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PubMed1989

Isometric contractile function recovery following tourniquet ischemia.

The purpose of this study was to document the recovery of isometric contractile function following tourniquet ischemia. Male Wistar rats (N = 27) were subjected to unilateral hindlimb tourniquet ischemia of 0 hr (control, N = 6), 1 hr (N = 5), 2 hr (N = 5), 3 hr (N = 5) and 4 hr (N = 3). Following a 2-week recovery period, isometric force measurements were made from both gastrocnemii of each rat with the contralateral limb acting as the control side. Each muscle was analyzed for maximal twitch (Pt, N/g), maximal rate of rise of twitch tension (DP/dt, N/sec), time to peak tension (TPT, msec), half relaxation time (RT 1/2, msec), maximal tetanus (P0, N/g, at 100 Hz), and fatigue (Burke Fatigue Protocol). Pt, P0, and DP/dt were significantly different from control values (P less than 0.05) for all hours of tourniquet ischemia. A strong negative correlation (P less than 0.001) was found for twitch (R = -0.84), tetanus (R = -0.78), and maximal rate of force development (R = -0.83) with respect to increasing hours of ischemia. The recovery of isometric twitch and tetanic function following tourniquet ischemia is inversely related to the ischemic interval. This study quantified the relationship between muscle ischemia and recovery of function following a 2-week interval and stresses the functional physiological changes which occur in skeletal muscle following tourniquet ischemia.

Animals↗
PubMed1992

Recovery functions of common peroneal, posterior tibial and sural nerve somatosensory evoked potentials.

We studied recovery functions of the somatosensory evoked potentials (SEPs) of common peroneal (CPN), posterior tibial (PTN) and sural nerves (SN) using a paired conditioning-test paradigm. The interstimulus interval (ISI) of paired stimuli ranged from 2 to 400 msec. In all SEPs with ISIs of 12-20 msec, the amplitude recovery was close to or beyond 100% of the control response, though their latencies and wave forms were not the same as the control. Further increases of the ISI resulted in significant depression of SEP (late phase suppression), most markedly in CPN, and less prominently in SN-SEP. With a longer than 50 msec ISI there was progressive recovery of SEP, but full recovery differed depending on the nerve stimulated; 400 msec ISI was required for CPN-, 250 msec for PTN- and 100 msec for SN-SEP. The peroneal nerve block by local anesthetic injected just distal to the stimulus electrodes abolished the late phase SEP suppression observed before the nerve block. These findings suggest that the late phase SEP suppression is attributable to the "secondary" afferents as a result of activation of peripheral receptors (muscle, joint and/or cutaneous) by the efferent volley initiated from the stimulus point. The greater and longer duration of peripheral receptor activation in CPN than in PTN or SN stimulation could explain the more pronounced and the longer duration of late phase suppression in CPN-SEP.

Adult↗
PubMed1983

[Functional recovery following surgical removal of traumatic epidural hematoma--factor analysis].

UNLABELLED: Factors contributing to functional recovery following evacuation of epidural hematoma were analyzed in 53 subjects. Subjects were limited to the cases with "pure" epidural hematoma. Fifty-three cases were classified into 3 groups based on presence or absence, and duration of preaggravation period (PAP) following occurrence of head trauma (Fig. 1). Level of consciousness at operation and at PAP is summarised in Fig. 2. Major neurological signs at operation are summarized in Table 1. Gradings of functional status were divided to 6 (Table 2). Gradings of 53 subjects which were judged 1 month after removal of epidural hematoma are summarized in Fig. 3. RESULTS: 1) As to outcome in relation to duration of preaggravation period (PAP) and consciousness level at operation (Fig. 4): The patients whose PAP was shorter and whose consciousness level at operation was more severe, took outcome of lower (worse) gradings. 2) As to outcome in relation to interval from the end of PAP to operation and PAP (Fig. 5): The patients whose PAP are within 3 hours, took outcome of relatively good recovery only when epidural hematoma was removed within 5.5 hours after the end of PAP. 3) As to outcome in relation to interval from the end of PAP to operation and consciousness level at operation (Fig. 6): The patients whose consciousness level at operation was better than semicoma took good recovery when epidural hematoma was evacuated within 5.5 hours after the end of PAP. This was right even in the patients who presented with decerebrate posture.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1980

Morphological and functional recovery of the canine gallbladder mucosa following two hours' ischemia.

Temporary interruption of the circulation to the canine gallbladder causes hemorrhagic necrosis of the mucosa and an abolition of active transport of glycine in vitro. The first signs of epithelial recovery following two hours' ischemia are seen in animals examined 7 days after the injury and are characterized by the appearance of a layer of cuboidal epithelial cells in which some mitotic figures are observed, accompanied by a decrease in the amount of necrosis and the presence of granulation tissue. At the same time, there is some slight resumption in glycine uptake. Two weeks after injury, the new epithelium covers a larger surface of the gallbladder wall but recovery is still incomplete. Four weeks after operation, structural and functional recovery has occurred in almost all the animals studied: the epithelium is columnar and does not differ greatly from that seen in the normal gallbladder. Mucosal folds are present although their morphological appearance is slightly altered in comparison with those of control specimens. The gallbladder wall is thickened by fibrosis. Measurements of active glycine transport in vitro confirm that the new epithelium functions normally.

Animals↗
PubMed1991

Contribution of serotonin neurons to the functional recovery after spinal cord injury in rats.

The contribution of serotonin neurons to the functional recovery after spinal cord injury was studied pharmacologically in rats with moderately severe neurologic impairment (complete paraplegia but responsive to tail pinching) 24 h after thoracic spinal cord (T11) compression-induced injury. Fourteen days after cord injury the levels of endogenous norepinephrine (NE, -33%), dopamine (DA, -50%) and serotonin (5-HT, -55%) in the lumbar cord in the injury control rats were decreased and there were significant correlations between the neurologic score and the NE level (rs = 0.562, P less than 0.01) and the 5-HT level (rs = 0.745, P less than 0.001) but not the DA level. Bilateral i.c.v. injection of 5,7-dihydroxytryptamine (200 micrograms/rat) 24 h after cord injury significantly retarded the neurologic recovery during the 14 days after injury, accompanied by a further reduction in the 5-HT level (-86%) but not in the NE or DA level. On the other hand, neither p-chlorophenylalanine (PCPA) (300 mg/kg, i.p., once daily starting 24 h after injury for 13 consecutive days) nor reserpine (1 mg/kg, i.p., 4 times, once 24 h after injury and then every fourth day) had any influence on the time course of the neurologic recovery during the 14 days after injury, although PCPA treatment further reduced the levels of NE (-50%) and 5-HT (-91%), and reserpine treatment further reduced the levels of NE (-95%), DA (-73%) and 5-HT (-85%).(ABSTRACT TRUNCATED AT 250 WORDS)

5,7-Dihydroxytryptamine↗
PubMed1989

Improvement in functional recovery of stunned canine myocardium by long-term pretreatment with oral propranolol.

We investigated the effect of long-term oral pretreatment with the beta-adrenergic antagonist, propranolol (Inderal LA, 160 mg daily for 8 days) on the functional recovery of myocardium after 15-minute coronary artery occlusion followed by 3 hours of reperfusion in barbital-anesthetized dogs. Propranolol-pretreated dogs (N = 9) displayed a significantly lower left ventricular peak-positive rise in ventricular pressure (dP/dt), heart rate, and rate-pressure product throughout the experiment compared with the control group (N = 15). Subendocardial percent segment shortening as measured by sonomicrometry recovered to 65.4 +/- 7.2% of the preocclusion level after pretreatment with propranolol, whereas the control group recovered to only 11.1% +/- 10.2% after 3 hours of reperfusion. To ascertain the beneficial role of a lower heart rate on the recovery of regional contractile function, a third group of dogs (N = 6) was pretreated with propranolol, but heart rate was maintained at control levels by atrial pacing. The beneficial effects of pretreatment with propranolol were abolished in this group. There were no differences between groups in myocardial perfusion in the normal region as measured by the radioactive microsphere technique. However, in postischemic, reperfused myocardium, there was a significantly higher blood flow to subepicardium, mid-myocardium, and subendocardium after reperfusion in the propranolol-pretreated, unpaced group. Thus long-term oral pretreatment with propranolol enhances the contractile recovery of postischemic, reperfused myocardium. This protective effect of beta-adrenergic blockade is primarily related to the reduction in heart rate and enhanced perfusion in the postischemic region.

Administration, Oral↗
PubMed1990

Macular recovery function (nyctometry) in diabetics without and with early retinopathy.

Nyctometry was used to assess macular recovery function in 234 diabetic patients; their retinopathy ranged from no retinopathy (99) to early background retinopathy (135). None had visual symptoms or macular oedema. Abnormal (reduced) nyctometry findings were significantly and directly related to the deterioration of diabetic retinopathy. There was no significant association between reduced or normal nyctometry findings and glycaemia at the time of the examination. The value of nyctometry in screening and follow-up is discussed.

Adaptation, Ocular↗
PubMed1978

Recovery function of short latency components of surface and depth recorded somatosensory evoked potentials in the cat.

Recovery functions of early components of surface and depth recorded somatosensory evoked potentials were studied in the cat. At interstimulus intervals of 50 msec or less differentiation of surface components was optimal. Component I showed less decrement at all ISI's than did component II and recovery curves of both were distinctly different from those of components III (anterior) and IV and the cortical SEP. The latter three potentials had similar recovery curves. Comparisons of latencies and recovery curves of surface recorded potentials with those of depth recorded potentials indicate that component I principally reflects activity in posterior column, that potentials in medial lemniscus, cuneate nucleus, and lateral cuneate nucleus contribute to component II, that the major generator for the contralateral component III is the ventral postero-lateral nucleus of the thalamus, and that component IV is largely due to activity in the sensory radiation. The results of this study support previous observations and conclusions about the origin of short latency, surface recorded somatosensory evoked potentials preceding the cortical SEP.

Animals↗
PubMed1988

Functional recovery after fractures of the distal forearm. Analysis of radiographic and other factors affecting the outcome.

Functional recovery of the wrist and hand after a fracture of the distal forearm in 207 consecutive patients was analysed. A good or excellent result was achieved in 77 percent, fair in 22.5 percent and poor in 0.5 percent of cases. The result in 14 unstable fractures treated with external fixation was as good as that of the whole series. Good functional results were associated with extra-articular fractures, good anatomical results, male sex and low age. Comminuted intra-articular fractures of the radiocarpal joint, fracture line into the distal radio-ulnar joint, fracture of the ulnar styloid and a poor anatomical result in addition to high age contributed to a poor result.

Adolescent↗
PubMed1993

Neurophysiological basis of functional recovery in the neonatal spinalized rat.

It had been shown previously that, following spinalization of the neonatal rat on postnatal day 7 (PN7), at the middle thoracic level, there was spontaneous recovery of coordinated stepping in the hindlimbs, enabling the animal to execute quadrupedal locomotion, with an ataxic gait. No significant recovery occurred in rats that were similarly spinalized on PN14. Despite the functional recovery in the PN7 group, their hindlimbs were paralyzed when not in contact with a surface. In the present experiments, at 16-18 weeks after spinalization, muscle spindle GpIa and cutaneous afferents were tested for functional connectivity to the alpha motoneurons (a-MNs) that innervate the right triceps surae (TS) muscles. The Hoffmann reflex (H-reflex), the tonic stretch reflex (TSR), and cutaneous reflexes were recorded from the right TS muscles in the nonanesthetized, intercollicular decerebrate preparation. The H-reflex and the TSR were readily elicited from the PN7 animals, but not from the PN14 animals. The PN14 preparations were characterized by prolonged (> 18 h in 3/8 cases), spontaneous discharge of motor units, and prominent M responses. There was widespread, bilateral convergence of cutaneous afferents from the hindquarters to the a-MNs of the TS muscles in both the PN7 and the PN14 preparations. In the nonspinalized, control preparation, only ipsilateral, cutaneous afferents activated the right TS a-MNs. These results demonstrate that in the chronic (> 3 months after spinalization), spinalized PN7 rat, but not in the PN14 rat, there is a tight functional connectivity between the hindlimb GpIa afferents and their homonymous a-MNs.

Animals↗
PubMed1987

Oral administration of nimodipine accelerates functional recovery following peripheral nerve damage in the rat.

Oral administration of the Ca2+-entry blocker nimodipine accelerates in a dose-dependent manner the recovery of sensorimotor function following a crush lesion of the rat sciatic nerve. The beneficial effect of nimodipine was apparent in both a foot shock withdrawal test and in a test analyzing the walking pattern of the rat. These data are the first demonstration of nimodipine-induced enhanced recovery following peripheral nerve damage.

Administration, Oral↗
PubMed1993

Exogenous epidermal growth factor fails to accelerate functional recovery in the autotransplanted ischemic pig kidney.

The reversibility of ischemic renal injury is dependent on epithelial cell regeneration and repopulation of the nephron. Renal cells produce and respond to many growth factors. In the rat, epidermal growth factor (EGF) is mitogenic for tubular cells and accelerates renal recovery after ischemia. We used a pig renal autotransplant model to evaluate the effect of exogenous EGF on renal recovery in a large animal more analogous to man. Group 1 animals underwent left autotransplant after 120 minutes of warm ischemia and received either a single intra-arterial dose of recombinant human EGF (EGF, 10(-7) M.) (N = 11) or vehicle alone (N = 6). Group 2 animals underwent left autotransplant after 72 hours of cold preservation with Collins' solution and received a similar intra-arterial dose plus a subcutaneous dose of EGF (0.5 ml. of 10(-3) M.) (N = 8) or vehicle alone (N = 6). Contralateral nephrectomy was performed in all animals. Daily creatinine measurements revealed no beneficial effect from EGF on recovery of renal function in Group 1 or 2 animals. Studies of EGF on pig proximal tubular cells demonstrated in vitro mitogenesis; autoradiography with 125I-EGF revealed binding of EGF throughout the kidney. Immunohistochemistry showed significant tubular cell proliferation in response to ischemic injury, without further enhancement from EGF. Thus, although exogenous EGF bound to pig kidney cells and stimulated cell proliferation, we were unable to demonstrate a clinically significant acceleration of recovery from ischemic injury.

Animals↗
PubMed1995

Contributing factors to poor functional recovery after delayed nerve repair: prolonged denervation.

The effects of prolonged denervation, independent from those of prolonged axotomy, on the recovery of muscle function were examined in a nerve cross-anastomosis paradigm. The tibialis anterior muscle was denervated for various durations by cutting the common peroneal nerve before a freshly cut tibial nerve was cross-sutured to its distal stump. Nerve regeneration and muscle reinnervation were quantified by means of electrophysiological and histochemical methods. Progressively fewer axons reinnervated the muscle with prolonged denervation; for example, beyond 6 months the mean (+/- SE) motor unit number was 15 +/- 4, which was far fewer than that after immediate nerve suture (137 +/- 21). The poor regeneration after prolonged denervation is not due to inability of the long-term denervated muscle to accept reinnervation because each regenerated axon reinnervated three- to fivefold more muscle fibers than normal. Rather, it is due to progressive deterioration of the intramuscular nerve sheaths because the effects of prolonged denervation were simulated by forcing regenerating axons to grow outside the sheaths. Fewer regenerated axons account for reinnervation of less than 50% of the muscle fibers in each muscle and contribute to the progressive decline in muscle force. Reinnervated muscle fibers failed to fully recover from denervation atrophy: muscle fiber cross-sectional area being 1171 +/- 84 microns2 as compared to 2700 +/- 47 microns2 after immediate nerve suture. Thus, the primary cause of the poor recovery after long-term denervation is a profound reduction in the number of axons that successfully regenerate through the deteriorating intramuscular nerve sheaths. Muscle force capacity is further compromised by the incomplete recovery of muscle fibers from denervation atrophy.

Anastomosis, Surgical↗
PubMedDate not supplied

Clinical implications of the impact of autologous blood donation on functional recovery.

The practice of depositing units of autologous blood to prepare for elective surgery is steadily increasing. This article outlines the advantages and limitations of autologous blood donations. Secondary analysis from a study of functional recovery following total knee replacement compares functional outcomes of people who predeposited autologous units with those who did not. Clinical implications and suggestions are made for managing the patient's physiologic status during the donation process, as well as hemodynamic status during the postoperative transfusion period.

Activities of Daily Living↗
PubMed1983

Improved functional recovery of the isolated rat heart after 24 hours of hypothermic arrest with a stable prostacyclin analogue (ZK 36 374).

Prostacyclin (PGI2) can protect the heart against ischemia, i.e. it can reduce myocardial damage [9, 10]. PGI2 protects the myocardium in vivo by preventing platelets from clumping and by dispersing preformed platelet aggregates [1,14]. However, also in the absence of platelets, PGI2 was shown to protect the myocardium against ischemia at concentrations that did not affect smooth muscle tone in the vessel wall [2]. This protective effect of PGI2 in vitro might be related to a stabilization of cell membranes in adrenergic nerve endings and hence to the prevention of ischemia-induced catecholamine release [13]. The instability of PGI2, both in vitro and in vivo, limits its application during long ischemic periods. Recently, a stable prostacyclin analogue, ZK 36 374, was demonstrated to have several prostacyclin-mimetic activities, both in vitro and in vivo [11,12]. In this communication we report upon the beneficial effect of this stable prostacyclin analogue at a low concentration (4 nM) on the extent of ischemic damage, on the recovery of myocardial function and on the occurrence of arrhythmias in the isolated rat heart after 24 h hypothermic cardiac arrest.

Animals↗
PubMed1994

Rate of glycolysis during ischemia determines extent of ischemic injury and functional recovery after reperfusion.

The efficacy of increasing glycolysis during ischemia for enhancing the salutary effects of reperfusion was evaluated in isolated perfused rabbit hearts subjected to low-flow ischemia followed by reperfusion. Control hearts were perfused with buffer containing 0.4 mM palmitate, 5 mM glucose, and 70 mU/l insulin. Additional groups of hearts were perfused with double glucose/insulin and 1 mM dichloroacetate or were subjected to substrate priming to increase preischemic glycogen content. Ischemic contracture was completely prevented in hearts perfused with high glucose/insulin and was delayed markedly by either dichloroacetate or enhanced preischemic glycogen [45 +/- 14 and 31 +/- 20 min, respectively; P < 0.01 each vs. control (11 +/- 10 min)] and inversely related to the rate of lactate production. With reperfusion, recovery of developed pressure was 56 +/- 23% of baseline in control hearts, 90 +/- 8% in hearts receiving high glucose/insulin, 92 +/- 5% in hearts receiving dichloroacetate, and 79 +/- 19% in hearts with increased glycogen (P < 0.05 each vs. control hearts). Creatine kinase release was reduced by > 55% in treated hearts. Thus enhancement of glycolysis by diverse mechanisms during ischemia decreased ischemic damage and improved the recovery of contractile function with reperfusion.

Animals↗