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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of reperfusion coronary vasodilatation on postischemic myocardial mechanical function has been investigated in the isolated working rat heart. After a working period to assess control function, all the hearts were subjected to a single infusion (10 ml) of St. Thomas' Hospital cardioplegic solution No. 1 at 4 degrees C and were kept immersed in the same solution for 4 hours at 4 degrees C. Then hearts (six in each group) were initially reperfused at 37 degrees C for 10 minutes, either with ordinary reperfusate (Krebs-Henseleit bicarbonate buffer) or with reperfusate containing additional coronary dilator. After this period, all hearts were subjected to a further 5 minutes of ordinary reperfusate before being put back into the working mode to assess functional recovery. Mean reperfusion coronary flows and the steady coronary flow measured after 10 minutes of reperfusion in ml/min +/- SEM were--Krebs (control): 17.4 +/- 0.39 and 13.4 +/- 0.40; adenosine (3.75 mumol/L): 19.9 +/- 0.6 and 16.7 +/- 0.8; papaverine (0.05 mmol/L): 21.8 +/- 2.3 and 17.3 +/- 1.8; dipyridamole (2 mmol/L): 20.7 +/- 1.7 and 17.9 +/- 1.0; nitroglycerin (15 mg/L): 20.5 +/- 0.45 and 19.9 +/- 1.4; diltiazem (0.05 mmol/L): 19.6 +/- 2.98 and 17.7 +/- 1.8; calcitonin gene-related peptide (0.03 mmol/L): 20.8 +/- 0.69 and 18.0 +/- 1.3; 5-hydroxytryptamine (0.01 mmol/L): 19.2 +/- 0.53 and 16.9 +/- 0.80. Mean postischemic recovery of cardiac output, peak aortic pressure, and differentiation of pressure were expressed as percent of preischemic control +/- SEM were--Krebs: 54.1 +/- 2.8, 69.1 +/- 2.8, and 53.9 +/- 3.0; adenosine: 78.0 +/- 5.6, 89.5 +/- 2.9, and 69.1 +/- 1.9; papaverine: 81.8 +/- 3.9, 91.8 +/- 3.1, and 71.0 +/- 4.1; dipyrdamole: 67.3 +/- 3.3, 84.3 +/- 2.3, and 75.0 +/- 2.7; nitroglycerin: 83.1 +/- 4.8, 79.7 +/- 2.7, and 69.0 +/- 0.5; diltiazem: 76.5 +/- 3.7, 85.9 +/- 2.9, and 73.3 +/- 1.7; calcitonin gene-related peptide: 79.5 +/- 3.6, 90.0 +/- 4.9, and 75.4 +/- 3.9; 5-hydroxytryptamine: 71.6 +/- 3.2, 85.5 +/- 3.5, and 67.9 +/- 4.8. There was a positive correlation between mean reperfusion coronary flow, steady coronary flow, and postischemic recovery of cardiac output, peak aortic pressure, and differentiation of pressure. Mean reperfusion coronary flow, steady coronary flow, and postischemic recovery of cardiac output, peak aortic pressure, and differentiation of pressure were significantly greater in groups reperfused with vasodilators (p < 0.05) compared with control values.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Enhancement of low coronary reflow improves postischemic myocardial function. 143 19

It was hypothesized that heterologous anti-rat visceral yolk sac serum (AVYS) exerts its teratogenic effect by reducing the endocytosis of serum proteins by the visceral yolk sac (VYS), thus reducing the supply of amino acids to the embryo and VYS. To evaluate this hypothesis, we studied the effect of teratogenic AVYS on the endocytic function of the VYS and the ultrastructure of the VYS and parietal yolk sac (PYS). Rat conceptuses were exposed to a teratogenic dose of AVYS on the 10th day of gestation in vivo or in vitro. Control and AVYS-exposed specimens were collected 24-192 hr later and prepared for scanning and transmission electron microscopy (SEM and TEM, respectively) utilizing standard procedures. The Endocytic Index was calculated for the VYS utilizing standard procedures. Approximately 97% of the in vivo exposed and 94% of the in vitro exposed embryos were morphologically abnormal. Ultrastructural observations showed that exposure to AVYS in vivo or in vitro caused severe damage to the VYS endodermal epithelial cells with loss of cellular borders, reduction in the number and length of microvilli, and increased cellular inclusions; and some damage to PYS endodermal cells with increased blebbling and decreased cell number. Recovery was evident at 72 hr and complete by 96 hr. The Endocytic Index was significantly reduced in the VYS 24 and 48 hr after injecting AVYS into the pregnant rat but was not significantly different at 96 and 192 hr. Our results show that the AVYS antiserum damaged visceral endodermal epithelium experienced ultrastructural recovery with parallel functional recovery. These studies suggest that transient yolk sac placental ultrastructural damage and dysfunction was probably sufficient to cause irreversible damage to the developing embryo during early organogenesis. We conclude that the proximate effect of the AVYS was on the plasma membrane of the visceral endoderm and that decreased pinocytosis is a consequence of this effect.
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PMID:Ultrastructure and function of the rat yolk sac: damage caused by teratogenic anti-VYS serum and recovery. 192 77

To determine whether halothane has protective effects on the ischemic heart, the influence of various concentrations (0.5%-1.5%) of halothane on metabolic and functional recovery during reperfusion after 60-min hypothermic (20 degrees C) and 40-min normothermic cardioplegic arrest was determined in the isolated rat heart. Halothane was administered either before and after arrest or intermittently during arrest. Hearts not receiving halothane demonstrated a reduction in adenosine triphosphate (ATP) content from a control value of 20.35 +/- 1.66 mumol/g dry wt (mean +/- SEM) (before arrest) to 9.34 +/- 1.12 mumol/g dry wt at the end of arrest (P less than 0.001). The myocardial ATP content, when measured 20 min after arrest and during reperfusion, remained decreased (9.57 +/- 0.62 mumol/g dry wt). Under these experimental conditions, aortic flow was reduced from 43.62 +/- 2.40 mL/min before arrest to 1.80 +/- 1.80 mL/min 20 min after arrest and during reperfusion (P less than 0.001). The administration of adrenaline after 20 min of reperfusion resulted in partial recovery to 22.01 +/- 8.36 mL/min. Administration of halothane (0.5%) before the cardioplegic period was associated with a reduction of ATP at the end of the normothermic arrest (4.02 +/- 0.38 mumol/g dry wt; P less than 0.01), but the ATP increased significantly (13.45 +/- 0.32 mumol/g dry wt) when measured after the arrest and after 20 min of reperfusion and stimulation with adrenaline.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Halothane does have protective properties in the isolated ischemic rat heart. 195 71

The present study adapted the overwintering strategy employed by freeze-tolerant amphibians and reptiles to freeze-preserve the isolated rat heart. The heart was flushed with a cardioplegic solution and supercooled to -1.2 and -3 degrees C. Then freezing was induced by inoculation of ice crystal. The viability of the heart explant was assessed after reanimation by the isolated working heart perfusion. There was no recovery of function in hearts flushed with solution containing 0.28 mM CaCl2. Lowering the concentration of CaCl2 to 0.15 mM, however, rendered good functional return. Furthermore, inclusion of 50 mM glycerol in the flush solution dramatically improved functional preservation. Under the best conditions defined here, the recoveries of aortic flow, coronary flow, cardiac output, systolic pressure, and work in hearts stored at -1.2 degrees C for 3 h were 72.8 +/- 6.8, 87.2 +/- 4.2, 77.6 +/- 5.4, 83.4 +/- 2.8, and 66.6 +/- 5.9% (mean +/- SEM, n = 8) of the unstored control levels, respectively. The myocardial ice content was 18.6 +/- 5.4% (n = 5) of tissue water. Prolonging the storage time to 5 h increased the ice content to 45.3 +/- 8.1% and reduced the recovery of cardiac output to 23 +/- 11% of the control value (mean +/- SEM, n = 5). Hearts frozen at -3 degrees C for 1.5 h showed 29.4 +/- 8.7% (n = 3) of control cardiac output during reperfusion. This novel approach may provide an opportunity to advance our knowledge about freezing preservation of not only the heart but other solid organs as well.
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PMID:Freezing preservation of adult mammalian heart at high subzero temperatures. 207 Jun 19

Isolated hearts from rabbits, hamsters, ferrets, gerbils, rats, mice and guinea pigs were used to investigate species differences in (i) stability during aerobic perfusion, (ii) susceptibility to ischemic injury and (iii) responsiveness to cardioplegic protection. During 120 minutes of continuous aerobic perfusion, the rate of functional deterioration differed between species. The rabbit was the most stable and the guinea pig the least: the mean +/- SEM of the left ventricular developed pressure falling, after 120 minutes of perfusion, to 82 +/- 4% and 60 +/- 6%, respectively. In studies with 30 minutes of ischemia and 60 minutes of reperfusion, the developed pressure recovered to 72 +/- 2, 71 +/- 2, 65 +/- 3, 64 +/- 2, 58 +/- 3, 50 +/- 8 and 50 +/- 2% of its pre-ischemic value in the rabbit, hamster, ferret, gerbil, rat, mouse and guinea pig, respectively. With 60 minutes of ischemia, the recovery of developed pressure in the guinea pig, rabbit, rat, mouse, hamster, ferret and gerbil was 5 +/- 1, 19 +/- 2, 22 +/- 3, 30 +/- 5, 55 +/- 4, 60 +/- 2 and 45 +/- 5%, respectively. Creatine kinase leakage and changes in tissue metabolite content generally reflected the degree of functional injury. In further studies, groups of 6 hearts were infused for 2 minutes with St. Thomas' Hospital Cardioplegic Solution, then subjected to 30 minutes of ischemia. Cardioplegia improved the recovery of developed pressure in the rabbit, hamster, gerbil, rat and mouse (from 72 +/- 2, 71 +/- 2, 64 +/- 2, 58 +/- 3 and 50 +/- 8% to 82 +/- 3, 103 +/- 3, 84 +/- 4, 77 +/- 2 and 78 +/- 5%, respectively; p less than 0.05 for each species). However, no protection was observed in the ferret and guinea pig (65 +/- 3 and 50 +/- 2% versus 66 +/- 3 and 47 +/- 6%, respectively; p = NS). With cardioplegia, tissue high-energy phosphates increased significantly in all species except the gerbil. Rat and guinea pig hearts were taken for time-response studies (ischemia for 15, 20, 30, 45, 50 and 60 minutes in the rat and 15, 30, 45 and 60 minutes in the guinea pig) with or without cardioplegia. In the rat, cardioplegia improved recovery over an ischemic time-window of 20-45 minutes, but in the guinea pig no improvement was detected. Creatine kinase leakage reflected the patterns of functional recovery. In contrast, high-energy phosphates were preserved better in both species after 30 minutes of ischemia.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Species differences in susceptibility to ischemic injury and responsiveness to myocardial protection. 210 1

The isolated perfused working rat heart model of cardiopulmonary bypass and ischaemic cardiac arrest has been used to investigate whether addition of various organic anti-oxidants to the St Thomas' Hospital cardioplegic solution can enhance the recovery of function of the rat myocardium after normothermic (37 degrees C) global ischaemic arrest. Five anti-oxidants were studied: (i) ascorbate (1.0 and 10.0 mmol.litre-1), (ii) methionine (1.0 and 10.0 mmol.litre-1), (iii) reduced glutathione (1.0 and 10.0 mmol.litre-1), (iv) dimethylthiourea (0.1, 1.0, 10.0 and 50.0 mmol.litre-1), (v) N-2-mercaptopropionyl glycine (0.1, 1.0 and 10.0 mmol.litre-1). The recovery of aortic flow in control hearts which were free of anti-oxidant was 50.7(SEM 0.5)%; ascorbate (1.0 or 10.0 mmol.litre-1) improved this recovery to 72.1(1.7) and 70.2(0.3)% respectively; methionine (1.0 and 10.0 mmol.litre-1) improved the recovery to 74.1(5.7)% and 67.7(1.7)%, respectively; reduced glutathione (1.0 and 10.0 mmol.litre-1) improved the recovery to 66.7(1.4)% and 74.0(1.7)% respectively. In further studies, the addition of dimethylthiourea (0.1, 1.0 and 10.0 mmol.litre-1) to the cardioplegic solution failed to improve recovery of aortic flow [47.3(8.0), 24.6(7.3), 48.0(7.7)% respectively] when compared to its anti-oxidant free control value of 40.4(6.1)% and at a concentration of 50.0 mmol.litre-1 a very poor recovery of aortic flow of 7.7(4.8)% was observed. Mercaptopropionyl glycine (0.1, 1.0 and 10.0 mmol.litre-1) also failed to improve the recovery of aortic flow [34.7(1.6), 34.7(7.7) and 25.6(5.4)% respectively.2+ Since biological membranes are highly permeable to dimethylthiourea and mercaptopropionyl glycine, it is possible that they accumulate in the intracellular compartment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Free radicals and cardioplegia: organic anti-oxidants as additives to the St Thomas' Hospital cardioplegic solution. 251 9

The effect of beta-adrenergic blockade on the salvage and functional recovery of reperfused myocardium was investigated in anesthetized dogs. Immediately after thrombotic occlusion of the left anterior descending coronary artery, the cardioselective beta-blocking agent metoprolol was given intravenously at a dose of 0.5 mg/kg infused over 10 min. One hour after the onset of occlusion, recanalization was initiated by intravenous infusion of recombinant human tissue-type plasminogen activator (rt-PA, 10 micrograms/kg/min for 30 min). Anatomic infarct size expressed as percent of the left ventricular mass (I/LV), global ejection fraction, and mean systolic shortening of the segmental radii (SS) of the infarcted area were measured either after 24 hr or 1 week in six groups of six dogs each: group I (rt-PA + metoprolol, evaluated at 24 hr), group II (rt-PA + metoprolol, evaluated at 1 week, group III (rt-PA alone, evaluated at 24 hr), group IV (rt-PA alone, evaluated at 1 week), group V (persistent occlusion, evaluated at 24 hr), and group VI (persistent occlusion, evaluated at 1 week). The smallest infarcts were found in reperfused dogs given metoprolol, but the differences from dogs receiving rt-PA alone were not statistically significant (I/LV, expressed as mean +/- SEM: 5.5 +/- 0.9% in group I, 6.7 +/- 1.9% in group II, 15.4 +/- 5.0% in group III, 11.4 +/- 3.5% in group IV, 23.6 +/- 2.5% in group V, and 26.9 +/- 2.3% in group VI).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reduction in infarct size and enhanced recovery of systolic function after coronary thrombolysis with tissue-type plasminogen activator combined with beta-adrenergic blockade with metoprolol. 310 51

Regional diastolic wall motion was studied with sonomicrometry in 30 open chest anaesthetised dogs after left anterior descending stenosis or occlusion. Post-systolic shortening and thickening, defined as the magnitude of segment shortening or wall thickening that occurred after end systole, was measured in peripheral and central ischaemic segments. These post-systolic events developed concurrently with impaired systolic shortening or thickening, either immediately after acute coronary occlusion or during progressive stenosis, and persisted with the development of dyskinesis and during reperfusion. The magnitude of these events in dyskinetic segments of 24 dogs was considerable, reaching 50(2)% (mean(SEM)) and 33(3)% of shortening or thickening that was present before coronary occlusion. Post-systolic shortening and thickening were maximum at 100(2) ms after peak negative dP/dt. Significant correlations were found between systolic shortening or thickening before coronary occlusion and post-systolic shortening (r = 0.74, 56 segments) or thickening (r = 0.84, 19 segments) after occlusion, but there was no correlation between post-systolic shortening or thickening and dyskinetic lengthening or thinning. In seven dogs followed for 4 h after coronary occlusion post-systolic shortening fell by 15% in peripheral segments and by 70% in central segments (p less than 0.002). In 17 dogs reperfused after 60 (n = 9) or 90 (n = 8) min of coronary occlusion the maximal recovery of systolic shortening early after reperfusion was significantly related to the magnitude of post-systolic shortening immediately before reperfusion (60 min occlusion r = 0.84, 90 min occlusion r = 0.88). These data show that post-systolic shortening is a marker of potential for early recovery of function of acutely ischaemic myocardium and suggest that it is due, at least in part, to an active process.
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PMID:Post-systolic shortening: a marker of potential for early recovery of acutely ischaemic myocardium in the dog. 344 Feb 62

Normal myocardium can derive energy for contraction and relaxation from oxidative metabolism of a variety of substrates. This investigation examined the influence of substrate availability early during reperfusion on the substrate pattern of oxidative metabolism and recovery of contractile function. For this purpose, isovolumically beating isolated rat hearts, perfused retrogradely with erythrocyte-supplemented buffer containing 0.4 mmol/L palmitate and 11 mmol/L glucose, were subjected to 40 minutes of no-flow ischemia. Hearts were reperfused with medium containing selected concentrations of palmitate and glucose. The substrate pattern for oxidative metabolism was determined on the basis of myocardial release of 14CO2 after equilibration of the hearts during the initial 15 minutes of reperfusion with either [1-14C]palmitate or [U-14C]glucose. In continuously perfused control hearts, glucose oxidation was largely inhibited by palmitate. During postischemic reperfusion, oxidation of glucose was increased by 59% (P < .05) and 467% (P <.01) in hearts reperfused after the ischemic period with 11 mmol/L glucose plus 0.4 or 1.2 mmol/L palmitate, respectively. Oxidation of palmitate was concomitantly reduced during reperfusion at low (0.4 mmol/L) but not at high (1.2 mmol/L) palmitate concentration. Compared with hearts reperfused with medium containing 0.4 mmol/L palmitate as sole substrate, hearts reperfused with medium containing 11 mmol/L glucose with 0.4 mmol/L palmitate exhibited lower left ventricular diastolic pressure (69 +/- 5 versus 90 +/- 3 mm Hg [mean +/- SEM], P < .05), less release of creatine kinase (31 +/- 5 versus 59 +/- 7 U/g wet wt, P < .05), and better recovery of left ventricular pressure development (26 +/- 9 versus 6 +/- 4 mm Hg, P < .05). Omission of palmitate or increasing the palmitate concentration to 1.2 mmol/L did not significantly alter postischemic myocardial contracture and enzyme release. The findings support the view that glucose oxidation early during reperfusion may be crucial for functional recovery. The results further indicate that interaction of substrates of oxidative metabolism is altered in severely injured postischemic myocardium. Inhibition of glucose oxidation by fatty acids was partially reversed during reperfusion.
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PMID:Substrate competition in postischemic myocardium. Effect of substrate availability during reperfusion on metabolic and contractile recovery in isolated rat hearts. 795 47

The pathogenesis and treatment of rupture of the Achilles tendon remain a source of controversy. This study presents the results of a biomechanical, functional, and morphological evaluation of a group of rats that had division and repair of the Achilles tendon. A total of 46 rats were used: 18 for biomechanical testing, 18 for functional evaluation, and 10 for histology. Morphological examination revealed an early inflammatory response with loose connective tissue formation that was replaced gradually by fibroblasts and a collagenous matrix. The functional evaluation (Achilles functional index [AFI]) was made from measurements of the hind pawprints of walking rats. Division and repair of the Achilles tendon produced a significant functional impairment (mean [+/- SEM] AFI = -87 +/- 8; p < 0.001), which gradually improved with healing time. The load to failure for the repaired tendons consistently improved with healing time, in a manner similar to the functional recovery. The average deformation (repair/control) varied considerably and was not related to healing time. The stiffness of the repaired tendons increased with healing time and was 60% of the corresponding control side by day 15. The major finding of this study was a strong correlation between the AFI and the failure load of the healing tendon-bone constructs (250-300 g group, r = 0.97, p < 0.001; 325-375 g group, r = 0.96, p < 0.001).
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PMID:Achilles tendon healing: a correlation between functional and mechanical performance in the rat. 828 36


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