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PubMed2000

The catalytic subunit DNA-dependent protein kinase (DNA-PKcs) facilitates recovery from radiation-induced inhibition of DNA replication.

Exposure of cells to ionizing radiation inhibits DNA replication in a dose-dependent manner. The dose response is biphasic and the initial steep component reflects inhibition of replicon initiation thought to be mediated by activation of the S-phase checkpoint. In mammalian cells, inhibition of replicon initiation requires the ataxia telagiectasia mutated ( ATM ) gene, a member of the phosphatidyl inositol kinase-like (PIKL) family of protein kinases. We studied the effect on replicon initiation of another member of the PI-3 family of protein kinases, the catalytic subunit of DNA-dependent protein kinase (DNA-PKcs) by measuring either total DNA synthesis, or size distribution of nascent DNA using alkaline sucrose gradient centrifugation. Exposure of human cells proficient in DNA-PKcs (HeLa or M059-K) to 10 Gy inhibited replicon initiation in a time-dependent manner. Inhibition was at a maximum 1 h after irradiation and recovered at later times. Similar treatment of human cells deficient in DNA-PKcs (M059-J) inhibited replicon initiation to a similar level and with similar kinetics; however, no evidence for recovery, or only limited recovery, was observed for up to 8 h after irradiation. In addition a defect was observed in the maturation of nascent DNA. Similarly, a Chinese hamster cell line deficient in DNA-PKcs (irs-20) showed little evidence for recovery of DNA replication inhibition up to 6 h after irradiation, whereas the parental CHO cells showed significant recovery and an irs-20 derivative expressing the human DNA-PKcs complete recovery within 4 h. Normal kinetics of recovery were observed in xrs-5 cells, deficient in Ku80; in 180BR cells, deficient in DNA ligase IV; as well as XR-1 cells, deficient in XRCC4, an accessory factor of DNA ligase IV. Since all these cell lines share the DNA double strand break rejoining defect of M059-J and irs20 cells, the lack of recovery of DNA replication in the latter cells may not be attributed entirely to the prolonged presence of unrepaired DNA dsb. We propose that DNA-PKcs, in addition to its functions in the rejoining of DNA dsb and in DNA replication, also operates in a pathway that in normal cells facilitates recovery of DNA replication after irradiation.

Animals↗

PubMedDate not supplied

Morphometric evidence that the total number of synapses on Purkinje neurons of old F344 rats is reduced after long-term ethanol treatment and restored to control levels after recovery.

Clinical symptoms of alcohol abuse may be confused with symptoms of age-related neuropathologies in human patients. It is important, therefore, to determine the relationships between alcohol abuse and changes in brain structures in well-controlled studies of ageing subjects. Currently there is little well-documented information of this type available. The purpose of this study was to determine whether long-term ethanol treatment during ageing would lead to reductions in synaptic input to cerebellar Purkinje neurons (PN) of old F344 rats that: (1) were more severe than those attributable to ageing alone; (2) might be responsible for an ethanol-related deletion of dendritic segments of PN in old F344 rats shown previously in this laboratory. The total number of synapses per PN dendritic arbor was determined after ethanol treatment of old F344 rats for 40 weeks between 12 and 22 months of age and in similarly treated rats given a subsequent 20-week period of recovery between 22 and 27 months of age. Groups of age-matched rats fed a chow diet and water and rats pair-fed an isocaloric liquid diet lacking ethanol served as controls. The volume of the molecular layer per PN arbor and the numerical density of synapses in the molecular layer was determined from light microscopic preparations of a fixed volume of the cerebellar cortex. Photographic montages of the ultrastructure of the molecular layer of the cerebellum were also prepared from each rat for measurements of synaptic numerical densities. From the volume of the molecular layer per PN arbor and the numerical density of synapses in the molecular layer, the total number of synapses per PN arbor was estimated for each rat. There was a significant reduction in synapses in the old ethanol-treated rats relative to age-matched chow-fed rats. There were also significant interactions between recovery and treatment prior to recovery. During recovery, synaptic numbers in the old, ethanol-treated rats were restored to pre-recovery control levels whereas synaptic numbers in the old, chow-fed rats were significantly reduced during the same period of time. There were no significant diet- or age-related changes in synaptic numbers in the pair-fed control rats during treatment or recovery. The pattern of reduction in synaptic numbers during ethanol treatment and restoration of synaptic numbers during recovery from treatment paralleled the pattern of ethanol-related segment loss and recovery-related segment regrowth noted earlier in PN arbors of old F344 rats, suggesting that reductions in the numbers of synapses and deletion of terminal dendritic segments were causally related in this strain.

Age Factors↗

PubMed1993

Histochemical and physiological correlates of training- and detraining-induced changes in the recovery from a fatigue test.

BACKGROUND AND PURPOSE: The primary purpose of this study was to evaluate the effects of endurance training and detraining on the development of and recovery from fatigue induced by isokinetic exercise. It was our hypothesis that the rate of recovery from fatigue would correlate with maximal oxygen uptake (VO2max). A secondary purpose was to determine whether changes in the development of fatigue and in the time course of recovery that occur with alterations in training status correlate with shifts in the proportions of type IIa and type IIb muscle fibers. SUBJECTS AND METHODS: Four subjects with no regular endurance exercise training participated in a 12-week program of intense endurance exercise training, and 6 endurance-trained subjects stopped all exercise training for 12 weeks. In addition, 11 subjects performed a single isokinetic fatigue test with recovery and a graded treadmill or bicycle ergometer test to determine VO2max. RESULTS: Maximal oxygen uptake increased 24% (SD = 10%) in response to the exercise training program and decreased 17% (SD = 6%) with detraining. The percentage of type IIa and type IIb muscle fibers changed with endurance training and detraining. The percentage of decline in torque during a 60-second isokinetic exercise test was unaffected by endurance training or detraining; however, there was a significant change in recovery of torque. CONCLUSION AND DISCUSSION: The results demonstrate a positive correlation (r = .75) between the percentage of reduction in torque at 30 seconds of recovery and the change in the proportion of type IIb fibers with both training and detraining. The results also demonstrate a high, negative correlation (r = -.84) between the percentage of reduction in torque at 30 seconds of recovery and VO2max. These results suggest the recovery of muscle torque reflects both the training- and detraining-induced changes in the proportion of type IIa and type IIb muscle fibers and maximal aerobic exercise capacity.

Adult↗

PubMed1985

In vitro fertilization in the rabbit after delayed ovum recovery.

Rabbit ovum donors were superovulated with pregnant mare's serum gonadotropin (PMSG) and human chorionic gonadotropin (hCG). Ova were recovered 16-17 h post-hCG from oviducts immediately after killing and from excised oviducts held in saline 30 min at 33 degrees or 38 degrees C prior to ovum recovery. In vivo-capacitated spermatozoa were used to inseminate both groups of ova. Data revealed a decrease in fertilization rates following a 30-min delay at 38 degrees C in ovum recovery. Thus, 64% (44/69 ova) were fertilized with rapid recovery, whereas 43% (39/90 ova) were fertilized following a 30-min delay. The decrease in fertilization imposed by delay in ovum recovery was apparently overcome when oviduct storage was at 33 degrees C. Under these conditions, 69% of inseminated ova were fertilized. Ova inseminated with in vitro-capacitated sperm showed a similar response to delayed ovum recovery. Embryonic development in culture of ova obtained from mated does was not affected by delay in recovery at 33 degrees or 38 degrees C provided mated does had been injected only with hCG. Ova from mated does receiving both PMSG and hCG were adversely affected by a 38 degrees C delay. The data emphasize the importance of rapid ovum recovery from oviducts and suggest the possibility of altering conditions to overcome damaging effects of delayed recovery.

Animals↗

PubMed1995

Comparison of the infusion requirements and recovery profiles of vecuronium and cisatracurium 51W89 in intensive care unit patients.

The selection and administration of neuromuscular blocking (NMB) drugs in intensive care unit (ICU) patients remain controversial. We compared the dose-response and recovery pharmacodynamics of a new intermediate-acting NMB drug, cisatracurium besylate, to the intermediate-acting NMB drug, vecuronium (VEC), in a prospective, randomized, double-blind, multicenter study in critically ill adults. After informed consent, 58 mechanically ventilated ICU patients from five medical centers were randomized to receive either cisatracurium or VEC. Fifty-four of the 58 patients received NMB drugs before entering this study but demonstrated at least partial recovery (> or = one twitch) in the train-of-four (TOF) response before initiation of the NMB study drug. NMB drug infusion was titrated by peripheral nerve stimulation to maintain at least one twitch in the TOF response. NMB drugs were infused for 1-5 days. After discontinuation of NMB drug infusion, recovery of neuromuscular transmission was monitored with an accelerometer. NMB drug infusion for 28 cisatracurium patients averaged 2.6 +/- 0.2 (mean +/- SEM) micrograms.kg-1.min-1 with a mean duration of 80 +/- 7 h. After discontinuing cisatracurium administration, recovery to 70% TOF ratio averaged 68 +/- 13 min. The mean infusion rate for 30 VEC patients was 0.9 +/- 0.1 micrograms.kg-1.min-1 with a mean duration of 66 +/- 12 h. Neuromuscular recovery after VEC averaged 387 +/- 163 min, which was significantly longer (P = 0.02) than that after cisatracurium. Prolonged recovery of neuromuscular function after discontinuation of NMB drug infusion (identified by the primary investigator at each medical center) was reported in two cisatracurium patients and 13 VEC patients (P = 0.002), and occurred despite the routine use of neuromuscular twitch monitoring. Seven VEC and one cisatracurium patients died during the infusion of study drug or within 48 h after discontinuation of the NMB drug infusion. In summary, we found recovery of neuromuscular function after discontinuation of NMB drug infusion in ICU patients is significantly faster with cisatracurium than with VEC. In addition, routine neuromuscular monitoring was not sufficient to eliminate prolonged recovery and myopathy in ICU patients.

Adult↗

PubMed1991

Midazolam improves electrophysiologic recovery after anoxia and reduces the changes in ATP levels and calcium influx during anoxia in the rat hippocampal slice.

Since blockers of excitatory transmission have been shown to reduce anoxic and ischemic neuronal damage, augmentation of inhibitory transmission by agents such as midazolam might have a similar protective effect. Rat hippocampal slices were maintained in vitro and used to determine whether and by what mechanism midazolam improves recovery of evoked responses after anoxia. The Schaffer collateral pathway in the slice was stimulated electrically, and an extracellular potential, the evoked population spike, was recorded from the CA1 pyramidal cells, which are postsynaptic. The slices were made anoxic by substituting artificial cerebrospinal fluid aerated with 95% nitrogen-5% carbon dioxide for fluid aerated with 95% oxygen-5% carbon dioxide. Percentage recovery was expressed as the amplitude of the evoked population spike 60 min after anoxia divided by its preanoxic amplitude. Protection in this model is defined as a significant (P less than 0.05) improvement in percentage recovery compared to the recovery of untreated slices. There was no recovery of the response recorded from CA1 pyramidal cells after 5 min of anoxia (4 +/- 2%) (mean +/- standard error of the mean [SEM]). Slices were treated with midazolam 10 min before, during, and 10 min after anoxia. Midazolam (1 microM) did not enhance recovery after anoxia when dissolved either in water (3 +/- 3%) or in dimethyl sulfoxide (DMSO) (1 +/- 1%). A higher concentration of midazolam (100 microM) did enhance recovery when dissolved in DMSO (27 +/- 7%) but not when dissolved in water (5 +/- 2%). To test whether prolonged pretreatment with midazolam dissolved in water would enhance recovery, slices were treated for 30 min prior to anoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗

PubMed1999

Isoflurane-enhanced recovery of canine stunned myocardium: role for protein kinase C?

BACKGROUND: Isoflurane enhances the functional recovery of postischemic, reperfused myocardium by activating adenosine A1 receptors and adenosine triphosphate-regulated potassium channels. Whether protein kinase C is involved in this process is unknown. The authors tested the hypothesis that inhibition of protein kinase C, using the selective antagonist bisindolylmaleimide, attenuates isoflurane-enhanced recovery of stunned myocardium in dogs. METHODS: Fifty dogs were randomly assigned to receive intracoronary vehicle or bisindolylmaleimide (2 or 8 microg/min) in the presence or absence of isoflurane (1 minimum alveolar concentration). Five brief (5 min) coronary artery occlusions interspersed with 5-min reperfusion periods followed by 180 min of final reperfusion were used to produce myocardial stunning. Hemodynamics, regional segment shortening, and myocardial blood flow (radioactive microspheres) were measured at selected intervals. RESULTS: There were no differences in baseline hemodynamics, segment shortening, or coronary collateral blood flow between groups. Isoflurane significantly (P<0.05) decreased heart rate, mean arterial pressure, rate pressure product, and the maximum rate of increase of left ventricular pressure (+dP/dt(max)) in the presence or absence of bisindolylmaleimide. Sustained contractile dysfunction was observed in dogs that received vehicle (recovery of segment shortening to 12+/-8% of baseline), in contrast to those that received isoflurane (75+/-7% recovery). Bisindolylmaleimide at a dose of 2 microg/min alone enhanced recovery of segment shortening (50+/-7% of baseline) compared with vehicle-pretreated dogs, and isoflurane in the presence of 2 microg/min bisindolylmaleimide further enhanced recovery of contractile function (79+/-8% of baseline). In contrast, 8 microg/min bisindolylmaleimide alone (32+/-12%) or combined with isoflurane (37+/-17%) did not enhance recovery of segment shortening compared with vehicle-pretreated dogs. CONCLUSIONS: The results indicate that protein kinase C inhibition using low doses of bisindolylmaleimide alone produces cardioprotection, and isoflurane further enhances this protection. In contrast, high doses of bisindolylmaleimide are not cardioprotective in the presence or absence of isoflurane. A role for protein kinase C during isoflurane-induced recovery of the stunned myocardium cannot be excluded.

Anesthetics, Inhalation↗

PubMed1994

Comparative effects of fluoxetine, amitriptyline and serotonin on functional motor recovery after sensorimotor cortex injury.

A recent investigation of the effects of the antidepressants desipramine and trazodone on behavioral recovery in brain-injured animals suggested that antidepressants, which act to increase noradrenergic activity in the brain, may facilitate the rate of recovery, whereas those that act to increase serotonergic (5-HT) activity may hinder recovery and reinstate deficits in recovered animals. The present study was designed to evaluate these findings further by assessing the effect of a single intraperitoneal injection of fluoxetine (a relatively pure 5-HT reuptake blocker), amitriptyline (a mixed 5-HT and noradrenergic reuptake blocker with alpha 1-adrenergic receptor blocking activity) or a single intraventricular infusion of 5-HT on recovery of beam-walking ability in animals with a unilateral sensorimotor cortex injury. None of the drugs significantly affected the rate of recovery. Although fluoxetine was ineffective in reinstating the motor deficit in recovered animals, amitriptyline reinstated the deficit in a dose-dependent fashion. Infusion of 5-HT resulted in an extremely transient reinstatement of the deficit, which was largely attributable to its short-term sedative properties. These results suggest that 5-HT may be less involved in functional recovery than previously thought. They also add further support to previous findings that indicate that drugs which act to antagonize alpha 1-adrenergic activity (e.g., phenoxybenzamine) may interfere with motor recovery after sensorimotor cortex injury. An appreciation of the potential impact of certain antidepressants on functional recovery in brain-injured patients appears warranted.

Amitriptyline↗

PubMed1994

Hyperbaric oxygen combined with nicardipine administration accelerates neurologic recovery after cerebral ischemia in a canine model.

OBJECTIVE: To evaluate the efficacy of combined therapy--hyperbaric oxygenation with nicardipine administration--for neurologic recovery after complete cerebral ischemia. DESIGN: Randomized, prospective, controlled, unblinded, study, with 14-day postischemic observation. SETTING: Laboratory of the Department of Anesthesiology, Tohoku University School of Medicine. SUBJECTS: Nineteen healthy mongrel dogs (mean weight 10.4 kg) divided randomly into two groups-ten dogs in the untreated group and nine dogs in the treated group. INTERVENTIONS: Fifteen minutes of complete global cerebral ischemia was achieved by occlusion of the ascending aorta and the caval veins. Dogs in the treated group each received a 0.01-mg/kg bolus injection of nicardipine immediately after the reestablishment of circulation, followed by a 0.03-microgram/kg/min continuous infusion of nicardipine for 3 days and hyperbaric oxygen therapy with 3 atmospheres absolute pressures in an FIO2 of 1.0 for 1 hr at 3, 24, and 29 hrs after ischemia. Neurologic recovery was evaluated based on the survival time and rate, the Electroencephalogram (EEG) Score (1 = normal, 5 = isoelectric), and the Neurologic Recovery Score (100 = normal, 0 = brain dead) over a 14-day postischemic period. MEASUREMENTS AND MAIN RESULTS: Neurologic Recovery Scores of the treated group were always higher than those scores of the untreated group throughout the 14-day period. The best Neurologic Recovery Score was 83.1 +/- 5.3 in the treated group and 46.9 +/- 5.2 in the untreated group (p < .01). The numbers of dogs that recovered to a Neurologic Recovery Score of > 85 (assessed as almost normal) was five of nine in the treated group and none of ten in the untreated group (p < .01). Recovery of EEG over 14-day period was better in the treated group. The survival rate and the predicted survival rate were 78% and 13.6 days in the treated group and 30% and 9.0 days in the untreated group, respectively (p < .04 for the survival rate and p < .05 for the survival time). CONCLUSION: Combined therapy, using hyperbaric oxygenation with nicardipine administration, given after 15 mins of complete global cerebral ischemia, accelerates neurologic recovery in dogs.

Animals↗

PubMed1994

Comparison of sedative recovery time after midazolam versus diazepam administration.

OBJECTIVE: To compare the sedative recovery rate pharmacology of intravenous midazolam vs. diazepam when used for short-term sedation. DATA SOURCES: English-language articles were identified through a search of the MEDLINE and InPharma databases. Bibliographies of retrieved articles were examined for relevant articles. STUDY SELECTION: Twenty-eight studies were identified based on a priori inclusion criteria. Eight trials had enough information to combine results for sedative recovery rate. DATA EXTRACTION: The difference in mean time to sedative recovery, weighted by sample size, was determined. DATA SYNTHESIS: Of the 28 trials, eight reported a significantly faster sedation recovery rate from diazepam vs. midazolam, whereas 19 trials reported no difference in sedative recovery time, and a single trial reported that midazolam offered significantly faster recovery from sedation than diazepam. A commonly defined time to sedative recovery event was available for only eight trials. The median dosing ratio for these eight trials was 2.1:1 for diazepam over midazolam. The weighted mean time difference was 4 mins 16 secs in favor of diazepam as the agent from which patients recover more quickly. CONCLUSIONS: These results firmly underscore the understanding that elimination half-lives of benzodiazepines do not necessarily correspond with their sedative pharmacodynamic effects, and we conclude that there are no clinically important sedative recovery rate differences between midazolam and diazepam, while midazolam is a more expensive agent.

Diazepam↗

PubMed1999

The influence of spinal canal narrowing and timing of decompression on neurologic recovery after spinal cord contusion in a rat model.

STUDY DESIGN: The effect of spinal canal narrowing and the timing of decompression after a spinal cord injury were evaluated using a rat model. OBJECTIVE: To evaluate whether progressive spinal canal narrowing after a spinal cord injury results in a less favorable neurologic recovery. Additionally, to evaluate the effect of the timing of decompression after spinal cord injury on neurologic recovery. SUMMARY OF BACKGROUND DATA: Results in previous studies are contradictory about whether the amount of canal narrowing or the timing of decompression after a spinal cord injury affects the degree of neurologic recovery. METHODS: Forty adult male Sprague-Dawley rats were equally divided into a control group, in which spacers of 20%, 35%, and 50% were placed into the spinal canal after laminectomy, and an injury group in which the spacers were placed after a standardized incomplete spinal cord injury. After spacer removal, neurologic recovery in both was monitored by Basso, Beattie, Bresnahan (BBB) Locomotor Rating Scale (Ohio State University, Columbus, OH) motor scores and transcranial magnetic motor evoked potentials for 6 weeks followed by histologic examination of the spinal cords. Subsequently, 42 rats were divided into five groups in which, after spacer placement, the time until decompression was lengthened 0, 2, 6, 24, and 72 hours. Again, serial BBB motor scores and transcranial magnetic motor evoked potentials were used to assess neurologic recovery for 6 weeks until the animals were killed for histologic evaluation. RESULTS: Spacer placement alone in the control animals resulted in no neurologic injury until canal narrowing reached 50%. All of the control groups (spacer only) exhibited significantly better (P < 0.05) motor scores compared with the injury groups (injury followed by spacer insertion). Within the injury groups the motor scores were progressively lower as spacer sizes increased from the no-spacer group to the 35% group. The results in the 35% and 50% groups were not statistically different. The results of the time until decompression demonstrated that the motor scores were consistently better the shorter the duration of spacer placement (P < 0.05) for each of the time groups (0, 2, 6, 24, and 72 hours) over the 6-week recovery period. Histologic analysis showed more severe spinal cord damage as both spinal canal narrowing and the time until decompression increased. CONCLUSION: The results in this study present strong evidence that the prognosis for neurologic recovery is adversely affected by both a higher percentage of canal narrowing and a longer duration of canal narrowing after a spinal cord injury. The tolerance for spinal canal narrowing with a contused cord appears diminished, indicating that an injured spinal cord may benefit from early decompression. Additionally, it appears that the longer the spinal cord compression exists after an incomplete spinal cord injury, the worse the prognosis for neurologic recovery.

Animals↗

PubMed1997

Diabetic neuropathy after pancreas transplantation: determinants of recovery.

Although simultaneous pancreas and kidney transplantation (SPK) achieves normoglycemia and correction of uremia in type I diabetic patients with renal failure, little data are available on long-term outcome and clinical determinants of recovery of peripheral neuropathy. In this prospective study, 219 electrophysiological studies using a standardized protocol were performed before and up to 8 years after SPK in 44 patients. Nine control diabetic recipients with functioning kidney but nonfunctioning pancreas transplants were studied on 35 occasions. Patients were 38.5+/-7.9 years old (mean+/-SD) with pretransplant diabetes present for 25.2+/-7.6 years. Significant polyneuropathy (total nerve conduction scores [NCS] <-1.0) was present in 89% before transplantation, which correlated with body weight (r=0.628, P<0.001). Two distinct patterns of neurological recovery were observed after SPK. Conduction velocity (CV) improved in a biphasic pattern, with a rapid initial recovery followed by subsequent stabilization. In contrast, the recovery of nerve amplitude was monophasic, and continued to improve for up to 8 years. Initial improvement in NCS was primarily due to an increase in CV (P=0.002 vs. baseline), and was best in shorter and younger patients. Recovery of total NCS at 6 months after SPK, assessed by multivariate analysis, was least in obese recipients and when performed in patients who had started dialysis before SPK, and was associated with lower transplant kidney isotopic glomerular filtration rate and HLA mismatch (P<0.05 to 0.001). Subsequent improvement was associated with less severe initial neuropathy, smaller body weight, and longer duration of diabetes (P<0.01 to 0.001). Fasting hyperinsulinemia was associated with impairment of initial recovery and subsequent NCS after SPK, but was worse in the control group. Recovery of nerve action potential amplitudes was predicted by better initial amplitudes and HLA mismatch, lower body weight, and the use of nifedipine (P<0.05 to 0.001). Nifedipine was used for hypertension in 33% of SPK and was associated with better CV and amplitudes, particularly in the upper limbs, where there was less neuropathy. The use of angiotensin-converting enzyme inhibitors also appeared beneficial, but this was confined to the lower limbs. SPK resulted in a gradual, sustained, and late improvement in nerve action potential amplitudes, consistent with axonal regeneration and partial reversal of diabetic neuropathy. These data suggest that early transplantation of uremic diabetic patients before onset of severe neuropathy, minimizing obesity and optimizing renal transplant function, maximizes neurological recovery after SPK. Furthermore, the preliminary data support randomized clinical trials for evaluation of nifedipine and angiotensin-converting enzyme inhibitors in diabetic neuropathy.

Adult↗

PubMed1994

Cerebral blood flow, plasma catecholamines, and electroencephalogram during hypoglycemia and recovery after glucose infusion.

Regional cerebral blood flow (rCBF) and plasma catecholamines were measured in separate experiments during the onset of insulin-induced hypoglycemia and during recovery. The purpose of these experiments was twofold: first, to study the relationship between plasma catecholamines and rCBF to determine if increased concentrations of plasma catecholamines were responsible for the increase in rCBF observed during insulin-induced hypoglycemia, and second, to study changes in rCBF after recovery from hypoglycemia. Male Long-Evans rats were fasted overnight, surgically prepared under isoflurane anesthesia, restrained, and allowed to awake from anesthesia. In the first series of experiments, plasma catecholamines, arterial blood pressure, arterial blood gases, and electroencephalogram (EEG) were measured during the onset of hypoglycemia produced by i.v. insulin and the recovery after i.v. glucose. The EEG showed a characteristic high-amplitude, slow-wave pattern during hypoglycemia (plasma glucose, 38 +/- 2 mg/dl; n = 3). Plasma epinephrine in the normoglycemic control rats was 529 +/- 122 pg/ml (n = 5) and increased 4.5 times as plasma glucose reached 50 +/- 3 mg/dl. After the initial increase, plasma epinephrine steadily decreased toward baseline over the next 90 min as the hypoglycemia became more severe. Plasma norepinephrine significantly increased by 60% when plasma glucose was 40 +/- 2 mg/dl and remained increased during much of the recovery period. In other studies, rCBF was measured in four groups of rats, one group with normoglycemia (control), one with hypoglycemia, one at 5 min of recovery, and one at 30 min of recovery. Regional CBF increased during hypoglycemia (plasma glucose, 39 +/- 1 mg/dl; n = 6) in most regions studied and ranged from 28 to 99% above control. After 5 min of the recovery (plasma glucose, 269 +/- 15 mg/dl), rCBF returned to or decreased below baseline. In a previous study, we determined that rCBF did not increase during hypoglycemia until plasma glucose decreased to 40 mg/dl. In the present study, the peak increase in plasma epinephrine occurred when plasma glucose was 50 mg/dl. At plasma glucose concentrations which rCBF began to increase, plasma epinephrine was decreasing from its peak level. Regional CBF and plasma norepinephrine increased in parallel during the onset of hypoglycemia; however, during the recovery period, plasma norepinephrine remained increased while rCBF decreased to or below baseline. The dissociation of rCBF and plasma catecholamines casts doubt on the hypothesis that plasma catecholamines are responsible for increases in rCBF.

Animals↗

PubMed2005

Integrated versus sealed-over recovery in schizophrenia: BORRTI and executive function.

Ego functioning of 222 outpatients with a diagnosis of schizophrenia or schizoaffective disorder was evaluated using the Bell Object Relations and Reality Testing Inventory (BORRTI). Sixty-one of these had BORRTI profiles identified as sealed-over recovery style, and 36 had profiles interpreted as integrated recovery style. Groups were compared on demographic characteristics, symptom profiles, and the Wisconsin Card Sorting Test, a performance measure of executive function. Groups had comparably low levels of positive symptoms, but the integrated recovery group had higher scores on the BORRTI uncertainty of perception scale. The integrated recovery group had significantly fewer minority patients, higher IQ, and higher levels of emotional discomfort. The sealed-over recovery group had higher levels of cognitive disorganization. When differences in ethnicity and IQ were controlled for, the integrated recovery group had better executive functioning. Wisconsin Card Sorting Test categories completed emerged as the significant predictor in a logistic regression, explaining 19% of the variance. These findings support the discriminant validity of these two recovery styles and reveal the importance of executive function in a recovery style that allows for investment in relationships, affect tolerance, and acknowledgment of symptoms.

Adaptation, Psychological↗

PubMed1998

Starvation recovery of Staphylococcus aureus 8325-4.

Nutrient limitation of Staphylococcus aureus induces a starvation-survival state which enables it to survive until sufficient nutrients become available to support growth. The response of starved S. aureus cells to nutritional upshift was analysed to characterize the recovery mechanism which results in the resumption of rapid growth. S. aureus 8325-4 starved for 7 d in a chemically defined medium limited for glucose was able to resume growth upon the addition of complex medium (brain heart infusion broth) or a mixture of amino acids and glucose. The addition of either glucose or amino acids alone did not lead to recovery of cells. Prior to the first cell division event, a lag period of about 120-150 min was observed, the duration of which was independent of the length of starvation survival. During this lag period, RNA synthesis increased immediately upon the addition of nutrients whilst protein synthesis was delayed by approximately 5 min. Cells rapidly enlarged within 30 min of recovery, and initiation of chromosome replication could be detected after 90 min. Changes in the profile of proteins expressed during the recovery period revealed that several starvation-specific proteins were down-regulated within 30 min, whilst other proteins were common to both starvation and recovery. Two proteins were identified which were only transiently expressed during the first 60 min of recovery. Protein synthesis could be detected during recovery even if the cells had been treated with the RNA synthesis inhibitor rifampicin for 30 min prior to the addition of recovery nutrients, demonstrating that several proteins are translated from long-lived mRNA transcripts present in starved cells.

Antibiotics, Antitubercular↗

PubMed1992

Effect of cold hardening on sensitivity of winter and spring wheat leaves to short-term photoinhibition and recovery of photosynthesis.

Photoinhibition of photosynthesis and its recovery were studied in wheat (Triticum aestivum L.) leaves grown at nonhardening (20 degrees C) and cold-hardening (5 degrees C) temperatures. Cold-hardened wheat leaves were less susceptible to photoinhibition at 5 degrees C than nonhardened leaves, and the winter cultivars, Kharkov and Monopol, were less susceptible than the spring cultivar, Glenlea. The presence of chloramphenicol, a chloroplastic protein synthesis inhibitor, increased the susceptibility to photoinhibition, but cold-hardened leaves still remained less susceptible to photoinhibition than nonhardened leaves. Recovery at 50 mumol m(-2) s(-1) photosynthetic photon flux density and 20 degrees C was at least biphasic, with a fast and a slow phase in all cultivars. Cold-hardened leaves recovered maximum fluorescence and maximum variable fluorescence in the dark-adapted state during the fast phase at a rate of 42% h(-1) compared with 22% h(-1) for nonhardened leaves. The slow phase occurred at similar rates (2% h(-1)) in cold-hardened and nonhardened leaves. Full recovery required up to 30 h. Fast-recovery phase was not reduced by either lowering the recovery temperature to 5 degrees C or by the presence of chloramphenicol. Slow-recovery phase was inhibited by both treatments. Hence, the fast phase of recovery does not require de novo chloroplast protein synthesis. In addition, only approximately 60% of the photochemical efficiency lost through photoinhibition at 5 degrees C was associated with lost [(14)C]atrazine binding and, hence, with damage to the secondary quinone electron acceptor for photosystem II-binding site. We conclude that the decrease in susceptibility to photoinhibition exhibited following cold hardening of winter and spring cultivars is not due to an increased capacity for repair of photoinhibitory damage at 5 degrees C but reflects intrinsic properties of the cold-hardened photosynthetic apparatus. A model to account for the fast component of recovery is discussed.

Journal Article↗

PubMed1993

Effect of voluntary tetanus on recovery of vecuronium block in the isolated forearm.

This study was conducted to investigate the effect of voluntary tetanus on the recovery from neuromuscular block produced by a nondepolarising drug, vecuronium, in the isolated forearm. We have studied the recovery indices and train of four fade at different levels of recovery following vecuronium in both isolated forearms simultaneously, in six sets of experiments. In one hand the volunteer performed a maximum contraction of his thumb repeatedly at fixed intervals. We found that following voluntary tetanus there is an increased rate of recovery from nondepolarising neuromuscular block; mean Recovery Index (7.4, SD 0.97) compared to control Recovery Index (10.55, SD 2.58), p < 0.05. The train-of-four fade also showed a sustained reduction in the isolated forearm which underwent voluntary tetanus. During the later phase of recovery the train-of-four fade showed significant difference statistically (p < 0.01). The findings of this study supports the hypothesis that more rapid recovery associated with voluntary tetanus is due to a reduction in the presynaptic block thus resulting in an increased rate of transmitter release.

Forearm↗

PubMed1994

Recovery of mivacurium and doxacurium versus vecuronium in the isolated forearm.

To assess rate of biophase recovery, the recovery from neuromuscular block with mivacurium in the isolated forearm was compared with that from vecuronium simultaneously administered into the other isolated forearm of six volunteers. In a second series of similar experiments, recovery from doxacurium was compared with that from vecuronium. Neuromuscular block was monitored using the adductor pollicis mechanomyographic response to ulnar nerve stimulation at 0.2 Hz. Comparable degrees of maximum twitch tension depression were obtained in each series. In the first series, mean (SD) 25-75% recovery index for mivacurium was 8.4 (1.5) min and 10.5 (1.9) min for vecuronium. In the second series, mean (SD) recovery index for doxacurium was 18.3 (4.2) min and 12.2 (5.0) min for vecuronium. The recovery index of doxacurium in the isolated forearm was significantly greater, and the recovery index of mivacurium significantly less, than the recovery index of simultaneously administered vecuronium. Mivacurium block in the isolated forearm recovers rapidly, although not faster than after systemic injection; this is consistent with a drug that is retained in the biophase despite rapid plasma metabolism. Doxacurium block in the isolated forearm is slow to recover, compared with vecuronium; this suggests that high affinity for the biophase may contribute to its long duration of action.

Forearm↗