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

Working rat hearts were perfused for 15 minutes at 37 degrees C before switching to a Langendorff perfusion (60 mm Hg aortic pressure) at 10 degrees C for 40 minutes of hypothermic arrest. Ventricular function was allowed to recover for 15 minutes at 37 degrees C by reestablishing the prehypothermic conditions. The perfusate was Krebs-Henseleit bicarbonate buffer containing 3% bovine serum albumin and either glucose (11 mmol/L) or glucose (11 mmol/L) plus palmitate (1.2 mmol/L) and gassed with 95% O2 and 5% CO2. In hearts receiving glucose alone as substrate, coronary flow was maintained constant during the 40 minutes of hypothermic arrest and returned to prehypothermic rates with rewarming. Ventricular function, as estimated by peak systolic pressure and heart rate, recovered to the prehypothermic level. When palmitate was added, coronary flow decreased continuously throughout the hypothermic perfusion (22% decrease by 40 minutes), and ventricular pressure development was lower throughout the rewarming perfusion. Tissue levels of adenosine triphosphate and creatine phosphate were well maintained and long-chain acyl coenzyme A and acyl carnitine decreased during hypothermia regardless of the substrate provided. With rewarming, tissue levels of adenosine triphosphate and creatine phosphate decreased in those hearts receiving palmitate. Omission of fatty acid either during hypothermia or during the first 5 minutes of rewarming improved recovery of function. Addition of oxfenicine to inhibit fatty acid oxidation, or inhibition of Ca2+ overload by verapamil and low perfusate Ca2+, prevented the effects of palmitate on ventricular function.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Fatty acids suppress recovery of heart function after hypothermic perfusion. 192 62

The effect of oxygenation of St. Thomas' Hospital cardioplegic solutions (ST solutions) was examined in isolated working rat hearts. They were subjected to hypothermic arrest (12 degrees C, 22 degrees C) for 3 hours with infusions of cardioplegic solutions repeated for 5 minutes every 30 minutes. Based on myocardial temperature and mode of oxygenation, the hearts were divided into six groups. Group I: 12 degrees C and non-oxygenated; Group II: 12 degrees C and 100%-oxygenated; Group III: 12 degrees C and 95% O2 + 5% CO2-oxygenated; Group IV: 22 degrees C and non-oxygenated; Group V: 22 degrees C and 100%-oxygenated; Group IV: 22 degrees C and 95% O2 + 5% CO2-oxygenated. The pH of ST solutions varied with the mode of oxygenation as follows: 7.9-8.2 in Groups I and IV; 8.7-8.9 in Groups II and V; 7.1-7.4 in Groups III and VI. In the two Groups (II and V) with 100%-oxygenated ST solutions, the functional recovery of the hemodynamic parameters was significantly inferior to that of Group I and III, VI with 95% O2 + 5% CO2-oxygenated ST solutions. It was concluded that 95% O2 + 5% CO2-oxygenated ST solutions were superior to 100%-oxygenated ones and the functional recovery at 22 degrees C of 95% O2 + 5% CO2-oxygenated ST solutions were comparable to that of non-oxygenated ones at 12 degrees C.
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PMID:[Oxygenation of St. Thomas' Hospital cardioplegic solutions--effects of myocardial temperature and carbon dioxide]. 203 29

A series of studies was undertaken to establish the optimal oxygenation of St. Thomas' Hospital cardioplegic solution (ST). Using an isolated working rat heart model of cardiopulmonary bypass and the cardioplegic arrest the effect of oxygenation of ST were investigated in this study. The effects of oxygenated ST with various O2/CO2 mixture (100% O2, 99% O2 + 1% CO2, 98% O2 + 2% CO2, 95% O2 + 5% CO2) upon post ischemic functional recovery were compared with those of non-oxygenated ST. Under both normothermic and hypothermic conditions, the pH of the St. Thomas' gassed with 99% O2 + 1% CO2 mixture was maintained at 7.8, and this cardioplegic solution showed highest percent recovery of aortic flow. On the contrary, the pH of St. Thomas' cardioplegic solution oxygenated with 100% O2 exceed 9.0 and it showed lethal effect upon postischemic cardiac function. Thus oxygenation of NaHCO3 containing crystalloid cardioplegic solution oxygenated with 100% O2 is rather harmful and the 99% O2 + 1% CO2 gas is the crucial gas mixture for clinical and experimental use with oxygenated ST.
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PMID:[The optimal oxygenation of cardioplegic solution--the buffer effect of carbon dioxide and pH control]. 212 55

Conventional suture repair of peripheral nerves results in a fibrotic reaction that is detrimental to nerve regeneration. As an alternative procedure known as "laser-assisted" repair, a laser can be used, along with a reduced number of sutures, to reanastomose served peripheral nerves. To explore the long-term implications of this technique, the right sciatic nerves of Sprague-Dawley rats were surgically cut and reanastomosed either by means of four epineurial sutures or two epineurial sutures and CO2 laser welds. Tensile strength, electrophysiology, histology, and functional studies were performed up to 11 months postoperatively. Tensile strength measurements indicate no long-term disadvantage with the laser-assisted technique, although the short-term tensile strength is lower than with conventional suture repair. The conduction velocities of the repaired nerves were similar for both techniques; however, laser-assisted repaired nerves were found to have lower stimulation thresholds and reduced branching compared to the suture repaired nerves. The measured functional recovery was similar for both repair techniques.
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PMID:Comparative study of suture and laser-assisted anastomoses in rat sciatic nerves. 255 2

The effects of hypoxia on hippocampal CA1 neurones in tissue slices of the rat brain were studied in vitro by intracellular recording. In response to superfusion of a hypoxic medium equilibrated with 95%N2-5% CO2, a majority of the neurones showed a transient depolarization followed by a hyperpolarization of 5-15 mV in amplitude and 4-12 min in duration. The hyperpolarization was, in turn, followed by a slow depolarization which within 20 min of hypoxic exposure reached a plateau level of about 25 mV above the prehypoxic resting potential. Both the initial hyperpolarization and subsequent depolarization were associated with a reduction in membrane resistance. The hyperpolarization reversed in polarity at a membrane potential of -83 mV. There was an almost linear relationship between amplitude of the hyperpolarization and membrane potential. The hyperpolarization was markedly enhanced in potassium-free media and was depressed in high-potassium solution. Superfusion of ouabain (5-7 microM)-containing medium in normoxic conditions produced hyperpolarizing and depolarizing responses similar to those elicited by hypoxic exposure. The slow depolarization was also mimicked by elevation of the extracellular potassium concentration to 10-20 mM. Evoked i.p.s.p.s were abolished within 4 min of hypoxic exposure while evoked e.p.s. p.s were maintained for about 20 min of hypoxic superfusion. Soma spikes of the neurones elicited by a depolarizing pulse were also well preserved. Their threshold was, however, raised, concomitant with a decrease in the peak amplitude. In a minority of the neurones the slow depolarization was suddenly followed by a rapid depolarization, after which the neurones showed no functional recovery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypoxia in brain slices. 273 Jun 2

In surgery of the knee, combining CO2 laser and arthroscopy provides the benefits of both techniques: work at a distance from the lesion and bleeding control for the laser, patient's comfort and functional recovery for the arthroscopy. This original method requires a CO2 laser of at least 40 watts, CO2 as gas for arthroscopy and the appropriate manual instruments. Forty patients totalling 52 lesions were operated upon by this method with 11 initial failures and 5 complications: 1 case of synovial fluid leakage due to skin burn, 2 cases of phlebitis and 2 cases of spontaneously regressive fever. The results obtained after 1 year follow-up in arthrolysis, adhesiotomy, treatment of chondromalacia patellae and partial meniscectomy are given. The CO2 laser-arthroscopy combination seems to be particularly suitable for arthrolysis and adhesiotomy.
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PMID:[Carbon dioxide laser in arthroscopic surgery of the knee]. 293 10

A marked decrease in the activity of the amiloride-sensitive Na+/H+ exchanger has been demonstrated in hearts from streptozotocin (STZ)-induced diabetic rats. The aim of this study was to investigate the contribution of other specific sarcolemmal transport mechanisms to intracellular pH (pHi) recovery upon reperfusion in STZ-induced diabetic rat hearts and their relation to recovery of ventricular function. Isovolumic rat hearts were submitted to a zero-flow ischemic period of 28 min at 37 degrees C and then reperfused for 28 min. The time course of pHi decline during ischemia and of recovery on reperfusion was followed by means of 31P-labeled NMR. The perfusion buffers used were either HEPES or CO2/HCO3-. An HCO3(-)-dependent (amiloride-insensitive) mechanism contributed to pHi recovery after ischemia in the diabetic rat hearts. Even when the Na+/H+ exchanger was blocked by amiloride in nominally HCO3(-)-free solution, a rapid rise in pHi occurred during the first 3 min of reperfusion. The early rise in pHi was reduced by external lactate and inhibited by alpha-cyano-4-hydroxycinnamate. This suggested that a coupled H(+)-lactate efflux may be a major mechanism for acid extrusion in the initial stage of reperfusion. The observation of a higher functional recovery on reperfusion in diabetic hearts is in accordance with previous studies using HCO3- buffer. However, this study shows that a good recovery of function occurred even more rapidly in diabetic hearts receiving HEPES-buffered solution than in those receiving HCO3(-)-buffered solution. This suggests that the HCO3(-)-dependent mechanism of regulation may be depressed in diabetic rat hearts.
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PMID:Mechanisms of intracellular pH regulation during postischemic reperfusion of diabetic rat hearts. 785 41

Recently we have shown that intracellular low molecular weight (LMW) iron increases during ischemia. It is hypothesized that this increase in LMW iron during ischemia underlies the reported hydrogen peroxide toxicity toward ischemic hearts. To investigate this hypothesis, rat hearts were subjected to 15 min of no-flow ischemia and reperfused with buffer saturated against 95% N2 and 5% CO2 (anoxic reperfusion) for 7 min. Hearts were then switched to buffer saturated against 95% O2 and 5% CO2 (reoxygenation) to assess functional recovery. The cardiac function recovered to 80 +/- 7% of the preischemic value. When the anoxic reperfusion was applied in the presence of 10 microM hydrogen peroxide, functional recovery after reoxygenation was 47 +/- 7%. Hearts that were perfused with deferoxamine before ischemia and then subjected to ischemia and anoxic reperfusion in the presence of 10 microM hydrogen peroxide recovered to 78 +/- 8%. Immediate reoxygenation after ischemia led to only 45 +/- 6% recovery of function. During ischemia, LMW iron increased from 49 +/- 45 to 183 +/- 45 pmol/mg protein (p < .05) and decreased to 58 +/- 38 pmol/mg protein (p < .05) during the subsequent anoxic perfusion. Rat hearts preloaded with deferoxamine showed a slightly higher LMW iron content than normal (85 +/- 23 and 49 +/- 45 pmol/mg protein, respectively; n.s.), which showed a small, nonsignificant increase up to 136 +/- 42 pmol/mg protein after 15 min of ischemia. No significant changes were found in reduced and oxidized glutathione content and glutathione peroxidase or catalase activities under those conditions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The increased susceptibility to hydrogen peroxide of the (post-)ischemic rat heart is associated with the magnitude of the low molecular weight iron pool. 800 30

Although preischemic hyperglycemia is known to aggravate damage due to transient ischemia, it is a matter of controversy whether or not this is a result of the exaggerated acidosis. It has recently been reported that although tissue acidosis of a comparable severity could be induced in normoglycemic dogs by an excessive rise in arterial CO2 tension, short-term functional recovery was improved, rather than compromised. In the present experiments we induced excessive hypercapnia (PaCO2, approximately 300 mm Hg) in normoglycemic rats before inducing forebrain ischemia of 10-min duration. This reduced the brain extracellular pH to values normally encountered in hyperglycemic rats subjected to ischemia. The events induced by hypercapnia clearly enhanced ischemic brain damage, as assessed histologically after 7 days of recovery. We hypothesize that the decisive event was an exaggerated decrease in extra- and intracellular pH and that the results thus demonstrate an adverse effect of acidosis. However, since postischemic seizures did not occur in the hypercapnic ischemic rats, the results also demonstrate that changes in intra-extracellular pH and bicarbonate concentrations modulated ischemic damage in an unexpected way.
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PMID:Acidosis induced by hypercapnia exaggerates ischemic brain damage. 811 21

The isolated working rat heart model was use to define the cardioprotective effects (function, metabolic and ultrastructure) of the oxygenated St. Thomas' Hospital No. 2 cardioplegic solution (STH) during lengthy, hypothermic ischaemia (20 degrees C, 4 hours and 5 hours). Hearts (n = 9 for each group) were arrested with and exposed to multidose reinfusion (2 min every 40 min interval) throughout the ischaemic period with the cold (4 degrees C) STH or oxygenated (95% O2:5% CO2) STH. Oxygenated STH significantly (p < 0.01) improved the postischaemic recovery of cardiac output from 49.5 +/- 11.1% to 96.8 +/- 1.5% (in 4 hours) and from 20.3 +/- 7.2% to 72.2 +/- 5% (in 5 hours). Other indices of functional recovery showed similar improved performance with the significant decrease in time from the onset of reperfusion to the return of regular sinus rhythm (57 +/- 8 v 495 +/- 150 s). The efflux of lactate during 5 hr ischaemic arrest was decreased (20.62 +/- 1.3 v 26.18 +/- 1.73 mumol/heart for oxygenated STH and STH, respectively, p < 0.05) and the progressive increase in the coronary vascular resistance was abolished in the oxygenated STH treated hearts. These improvements were associated with the reduction in the decline of the myocardial adenosine triphosphate (14.49 +/- 2 v 3.3 +/- 0.19 mumol/g dry wt), creatine phosphate (24.61 +/- 3.47 v 7.48 +/- 1.34 mumol/g dry wt) and guanosine triphosphate (1.69 +/- 0.2 v 0.84 +/- 0.08 mumol/g dry wt) during ischaemia, total resynthesis after reperfusion (ATP: 103% v 36%, CP: 105% v 69% and GTP: 203% v 61% of control) and the total absence of myocardial cells and microvasculature injuries in ischaemic (non-reperfused) hearts. These results confirm that the provision of additional oxygen to the St. Thomas' Hospital solution (with 95% O2:5% CO2) can meet the metabolic demand of the ischaemic myocardium and thus increase the safe duration of cardiac arrest.
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PMID:Protective effects of oxygenated St. Thomas' Hospital cardioplegic solution during ischaemic cardiac arrest: improved function, metabolism and ultrastructure. 828 49


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