isolation and in sequence and the course of motor recovery was studied on the test performances. The deep nuclei were lesioned by kainic acid injections, the sensory cortex was removed by ablation. Cerebellar lesions in isolation produced obvious deficits at proximal and distal joints, affecting both slow and fast motor adjustments. Only lesions of the anterior portions of the intermediate and lateral deep nuclear complexes produced deficiencies in voluntary movements. Lesions of the posterior portions produced postural disturbances. The process of recovery following cerebellar lesions was slow and, depending on the nature of the task, was found to be differentially disruptive for motor performances requiring fast and slow motor adjustments. The deficits at distal joints appeared to be more enduring than those at proximal joints. Sensory cortical lesions in isolation produced much less severe and more transient motor deficits. They consisted of hand clumsiness and their recovery was fast and reached higher levels of performance than following cerebellar lesions. When the sensory cortex was removed secondarily to a cerebellar lesion and after recovery from the cerebellar deficits, the initially recovered motor performance became much worse again (decompensation). Removal of the sensory cortex prior to a cerebellar lesion exaggerated the cerebellar deficits and severely limited their recovery. Slow and fast motor performances were completely abolished for three weeks following sequential lesions. Signs of recovery subsequently appeared and stabilized at low levels of performance by five to seven weeks. The effects of combined, sequential cerebellar and sensory cortical lesions were much worse than expected if the effects from the two lesions were merely additive. This indicates that there is some functional interrelationship between the sensory cortex and the cerebellum, which promotes compensation. The somatosensory cortex appears to play a crucial role in the process of recovery from cerebellar motor deficits and it is likely that sensation is an important component in the process of recovery. It is suggested that the sensory cortex exerts its compensatory actions via a structure or structures which receives convergent cerebellar and sensory cortical inputs.

Adaptation, Physiological↗

PubMed1975

Kinetics of inactivation and recovery of the slow inward current in the mammalian ventricular myocardium.

In order to study the kinetics of inactivation and recovery of the slow inward current in the mammalian ventricular myocardium voltage clamp experiments using the double sucrose gap technique were performed on isolated trabeculae and papillary muscles of cats. The separation of the slow inward current from the fast Na current was achieved by use of the conditioning clamp procedure. 1. The decay of the Ca current reflects the inactivation which develops due to depolarization. The rate of inactivation depends upon the membrane potential. Excess Ca (8.8 mM) accelerates the inactivation speed indicating that Ca ions not only act as charge carrier of the slow inward current but might influence in addition the kinetics of the slow membrane channel. In the presence of a lowered temperature a deceleration of inactivation (Q10 2.3) occurs. 2 If the membrane is repolarized a recovery process takes place restoring the availability of the slow membrane channel. As the inactivation the recovery rate depends upon the membrane potential. Excess Ca causes an acceleration whereas a decrease in temperature diminishes the recovery speed (Q10 2.3). Consequently, the Ca supply to the myocardial cell can be modified not only by changes of the transmembrane Ca concentration gradient or by an alteration of the Ca conductance of the slow channel but also by changes in the degree of recovery after a preceding Ca current. 3. Compared with the inactivation the recovery proceeds very slowly. Assuming that this slow recovery represents an inherent kinetic feature of the slow channel the kinetics of inactivation and removal of inactivation are not describable by a single inactivation variable (called as f by Reuter, 1973) which is of the Hodgkin-Huxley type. If a second inactivation variable (called as l) would be introduced additionally a formulation of the inactivation-recovery process of the slow membrane channel on the basis of the Hodgkin-Huxley model becomes feasible.

Action Potentials↗

PubMed1996

A comparison of the adrenocortical response during septic shock and after complete recovery.

OBJECTIVE: To compare the adrenocortical response to corticotropin during septic shock and after complete recovery. DESIGN: Prospective clinical study. SETTING: Multidisciplinary intensive care unit in a university hospital. PATIENTS: 20 consecutive patients surviving septic shock. All patients met the American College of Chest Physicians/Society of Critical Care Medicine criteria for septic shock. In addition, the presence of high-output circulatory failure with a cardiac index > 41/min per m2 was a criterion for enrollment in the study. Complete recovery from septic shock was defined as discontinuation of any supportive therapies. Severity of illness during septic shock and after recovery was graded using the Acute Physiology and Chronic Health Evaluation (APACHE) II scoring system. INTERVENTIONS: In each patient, two short corticotropin stimulation tests were done during septic shock and after recovery. MEASUREMENTS AND RESULTS: Basal cortisol levels recorded during septic shock and after recovery did not differ (medians: 18.8 vs 18.9 micrograms/dl). However, the response to corticotropin was significantly attenuated during septic shock when compared with the response after recovery (medians: 7.7 vs 14.7 micrograms/dl; p = 0.02). After recovery, patients' stress response was less, as indicated by a reduction in APACHE II scores (medians: 21 vs 5 points; p < 0.01). CONCLUSIONS: Adrenocortical response to corticotropin is attenuated in patients with septic shock and high-output circulatory failure compared to the response in the much less stressful condition after recovery. The attenuated adrenocortical responsiveness may be explained by effects of circulating mediators from the systemic inflammatory response.

APACHE↗

PubMed1992

Electrode recovery potential.

In some instances the same electrodes are used for stimulation and then for recording a bioelectric event immediately after the stimulus. However, after the current pulse there remains an electrode potential that decays quasiexponentially. We have designated this falling potential the electrode-recovery potential. This study investigated the recovery potentials of single electrodes of rhodium, stainless steel, platinum and platinum-iridium in contact with 0.9% saline at room temperature (25 degrees C) over a current density ranging from 0.1 to 100 mA/cm2 using a constant-current pulse. In all cases, with increasing current density, there was a decrease in the time for the electrode potential to fall to one half of the immediate post-stimulus value. Above about 20 mA/cm2 the decrease in recovery time was smooth with increasing current density. Below 20 mA/cm2, the recovery time was slightly irregular. The shortest recovery times were for platinum and platinum-iridium. The largest decrease in recovery time with increasing current density was for stainless steel, which decreased 10 fold from 0.1 to 100 mA/cm2. The recovery time for rhodium decreased about three-and-one half fold over the same current density range. It was found that the waveform of the recovery potential is not a simple exponential because the Warburg and Faradic components of the electrode-electrolyte interface are current-density dependent. In general, for all current densities studied (0.1-100 mA/cm2), there was a sudden initial fall in electrode potential with cessation of current flow, followed by a very gradual nonexponential decrease in potential.

Electric Conductivity↗

PubMed1996

[The effects of age on onset and recovery from atracurium, rocuronium and vecuronium blockade].

UNLABELLED: Elderly patients may show an age-related decline in physiologic functions, which may be responsible for the prolonged duration of some neuromuscular blocking agents. Previous studies have yielded conflicting results as to the effects of these drugs in the elderly. METHODS: After obtaining informed consent and approval of the Ethics Committee, we compared onset and recovery times of single IV doses of atracurium, rocuronium, and vecuronium given to 108 patients divided into three groups according to age (18-50, 51-64, > or = 65 years). Following oxazepam premedication and fentanyl and thiopentone induction, patients were randomly allocated to receive atracurium, rocuronium or vecuronium (0.5, 0.6, or 0.1 mg/kg, respectively) in < or = 0.8 vol.% enflurane (end-tidal)-nitrous oxide anaesthesia. Muscular relaxation was assessed by electromyographic (EMG) recording of the adductor pollicis muscle after supramaximal single-twitch stimulation of the ulnar nerve every 10 s. Onset time and recovery to 25%, 75% and 90% of twitch control values (DUR25, 75, 90) were recorded. Creatinine clearance predicted from serum creatinine (Ccr) was correlated with recovery from neuromuscular block. RESULTS: Onset time was not different among groups or relaxants. The results showed a prolonged duration of action for atracurium (DUR75, DUR90), rocuronium (DUR25, DUR75), and vecuronium (DUR25) in the elderly. A number of patients did not reach DUR75 or DUR90. There was a significant relationship between age and failure to return to control values during recovery from neuromuscular block, especially after atracurium and rocuronium. Ccr showed a negative correlation with age for all relaxants, but a negative significant correlation between Ccr and recovery was found only for rocuronium. CONCLUSIONS: This study suggests that onset time for atracurium, rocuronium and vecuronium is not age-dependent. Recovery was prolonged in the elderly for all three relaxants. This effect appears to be secondary to changes in body composition and function accompanying the aging process. Neither atracurium nor vecuronium depends significantly on the kidney for elimination, but the negative correlation between Ccr and rocuronium suggests an appreciable role for the kidney in the elimination of this relaxant. The long recovery times observed in this study could also be related to enflurane anaesthesia. We suggest that failure of EMG responses to return to baseline values during recovery from neuromuscular block may be related to age, especially for atracurium and rocuronium.

Adolescent↗

PubMed1997

The association between blood lactate concentration on admission, duration of cardiac arrest, and functional neurological recovery in patients resuscitated from ventricular fibrillation.

OBJECTIVE: To assess the association between arterial lactate concentration on admission and the duration of human ventricular fibrillation cardiac arrest, and to what degree the arterial lactate concentration on admission is an early predictor of functional neurological recovery in human cardiac arrest survivors. DESIGN: Cohort study. Arterial lactate concentrations and out-of-hospital data concerning cardiac arrest and cardiopulmonary resuscitation were collected retrospectively according to a standardized protocol. Functional neurological recovery was assessed prospectively at regular intervals for 6 months. SETTING: Emergency department of an urban tertiary care hospital. PATIENTS: A total of 167 primary survivors of witnessed out-of-hospital ventricular fibrillation cardiac arrest. MEASUREMENTS: The association between arterial lactate concentration on admission, the duration of cardiac arrest, and functional neurological recovery was assessed. Further, we assessed whether admission concentrations of arterial lactate and duration of cardiac arrest can predict unfavorable functional neurological recovery. Functional neurological recovery was measured in cerebral performance categories (CPC). No or minimal functional impairment (CPC 1 and 2) was defined as favorable outcome; the remaining categories (CPC 3, 4 and 5) were defined as unfavorable functional neurological recovery. RESULTS: In 167 patients, a weak association between total duration of cardiac arrest and admission levels of lactate (r = 0.49, P < 0.001) could be shown. With increasing admission concentrations of arterial lactate functional neurological recovery was more likely to be unfavorable (OR 1.15 per mmol/l increase, 95% CI 1.04-1.27). Nevertheless, only at very high levels of lactate (16.3 mmol/l) could unfavorable neurological recovery be detected with 100% specificity, yielding a very low sensitivity of 16%. CONCLUSIONS: The arterial admission lactate concentration after out-of-hospital ventricular fibrillation cardiac arrest is a weak measure of the duration of ischemia. High admission lactate levels are associated with severe neurological impairment. However, this parameter has poor prognostic value for individual estimation of the severity of subsequent functional neurological impairment.

Aged↗

PubMed1996

Bone mineral density and turnover following forelimb immobilization and recovery in young adult dogs.

The purpose of this experiment was to study changes in bone mass, structure, and turnover in the canine forelimb after unilateral immobilization and recovery. The right forelimbs of 14 adult mongrel dogs were immobilized for 16 weeks. Six dogs served as controls. Seven immobilized and three control dogs were euthanized at the end of the immobilization period. Recovery consisted of 16 weeks of kennel confinement followed by 16 weeks of treadmill exercise. Seven once-immobilized and three control dogs were euthanized at the end of the recovery period. Bone mineral density of both the proximal (PBMD) and central (CBMD) radius was determined by dual X-ray absorptiometry. Standard histomorphometric endpoints for bone mass and turnover were determined in the cancellous bone of the proximal radius. After immobilization, PBMD, CBMD, and trabecular thickness were lower in the immobilized limb than in either the contralateral or control limbs (P < 0.05). Only CBMD remained significantly lower (P < 0.05) after recovery. At the end of immobilization, bone formation endpoints were significantly higher in the immobilized limb than both the contralateral and control limbs. Bone turnover was also significantly lower in the contralateral limb than in the immobilized and control limbs. After recovery, all differences in bone turnover had resolved. Immobilization of 16 weeks duration caused an elevation in cancellous bone formation rate and reduced bone density in both cortical and cancellous bone. After 32 weeks of recovery, turnover abnormalities disappeared, cancellous bone normalized, but cortical bone mass remained low. Recovery of cortical bone from immobilization takes longer than recovery of cancellous bone.

Animals↗

PubMed2002

Accelerated recovery from irradiation injury by angiotensin peptides.

PURPOSE: Angiotensin peptides have been shown to affect the proliferation and chemotaxis of multiple cell types. More recent studies in this laboratory have shown that angiotensin II (AII) can increase colony formation and proliferation by hematopoietic progenitors and mesenchymal cells in vitro. As white blood cell (WBC) recovery after bone marrow injury requires progenitor proliferation, the effect of AII and angiotensin (1-7) [A(1-7)], a non-hypertensive fragment of AII, on recovery from total body irradiation was evaluated in C57Bl/6 mice. MATERIALS AND METHODS: The effect of angiotensin peptides on hematopoietic recovery and the number of progenitors in the bone marrow of irradiated C57Bl/6 mice was evaluated. RESULTS: Treatment of animals with angiotensin peptides accelerated hematopoietic recovery and increased the number of hematopoietic progenitors in bone marrow and in the blood. The increase in WBC concentration continued for a longer time after cessation of AII therapy than after treatment with filgrastim. Specifically, the number of WBCs continued to increase 21 days after irradiation with 7 days of angiotensin peptide administration. In contrast, the number of WBCs increased through day 13 with 7 days of filgrastim administration. On day 35 after irradiation (28 days after the last treatment), AII was shown to have increased the number of CFU-GM in the bone marrow of irradiated mice, whereas filgrastim administration had not. Angiotensin peptides also reduced the drop in platelet concentration after irradiation and increased the number of megakaryocyte precursors and megakaryocytes in the bone marrow. Receptor blocking studies indicated that losartan, an antagonist of the angiotensin type 1 receptor, blocked recovery of WBC levels in response to treatment with AII. In contrast, the increase in WBC levels in response to treatment with A(1-7), a ligand for other angiotensin receptors, was not affected by losartan. CONCLUSIONS: These findings suggest that these peptides utilize distinct receptors in the stimulation of hematopoietic recovery. In summary, systemic administration of angiotensin peptides led to an acceleration in hematopoietic recovery after irradiation. These peptides act to stimulate the formation of bone marrow progenitors, thereby facilitating recovery after myelosuppressive irradiation.

Angiotensin I↗

PubMed1998

Barrier recovery is impeded at neutral pH, independent of ionic effects: implications for extracellular lipid processing.

Epidermal permeability barrier homeostasis requires the postsecretory processing of polar lipid precursors into nonpolar lipid products within the stratum corneum (SC) interstices by a family of lipid hydrolases. A specific requirement for beta-glucocerebrosidase (beta-GlcCer'ase), which exhibits a distinct acidic pH optimum, is particularly well documented. Therefore, we sought to determine whether the recovery of the barrier after acute insults requires acidification of the SC. We examined permeability barrier recovery by assessing changes in transepidermal water loss (TEWL), SC membrane ultrastructure utilizing ruthenium tetroxide (RuO4) postfixation, and beta-GlcCer'ase activity by in situ zymography at an acidic vs neutral pH. Barrier recovery proceeded normally when acetone-treated skin was exposed to solutions buffered to an acidic pH. In contrast, the initiation of barrier recovery was slowed when treated skin was exposed to neutral or alkaline pH, regardless of buffer composition. In addition, enhancement of the alkaline buffer-induced delay in barrier recovery occurred with Ca2+ and K+ inclusion in the buffer. Moreover, the pH-dependent alteration in barrier recovery appeared to occur through a mechanism that was independent of Ca(2+)- or K(+)-controlled lamellar body secretion, since both the formation and secretion of lamellar bodies proceeded comparably at pH 5.5 and pH 7.4. In contrast, exposure to pH 7.4 (but not pH 5.5) resulted in both the persistence of immature, extracellular lamellar membrane structures, and a marked decrease in the in situ activity of beta-GlcCer'ase. These results suggest first that an acidic extracellular pH is necessary for the initiation of barrier recovery, and second that the delay in barrier recovery is a consequence of inhibition of postsecretory lipid processing.

Animals↗

PubMed1995

Incomplete, delayed functional recovery late after reperfusion following acute myocardial infarction: "maimed myocardium".

The objective of the current editorial is to introduce a new concept ("maimed myocardium") that we believe describes more accurately the incomplete, delayed recovery of LV function that may occur late after reperfusion after AMI. It has been demonstrated previously that myocardium remains viable for a prolonged period in many patients with nonsustained coronary occlusion, despite the occurrence of myocardial necrosis; late reperfusion may result in myocardial salvage in reversibly ischemic (stunned) segments (complete recovery) and in intensely injured (maimed) segments that display partial return of LV function over time (incomplete recovery). Clinically, the basis for maimed myocardium is the observation that delayed, LV functional recovery may occur in partially infarcted segments where there has been an antecedent ischemic insult of sufficient duration to result in some degree of myocardial necrosis. Certain acute coronary syndromes characterized by nonsustained coronary occlusion followed by spontaneous reperfusion (e.g., non-Q-wave AMI) or drug-induced reperfusion induced by the exogenous administration of thrombolytic therapy are associated with incomplete, delayed recovery of LV function as detected clinically by partial improvement in serial radionuclide-ejection measurement, enhanced metabolic integrity of cardiac tissue by F-18 deoxyglucose myocardial imaging, and scintigraphic findings of reverse thallium redistribution--findings that support the presence of partially viable myocardium that has been incompletely salvaged during reperfusion late after AMI. Experimentally, delayed LV functional recovery has been reported in animal models in which prolonged coronary occlusion (hours to days) followed by reperfusion is associated with late recovery of regional LV function in myocardial segments subtending border (stunned) zones and central infarct (maimed) zones. In studies in animals and human beings, postextrasystolic potentiation and pharmacologic inotropic interventions may augment maimed and stunned segments, although the magnitude of regional contractile reserve that can be unmasked with these interventions is quantitatively less in the maimed than in stunned segments. In summary, the propensity of intensely injured or partially infarcted LV segments to display intermediate functional recovery followed by reperfusion late after coronary occlusion suggests that even severely depressed but residually viable cardiac muscle can be salvaged incompletely over time.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1993

Continuously updated 12-lead ST-segment recovery analysis for myocardial infarct artery patency assessment and its correlation with multiple simultaneous early angiographic observations.

Early angiography may not adequately subgroup patients with myocardial infarction if cyclic changes in coronary flow occur frequently. From a pilot experience using a new 12-lead ST-segment monitor, a continuously updated, self-referenced ST-recovery analysis method was developed to quantify both instantaneous recovery, as a noninvasive marker of patency, and cumulative ST recovery over time, as a marker of the speed, stability and duration of reperfusion. In 22 patients with acute infarction in whom 44 observations of unique angiographic patency were noted within 6 hours of presentation, serial patency assessments simultaneous with all angiographic observations predicted coronary occlusion with 90% sensitivity and 92% specificity. Of the 22 patients, 11 (50%) had multiple ST trend transitions suggesting cyclic changes in coronary flow before catheterization. Speed, stability and duration of ST-segment recovery were defined by the time to first 50% ST recovery, total number of ST-trend transitions and patent physiology index (percentage of monitoring period showing ST recovery), respectively. Subgrouped angiographically, the median (interquartile range) for cumulative ST parameters with patent (n = 8) versus occluded (n = 14) arteries were, respectively--time to 50% recovery, 1.57 (1.16, 1.70) versus 0.17 (-0.47, 0.32) hours; number of reelevation/recovery events, 1.5 (1, 3) versus 3 (1, 3); and patent physiology index, 52 (47, 59) versus 50 (5, 73). Thus, continuous ST-segment recovery analysis appears to predict simultaneous angiographic patency over serial assessments, whereas cumulative parameters appear to contain independent information, probably because of patency changes before or after angiography.

Cardiac Catheterization↗

PubMed1989

Difference in recovery patterns of striatal dopamine content, tyrosine hydroxylase activity and total biopterin content after 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) administration: a comparison of young and older mice.

Striatal dopamine (DA) content, tyrosine hydroxylase (TH) activity, and total biopterin content were measured as parameters of recovery, after administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in 7-week-old (young) and 28-week-old (older) C57 BL/6 mice. After 10 consecutive days of injection of MPTP (30 mg/kg/day) young mice were sacrificed at one day and 2, 4, 8, 12 and 20 weeks; older mice (20 mg/kg/day) at one day and 4, 8, and 12 weeks. All 3 parameters were markedly reduced one day after the last injection of MPTP. During the observation period, the parameters showed a gradual and partial recovery. The recovery rates of the 3 parameters differed significantly, especially during the early phases of 2-8 weeks. Total biopterin content showed a greater rate of recovery than TH activity and TH activity, a greater rate of recovery than DA content. In the older mice group, the recovery of all 3 parameters was retarded significantly, and dissociation of the recovery rates between the 3 parameters was more prominent. The results of our present study suggest that, following neurotoxic injury, the recovery of biopterin may play a significant role in dopaminergic terminal regeneration.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗