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Query: UMLS:C0599766 (functional recovery)
 13,441 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Regenerative growth at the lesion site, reinnervation of a target nucleus and functional manifestations of recovery were studied in aged (20 and 30 months old) rats subjected to long-term transection of catecholaminergic (CA) fibers which contact and influence neurons of the supraoptic nucleus (SON). Small bilateral knife cuts were placed stereotaxically just caudal and medial to the SON. CA histofluorescence, induced by formaldehyde-glutaraldehyde (FAGLU) or aluminum-formaldehyde (ALFA) methods, was examined in hypothalamus at 2, 14, 21 and 60 days postsurgically. Water consumption, and urine volume and osmolality, were monitored presurgically, and through survival times. Subtotal CA denervation in the SON, and typical axonal transmitter "pile-up" at the lesion site, were evident two days after surgery. Among these degenerative profiles, which persisted for up to three weeks, fine-sized new fibers were apparent at the lesion, beginning between 2 and 14 days, and persisting throughout the period studied. At 21 days, and progressively thereafter, SON neurons were rimmed with fluorescent varicosites. Water consumption initially was depressed, but returned to presurgical mean levels by nine days. Urine volume returned to normal by 32 days. Urine osmolality showed a recovery by approximately three weeks. These functional parameters rebounded to levels higher than presurgical means among 20 month old, but not 30 month old, rats beyond 6 weeks survival, concurrent with a morphological hyperinnervation. The results reaffirm morphological regeneration, and support reinnervation and functional recovery, which extend considerably into the aging process.
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PMID:Plasticity of catecholaminergic neurons in aged rat brain: reinnervation and functional recovery after axotomy. 653 17

Long-Evans rats received septal lesions or sham operations and were tested for performance in a radial arm maze, level of activity and water intake in order to test whether recovery of function was mediated by sprouting of peripheral sympathetic fibers. Animals receiving septal lesions displayed an initial deficit in radial arm maze performance followed by recovery. No critical changes occurred in activity level and no recovery was seen in water intake. Subsequent superior cervical ganglionectomies had no effect on recovery of radial arm maze performance. There was a significant relationship between behavioral recovery and the degree of hippocampal AChE depletion. It is concluded that recovery of radial arm maze performance is not mediated by sympathetic sprouting following septal lesions but might be mediated by residual septohippocampal fibers.
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PMID:Medial septal lesions, radial arm maze performance, and sympathetic sprouting: a study of recovery of function. 683 Dec 31

Reperfusion conditions significantly affect recovery following global myocardial ischemia. Using an isolated dog heart model, we investigated the effect of initial (first 10 minutes) reperfusion temperature and pressure on the metabolic and functional recovery of the preserved heart. Four groups of five or six dogs each underwent 2 hours of ischemic cardioplegic arrest at 15 degrees C following single-dose crystalloid cardioplegia. Hearts were initially reperfused at 37 degrees C (high temperature) or 28 degrees C (low temperature) and at 50 mm Hg (low pressure) or 80 mm Hg (high pressure), giving four groups: (1) high-temperature, high-pressure; (2) high-temperature, low-pressure; (3) low-temperature, high-pressure; and (4) low-temperature, low-pressure. Septal temperatures were continuously recorded. Ventricular function curves 1 and 2 hours following reperfusion were significantly depressed in the high-temperature, high-pressure group (70%, p less than 0.01, and 83%, p less than 0.02) and the low-temperature, high-pressure group (78%, p less than 0.03, and 85%, p less than 0.03) but were normal in the low-temperature, low-pressure and the high-temperature, low-pressure groups. All groups showed edema 1/2 hour after reperfusion as measured by water and sodium content in myocardial biopsy specimens but only the high-temperature, high-pressure and the low-temperature, high-pressure groups showed persistent edema at 3 hours (3.95 +/- 0.2 ml H2O/gm dry weight, p less than 0.03 and 3.99 +/- 0.16 ml/gm, p less than 0.02, respectively). Only low-temperature, high-pressure reperfusion resulted in statistically significant reductions in adenosine triphosphate (ATP) 1/2 hour and 2 hours following reperfusion (a 15% reduction from baseline). Maximum rewarming rates were measured for each group. High-temperature, high-pressure = 2 degrees C per second; low-temperature, high-pressure = 1 degree C per second; high-temperature, low-pressure = 0.75 degrees C per second; and low-temperature, low-pressure = 0.4 degrees C per second. High-pressure reperfusion following global myocardial ischemia results in rapid rewarming and is associated with prolonged myocardial edema, depressed ATP levels, and delayed functional recovery. Therefore, we employ 10 minutes of low-pressure reperfusion in our patients undergoing potassium cardioplegic arrest.
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PMID:Effect of reperfusion temperature and pressure on the functional and metabolic recovery of preserved hearts. 687 60

The calcium channel blocker, diltiazem, has been studied in the same model used for evaluation of cold blood-potassium cardioplegia. Six dogs (Group 1) had one hour of myocardial ischemia with topical ice (myocardial temperature, 7 degrees +/- 2 degrees C) after coronary perfusion with 200 ml of cold blood (5 degrees +/- 1 degree C) containing diltiazem, 400 micrograms per kilogram of body weight. Seven dogs (Group 2) had two hours of ischemia after perfusion with 200 ml of cold blood containing 200 micrograms/kg and reperfusion every 30 minutes with 100 ml of cold blood and diltiazem, 100 micrograms/kg. Baseline studies were repeated after rewarming and 40 minutes of reperfusion. No inotropic agents or calcium were used. Heart rate, peak systolic pressure, velocity of the contractile element, peak + rate of rise of left ventricular pressure (dP/dt), peak - dP/dt, dP/dt over common peak isovolumic pressure, left ventricular compliance and stiffness, and heart water were unchanged in Group 1. In Group 2, heart rate slowed (p less than 0.025) and compliance decreased (p less than 0.02). In both groups, coronary vascular resistance declined (p less than 0.001) and recovery of adenosine triphosphate (p less than 0.001), adenosine diphosphate (p less than 0.025), and the adenosine pool (p less than 0.001) was impaired. Ultrastructure was well preserved, but myofibrillar lesions were noted in Group 2. Diltiazem cardioplegia was associated with good functional recovery, but there was impairment of high-energy phosphate metabolism.
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PMID:Cold blood-diltiazem cardioplegia. 706 65

The hypothesis tested was that the composition of the prime and the perfusate at the time of reperfusion had an influence on postischemic cardiac performance. Twelve dogs in two equal groups had long (210 +/- 10 minutes) hypothermic (25 degrees +/- 1 degree C) perfusions. Each had 180 minutes of global ischemia and were given 500 ml of the same cold (4 degrees C) cardioplegic solution (CPS) every 45 minutes and topical hypothermia with a resultant average myocardial temperature of 10 degrees +/- 2 degrees C. Group A had a prime (1,958 ml) consisting of a 50/50 mixture of 5% dextrose in water and 5% dextrose in Ringer's injection to which mannitol (12.5 gm), furosemide (20 mg), and heparin (6,000 units) were added. Group B received a prime (1,868 ml) of 5% dextrose in Ringer's injection (1 L) and 750 ml of 6% helastarch in normal saline to which NaHCO3 (10 mEq), furosemide (20 mg), mannitol (25 gm), and heparin (6,000 units) were added. During perfusion, Group A received lactated Ringer's solution and Group B received a 1 : 2 portions of Ringer's injection and 6% helastarch. Additionally, Group B received additional furosemide and mannitol 5 minutes prior to the reperfusion interval. The results showed a marked difference between groups in postischemic cardiac recovery 120 minutes after cessation of cardiopulmonary bypass. The Group B dogs had statistically (less than 0.02) greater cardiac output, stroke volumes, and stroke work index at equal preloads and lower total peripheral resistances. Arterial systolic, diastolic, and mean pressures and right atrial pressures were not different. The Group A dogs required nearly threefold the volume of fluid additions required during bypass and twice the amount of NaHCO3 as Group B dogs. It is concluded that the composition of the prime and fluids used during bypass and use of agents to counteract tissue water accumulation during the ischemic and reperfusion intervals strongly influences postischemic cardiac performance. Further, these data suggest that the composition of the perfusate may have a greater influence on the functional recovery of the heart than the composition of various CPSs.
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PMID:Adequacy of the perfusate: its influence on successful myocardial protection. 713 9

The stress-induced changes in peripheral benzodiazepine receptors (PBR) can be observed in a number of different tissues, depending upon the nature and chronicity of the aversive experience. In addition, virtually all stress procedures that cause rapid changes in PBR simultaneously increase the physical activity or metabolic rate of the subjects. The present study analyzed the contributions of rapid alterations in activity or metabolic rate with and without aversive stimulation and their subsequent impact on PBR. Mechanically induced increases in activity by forced running stress results in a significant reduction in [3H]Ro 5-4864 binding to PBR in olfactory bulb, opposite to the PBR changes in this tissue following forced cold-water swim stress. Pharmacological induction of increased locomotor activity as well as metabolic rate by d-amphetamine causes a significant increase in cardiac PBR binding, again, opposite to the response typically observed following inescapable shock stress. Finally, administration of the anxiogenic beta-carboline, FG-7142, causes increases in both hippocampus and adrenal gland PBR binding reminiscent of acute noise stress exposure. These experiments demonstrate that increased locomotor activity or metabolic rate alone is not a necessary and sufficient condition for previous stress-induced changes in PBR. Conversely, increased metabolic rate coupled with an aversive stimulus appears to be an important factor for inducing stress-like changes in PBR. This data, coupled with previous reports, suggests that rapid alterations in these sites are stressor and tissue dependent. Finally, we propose that the PBR may be involved in many aspects of the stress response including: a) a blowarning system in adrenal gland, b) participation in stress-induced hypertension via renal PBR, and c) a modulator of stress-induced immunosuppression and subsequent recovery of function or recuperation by actions on immune cells.
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PMID:Environmentally induced changes in peripheral benzodiazepine receptors are stressor and tissue specific. 761 1

At least theoretically, ACE-inhibitors may influence each of the factors involved in the regulation of salt and water metabolism. Angiotensin II exerts an antidiuretic and antinatriuretic action on the kidney through influences on the glomerular filtration coefficient, glomerular filtration rate, mesangial tone, filtration fraction, proximal and distal tubule. Angiotensin II and renin also regulate the input of water and salt through an unequivocal dipsogenic effect. In congestive heart failure angiotensin II participates in the preservation of the glomerular filtration rate through its vasoconstrictor properties on the systemic vessels (maintenance of the perfusion and filtration pressure) as well as on the efferent arteriole (maintenance of the filtration pressure). ACE-inhibition weakens or abolishes these influences. However, two favorable mechanisms may also come into action: rise of cardiac output and improvement in renal blood flow; widening of the filtration surface and increment of the filtration coefficient. The efficacy of these factors depends on renal function, age, functional recovery of the heart, treatment with diuretics, duration of treatment with ACE-inhibitors, duration of action of the ACe-inhibitor used, blockade of the facilitating action on the adrenergic vasoconstriction, formation of vasodilating prostaglandins, reduced degradation of kinins. All these effects may account for the variable and often contradictory clinical results, in particular as concerns the relationship between ACE-inhibition and use of diuretics in congestive heart failure. This also explains the variability of efficacy (from the development of pulmonary edema and requirement of diuretics to diuretic withdrawal and clinical improvement) of the ACE-inhibitors as monotherapy in mild to moderate heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[ACE-inhibitors and water metabolism in heart failure]. 763 56

The purpose of this study was to develop a bilateral model of frontal cortical contusion in the rat that would demonstrate reproducible deficits typically found after frontal lobe injury in humans. We used a pneumatically controlled cortical impactor to create bilateral contusions of the medial prefrontal cortex (PFC) in adult male Sprague-Dawley rats. Cognitive, neurologic, physiologic, and histopathologic measures were used to evaluate changes caused by the injury. The cognitive task employed the Morris water maze (MWM). Contused rats performed worse than sham-operated controls on measures of time taken to find a submerged platform, distance to the platform, and swim strategy. Neurologic measures revealed impairments of tongue mobility and transient deficits of forelimb placing. Body weights of the contused rats were chronically reduced with respect to controls, indicating that cortical contusion produces disruption in homeostasis. All rats given bilateral PFC contusions developed marked necrotic cavities at the site of impact. The borders surrounding the cavities were heavily lined with astrocytes and ameboid microglia. There was subcortical gliosis in the medial caudate that extended throughout the rostral-caudal length of the caudate-putamen and into the mediodorsal (MD) and ventrolateral (VL) nuclei of the thalamus. The thalamus was also the site of distal transneuronal degeneration. In both the MD and the VL, there was significant neuronal loss in the contused rats as compared with sham-operated controls. This method of bilateral cortical contusion demonstrates clear, reproducible results that would be required for the development of future pharmacologic therapies designed to promote functional recovery.
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PMID:Bilateral frontal cortical contusion in rats: behavioral and anatomic consequences. 783 82

Previous studies from the authors' laboratory have shown that controlled limb perfusion after prolonged, acute ischaemia minimizes reperfusion injury. The present study was performed to investigate the role of osmotic and colloid-osmotic pressure in the initial reperfusate in order to reduce postischaemic limb oedema and subsequent reperfusion injury. A total of 96 isolated rat hindlimbs were used: 18 were perfused immediately after amputation (no ischaemia; untreated) and 78 limbs were subjected to 4 h of warm ischaemia in a moist chamber. Thereafter eight limbs were used to investigate the effects of the addition of mannitol to the initial reperfusate. The remaining 70 limbs received controlled reperfusion (modified reperfusate with various osmotic (315-580 mosmol/l) and colloid-osmotic pressure (0-50 mmHg. perfusion pressure 50 mmHg) during the first 30 min after ischaemia. Controlled reperfusion was always followed by uncontrolled reperfusion (30 min. perfusion pressure 100 mmHg) to simulate the clinical condition where normal blood perfusion at systemic pressure will follow controlled reperfusion. Functional recovery, limb weight, water content of the soleus muscle, limb flow and tissue high-energy phosphates were assessed at the end of the experiment. Results show that a reperfusate without colloid-osmotic pressure (i.e. without macromolecules) produces severe limb oedema (84.6(2.0)% water content) and allows no functional recovery after prolonged warm ischaemia. Addition of mannitol to the initial reperfusate does not prevent severe reperfusion injury. In contrast, a hyperosmotic reperfusate with a colloid-osmotic pressure of 26 mmHg effectively prevents limb oedema (78.6(0.9)% water content, 110.8(2.4)% of control weight). Physiological osmotic pressure (315 mosmol/l), however, will not reduce oedema formation (82.7(0.4)% water content). Furthermore, colloid-osmotic pressure > 26 mmHg increases the viscosity of the reperfusate (flow decreases to < 50% of control) and does not allow an optimal functional recovery. Macromolecules used to create the colloid-osmotic pressure should be of similar molecular weight to albumin (69,000 Da); those with a smaller molecular weight (e.g. hydroxyethyl starch40,000/0.5) produce excessive limb oedema (184.9(13.5)% control weight; 85.7(1.4)% water content) without functional recovery (0% control contractions). The present data suggest that after prolonged limb ischaemia: (1) addition of mannitol to a crystalloid solution does not prevent oedema; (2) hyperosmotic reperfusates (380-480 mosmol/l) with a colloid-osmotic pressure of 26 mmHg are most effective in preventing limb oedema; and (3) macromolecules used to achieve colloid-osmotic pressure should have a molecular weight similar to albumin.
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PMID:Reperfusion injury in skeletal muscle: interaction of osmotic and colloid-osmotic pressure in the initial reperfusate for oedema prevention. 785 91

In studies on aged and brain-lesioned rats the chronic administration of the ACTH(4-9) analog Org2766 has been demonstrated to improve the behavioral performance. Those results suggest that maintenance of hippocampal functioning in senescence and facilitation of functional recovery after brain damage are not due to facilitated reinnervation of denervated structures as suggested in previous studies concerning regeneration of the PNS. Alternative explanations may refer to either the neuroprotective properties of the peptide as demonstrated when chronic treatment immediately follows the damage, or a peptide-induced general change in attention that indirectly may contribute to functional recovery. The behavioral effects after acute treatment with ACTH-like peptides have been previously associated with sustained attention by enhanced neuronal excitability of limbic structures. Now, a hypothesis accounting for both neuroprotection and enhanced attention is forwarded by supposing that the peptide exerts its influence by modulation of NMDA receptor activation. Therefore, the acute effects and interactions between the peptide and the NMDA receptor antagonist AP5 (D,L-2-amino-5-phosphonopentanoic acid), and the peptide and NMDA were studied in a water maze and an open field. Impaired water maze performance induced by an acute intracerebroventricular administration of AP5 was counteracted by the ACTH(4-9) analog Org2766, whereas the peptide alone did not affect spatial orientation. NMDA induced extreme locomotor activity at the periphery of the open field. Interestingly, the ACTH(4-9) analog strongly suppressed NMDA-induced enhanced locomotor activity and normalized the pattern of exploratory behavior.
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PMID:The ACTH(4-9) analog Org2766 modulates the behavioral changes induced by NMDA and the NMDA receptor antagonist AP5. 791 Feb 5


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