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 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the effect of mild whole-body hyperthermia before and after 16 minutes of global cerebral ischemia on metabolic recovery during recirculation in cats using in vivo phosphorus-31 nuclear magnetic resonance spectroscopy. Hyperthermia (temperature 40.6 +/- 0.2 degrees C) was induced greater than or equal to 1 hour before ischemia and was maintained during 1.5-2 hours of recirculation in nine cats; four cats were subjected to hyperthermia without cerebral ischemia, six to hyperthermia during recirculation (after return of intracellular pH to preischemic values), and 14 to normothermic ischemia and recirculation. Our data indicate that preischemic hyperthermia results in an intracellular cerebral pH during recirculation significantly lower than that in normothermic cats. In hyperthermic cats beta-ATP and phosphocreatine (PCr) concentrations and the ratio of PCr to inorganic phosphate failed to return to preischemic levels during recirculation in contrast to normothermic cats. Hyperthermia without ischemia and hyperthermia during recirculation had no significant effect on intracellular pH. Thus, preischemic hyperthermia has a detrimental effect on metabolic recovery after transient global cerebral ischemia.
Stroke 1988 Dec
PMID:Effect of mild hyperthermia on recovery of metabolic function after global cerebral ischemia in cats. 320 11

To test the effect of a high dietary calcium intake on blood pressure, we fed stroke-prone spontaneously hypertensive (SHR-SP) and Wistar-Kyoto rats (WKY) diets containing (a) 0.25% Ca/0.08% Mg, (b) 4.0% Ca/0.02% Mg, and (c) 4.0% Ca/0.08% mg, beginning at 6 weeks of age. SHR-SP and WKY rats receiving 4% Ca with the lower Mg content had lower blood pressures, hypomagnesemia, and hypomagnesuria, and grew poorly. SHR-SP receiving 4% Ca and the higher Mg diet had blood pressures no different from those of rats receiving the 0.25% Ca diet, in spite of having lower body weights. Rubidium flux studies in erythrocytes were not influenced by Ca or Mg in the diets. Plasma phosphate values were moderately reduced in rats receiving 4% Ca diets. Epinephrine and norepinephrine values were higher in SHR-SP than in WKY rats. Norepinephrine increased with stress in both strains, independent of diet. Epinephrine values were lower in SHR-SP receiving the 4% Ca diets and showed less of an increase with stress compared to SHR-SP receiving the 0.25% Ca diet. After 26 weeks of diets, SHR-SP and WKY rats were given 0.9% NaCl in their drinking water. NaCl increased blood pressure in SHR-SP irrespective of Ca content of the diet. These data suggest that a high Ca diet influences Mg homeostasis and adrenal medullary function in SHR-SP. Further, SHR-SP appear resistant to any blood pressure lowering effect of Ca irrespective of NaCl intake.
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PMID:Effect of high calcium diet on magnesium, catecholamines, and blood pressure of stroke-prone spontaneously hypertensive rats. 335 96

We report on a patient with a large ischemic hemispherical stroke studied serially by 31P nuclear magnetic resonance spectroscopy. Persistent hyperglycemia was associated with prolonged acidosis in ischemic brain and failure of high-energy phosphate metabolism to recover. These in vivo human data support the concept that hyperglycemia adversely affects ischemic brain metabolism, pH, and clinical outcome.
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PMID:Prolonged deterioration of ischemic brain energy metabolism and acidosis associated with hyperglycemia: human cerebral infarction studied by serial 31P NMR spectroscopy. 338 81

The cardioprotective effect of the addition of the slow calcium-channel blocker nifedipine to cardioplegic solution was tested in two double-blind placebo controlled randomized studies. The first study included 24 patients undergoing aortic-coronary bypass grafting, and the second included 24 patients undergoing aortic valve replacement. Nifedipine at a dose of 200 micrograms/L or placebo was added to St. Thomas' Hospital cardioplegic solution. The following markers of ischemia were used: adenosine triphosphate and its catabolites, creatine phosphate and inorganic phosphate, determined in transmural left ventricular biopsy specimens taken before, at the end of, and after aortic cross-clamping; hemodynamic recovery 15 minutes after cessation of cardiopulmonary bypass; clinical outcome in terms of the incidence of arrhythmias, low cardiac output, positive inotropic support immediately after operation, and follow-up at 15 months. The main difference between the two studies was that myocardial temperature during cross-clamping remained constant at 14 degrees C in coronary bypass grafting but increased to 25 degrees C in valve operations despite the application of the same amounts of cardioplegic solutions. This lower temperature resulted in better preservation of high-energy phosphates in coronary bypass operations as compared to the placebo group having valve replacement operations. According to analysis of variance, a drug effect could be demonstrated only in the aortic valve replacement study: Accumulation of breakdown products of the adenine nucleotide pool was less in the nifedipine group than in the placebo group (p less than 0.05). Adenosine triphosphate decreased only to 84% in the nifedipine group and to 72% in the placebo group. Despite this adenosine triphosphate-sparing effect, weaning from cardiopulmonary bypass was more difficult in the nifedipine group. Left ventricular stroke work index 15 minutes after bypass was decreased to 72% of the prebypass value in the nifedipine group (t test, p less than 0.01) and only to 86% in the placebo group (p = NS). In contrast, after the patients were admitted to the intensive care unit, the incidence of low cardiac output tended to be lower in the nifedipine group than in the placebo group: 33% versus 58% (p = NS). In conclusion, ischemia-induced degradation of nucleotides as it occurs when myocardial cooling is inadequate can be prevented by the addition of nifedipine to the St. Thomas' Hospital cardioplegic solution. This effect, however, is not associated with an improved clinical outcome.
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PMID:Nifedipine as an adjunct to St. Thomas' Hospital cardioplegia. A double-blind, placebo-controlled, randomized clinical trial. 351 8

The intracellular Na+ content of washed erythrocytes from stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto normotensive rats (WKY) was measured by a high resolution 23Na-nuclear magnetic resonance (NMR) technique using a non-permeant aqueous shift reagent, dysprosium triethylenetetramine hexaacetic acid, Dy(TTHA)3-. The initial intracellular Na+ of freshly isolated and washed erythrocytes was very low (approximately 5 mmol/l) and increased progressively with prolonged incubation in isotonic salt solution at 37 degrees C. There was no significant difference in the erythrocyte Na+ concentration between SHRSP and WKY over the entire period of measurement, nor was any difference detected in their osmotic fragility or total cellular volume, although the osmotic fragility decreased with incubation time. The high energy phosphate metabolites were also studied in the same erythrocytes by 31P-NMR. The level of intracellular ATP decreased with incubation at 37 degrees C but showed no difference between the SHRSP and WKY samples. Inclusion of 1 mmol/l ouabain in the incubation medium substantially retarded the breakdown of intracellular ATP and resulted in a concomitant increase in intracellular Na+. However, neither the ouabain-sensitive nor the ouabain-insensitive component of Na+ influx altered in SHRSP erythrocytes compared with WKY erythrocytes in paired experiments. Our results do not support the hypothesis that altered Na+ transport, resulting in an increase in erythrocyte Na+ concentration, is associated with spontaneous hypertension.
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PMID:High resolution 23Na-nuclear magnetic resonance study of stroke-prone spontaneously hypertensive rat erythrocytes. 361 83

A synthesis of the postulated sequence of events for development of the inappropriate response of the myocardium to a demand for increased cardiac index is schematically represented in Fig. 10. In sepsis, bacteremia and/or the release of endotoxin activate the macrophages which release a spectrum of mediators. Some of these mediators (and possibly also endotoxin itself) have a negative influence on myocardial contractile function either directly and/or through altering cellular calcium flux. This results in impaired myocardial function manifested initially by decreased stroke volume. Subsequently, stroke volume will be either partially or completely restored to normal through the action of circulating catecholamines, the concentration of which is markedly elevated due to the presence of endotoxin and/or macrophage-produced mediators. Endotoxin and/or these mediators also act on the SA node increasing its sensitivity to beta-adrenergic stimulation. This will result in elevated heart rates. The latter, combined with the restored stroke volume, will yield an increased cardiac index which is the hallmark of the hyperdynamic phase of sepsis. In the cecal ligation and puncture model of sepsis, where cardiac index is maintained at the original level, the partially restored stroke volume and the elevated heart rate will combine to maintain cardiac index. Although this mechanism of increasing cardiac index through tachycardia is not energy efficient, the myocardium is able to cope with these changes and also to maintain its high energy phosphate concentrations, since the utilization of the three major myocardial substrates (fatty acids, lactate and glucose) is not affected by sepsis. Although this putative sequence of events is consistent with the observed experimental findings, further work is needed to substantiate its applicability to the etiology of myocardial dysfunction in man during sepsis.
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PMID:Myocardial dysfunction in sepsis. 361 52

In vivo 31P nuclear magnetic resonance spectroscopy was used to monitor the time course of intracellular pH in cat cerebral cortex subjected to global cerebral ischemia under control and hyperglycemic pretreatment conditions. Transient (16 minutes) global cerebral ischemia was induced in 14 cats using an inflatable cervical cuff combined with systemic arterial hypotension. Six cats were pretreated with infusion of 1.5 g/kg glucose prior to ischemia. Relative concentrations of high-energy phosphate metabolites and intracellular pH were continuously monitored before, during, and for 2 hours after cerebral reperfusion. During ischemia, intracellular pH fell to the same level and followed a similar time course in both groups. However, during initial reperfusion in the hyperglycemic group, there was a severe further decline (p less than 0.003) in intracellular pH. We suggest that the increased neurologic deficit and mortality found in hyperglycemic animals subjected to cerebral ischemia may be attributed to this transient severe tissue acidosis.
Stroke
PMID:Intracellular acidosis during and after cerebral ischemia: in vivo nuclear magnetic resonance study of hyperglycemia in cats. 362 52

The present study examines the effects of resuscitation fluid composition on myocardial function, myocardial high-energy phosphate content, and survival following third-degree anesthetic burn to 35-40% body surface area in the guinea pig. Treatment regimens used were 1) no resuscitation, 2) isotonic saline, 3) Ringer's lactate and 4) Ringer's acetate. Fluids were administered at the rate of 0.334 ml/kg/hr/% burn for 4 hr following injury, at which time myocardial function was assessed. Nonburned animals served as controls. In isolated working hearts, significant depression of myocardial function was observed in nonresuscitated and saline-resuscitated animals as evidenced by decreased cardiac output, dP/dt, -dP/dt, and stroke work. Lactate resuscitation produced some improvement in these parameters but did not restore them to those of nonburned control animals. In contrast, Ringer's acetate resuscitation resulted in normal cardiac output and contractility. Myocardial ATP content of hearts obtained from the various resuscitation groups did not differ from that of nonburned control hearts, except for hearts from Ringer's lactate group, which were significantly lower in myocardial ATP than those of the other groups. No differences were found in creatine phosphate content. Resuscitation with the different fluid regimens for 48 hr produced significant differences in survival. Fluids were given at the rate of 4 ml/kg/% burn for 24 hr. Half of the fluid was given in the first 8 hr and the rest during the remaining 16 hr. Nonresuscitated and saline-resuscitated animals showed significant mortality by 24 hr, whereas lactate- and acetate-treated animals had survival rates of 100% and 87.5%, respectively. However, by 48 hr, only acetate-treated animals survived. These data indicate that important differences exist in the effectiveness of different resuscitation fluids and that Ringer's lactate, the fluid most often utilized clinically, may not provide optimum benefit. In light of these results, serious consideration should be given to the substitution of acetate for lactate during the resuscitation of burn shock patients.
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PMID:Resuscitation fluid composition and myocardial performance during burn shock. 369 Aug 12

Attempts were made to define the effects of epinephrine and dobutamine on the myocardium during early reperfusion for 60 minutes following hypothermic global ischemia at a myocardial temperature of 28 degrees C for 60 minutes under cardiopulmonary bypass. Ischemia was induced by cross-clamping the dog aorta. Epinephrine (0.1 microgram/kg/min) and dobutamine (5 micrograms/kg/min) were given throughout the reperfusion period by intravenous drip infusion, a control group was treated with saline infusion. Comparison of hemodynamic parameters was made before cardiopulmonary bypass, and at 30 and 60 minutes of reperfusion. Epinephrine and dobutamine significantly increased stroke volume index, left ventricular stroke work index and tissue calcium content compared with saline, however, myocardial water content was only slightly higher in the group given saline, compared with the other two groups. Myocardial mitochondrial membranes and cristae were slightly damaged and creatine phosphate content was reduced. Ultrastructural integrity was related to myocardial tissue calcium content, with a significant negative correlation. These results suggest that epinephrine (0.1 microgram/kg/min) will improve stroke volume index and left ventricular stroke work index, as does dobutamine (5 micrograms/kg/min), however, both agents had a minimal effect on reducing myocardial morphological and biochemical integrity, although catecholamines have detrimental effects on the myocardium in early reperfusion following ischemia.
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PMID:Effects of catecholamines on myocardial viability in early reperfusion following hypothermic global ischemia in dogs--comparison between epinephrine and dobutamine. 383 1

Fluosol-DA (Perfluorochemical Blood Substitute) was investigated in a previous study and found to provide some protection from ischemia and possible usefulness in limiting the size of infarction. In the present study, larger doses over longer periods of acute focal cerebral ischemia were used. Twenty four cats had transorbital ligation of the middle cerebral artery (MCA). The 12 experimental animals were given 20% Fluosol-DA. The control group of 12 received isotonic saline solution. Twenty-four hours after the MCA occlusion, the cats were perfused with saline and phosphate-buffered formalin. The brains were removed and immersed in 10% formalin for 2 weeks. The results of macroscopic and histological examination suggested that, although Fluosol-DA did not provide complete protection from ischemic injury to the brains of the cats treated, it may have helped to slow the development of the pathological changes.
Stroke
PMID:Modification of cerebral ischemia with Fluosol. 396 63


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