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G Bloch

Publications and source records attributed to G Bloch.

At least 55 records · Page 3Linked to original sources
PubMed1996

Patterns of changes in neutrophil adhesion molecules during normothermic cardiopulmonary bypass. A clinical study.

The adhesion of activated neutrophils to endothelial cells is a key feature of the inflammatory response to cardiopulmonary bypass (CPB) because it "unlocks" a cascade of cytotoxic events. This adhesion is made possibly by the sequential involvement of two sets of neutrophil cell surface receptors: L-selection and beta 2 integrins (CD 11 a/CD 18; CD 11 b/CD 18; CD 11 c/CD 18). We have assessed the changes in the expression of these adhesion molecules in ten patients who underwent various open-heart procedures with the use of "warm" (33.4 degrees-37 degrees C) CPB. Arterial blood samples were obtained before, during and after bypass and processed for immunofluorescent flow cytometric analysis. CD 11 a expression remained unchanged throughout the study period. Conversely, CD 11 b drastically increased early after the onset of bypass (at 15 min on bypass: 172 +/- 17 [mean fluorescence (arbitrary units), mean +/- SEM] versus 63 +/- 13 before bypass. P < 0.02) and was still markedly elevated 30 min after the end of bypass (160 +/- 38, P < 0.05 versus the pre-by-pass value). CD 11 c expression underwent a similar upregulation (at 15 min of bypass: 54 +/- 5 versus 34 +/- 5 at baseline, P < 0.01). L-selectin expression did not change significantly during the period of observation. Put together, these results suggest that CPB is associated with an increased adhesive potential of neutrophils, which enhances their binding to the vascular endothelium and thereby initiates tissue damage through the release of cytotoxic mediators from adherent cells. Manipulation of integrin expression could therefore represent an effective means of alleviating the component of bypass-induced inflammatory tissue damage which is more specifically neutrophil-mediated.

Adult↗
PubMed1996

In vivo NMR evidence for moderate glucose accumulation in human skeletal muscle during hyperglycemia.

Although the absence of intracellular (IC) free glucose is direct evidence of glucose transport being the rate-limiting step for muscle glucose disposal at euglycemia, the scarcity of data in humans during hyperglycemia precludes any definitive conclusion. In the present study, 13C and 31P in vivo nuclear magnetic resonance (NMR) data from two separate groups of subjects were combined to measure IC free glucose in the human skeletal muscle. When these noninvasive tools were used with an infusion of [1-13C]glucose, a steady-state concentration of 1.2 +/- 0.2 mmol IC glucose/l IC water was observed at the end of a 2-h hyperglycemic clamp with somatostatin infusion, during which glycemia was maintained at approximately 22 mmol/l and insulinemia at approximately 5 mU/l. Despite this moderate glucose accumulation, the persistence of a large transmembrane glucose gradient suggests that the posttransport steps do not play a significant role in the control of muscle glucose disposal in these specific conditions, relevant to insulinopenic diabetic patients.

Adult↗
PubMed1995

Influence of temperature on neutrophil trafficking during clinical cardiopulmonary bypass.

BACKGROUND: The adhesion of neutrophils to endothelial cells and their subsequent transendothelial migration play a major role in inflammatory damage elicited by cardiopulmonary bypass (CPB) because these events are linked to the release of cytotoxic proteases and oxidants. However, the patterns of neutrophil trafficking in relation to systemic temperature during clinical CPB have not yet been characterized. METHODS AND RESULTS: Twenty case-matched patients undergoing warm (31.8 +/- 0.4 degrees C) or cold (26.3 +/- 0.5 degrees C, P < .0001 versus warm) bypass were studied. Blood samples were simultaneously collected from the right and left atria before, at the end of, and 30 minutes after CPB. Plasma levels of C3a, P- and E-selectins, elastase, and interleukin-8 were determined by immunoassays. The results demonstrate: (1) a rise in C3a, reflecting complement activation, (2) a fall in soluble E-selectin consistent with an increased adhesiveness of activated neutrophils, (3) a rise in soluble P-selectin expected to enhance endothelial adhesion of these neutrophils, (4) a rise in elastase, suggesting an adhesion-triggered neutrophil degranulation, and finally (5) a rise in interleukin-8 that is likely to promote transendothelial migration of adherent neutrophils. All of these changes occurred in the two groups of patients and were significant compared with prebypass values. However, in none of the groups was there a significant difference between right and left atrial values for any of the markers. The single difference between cold and warm bypass patients was a significant reduction of elastase release in the cold group (P < .001 versus the warm group). CONCLUSIONS: Clinical CPB is associated with biological changes suggesting the occurrence of neutrophil trafficking. Hypothermia provides only partial protection through a reduced release of elastase. Overall, these results reinforce the rationale for the development of therapeutic strategies targeted at blunting the neutrophil-mediated component of bypass-induced inflammatory damage.

Body Temperature↗
PubMed1995

Hypothermia during cardiopulmonary bypass delays but does not prevent neutrophil-endothelial cell adhesion. A clinical study.

BACKGROUND: An accurate evaluation of warm heart surgery cannot be limited to the assessment of the myocardial effects of warm blood cardioplegia but should also address the effects of systemic normothermia on the inflammatory response to cardiopulmonary bypass. A major component of this response is the endothelial adhesion of neutrophils, because it is linked to the release of cytotoxic compounds. This study was designed (1) to characterize the bypass-induced changes in the expression of neutrophil adhesion molecules (L-selectin and beta 2-integrins) and (2) to assess the influence of bypass temperature on these changes. METHODS AND RESULTS: Twenty case-matched patients undergoing open-heart procedures were divided into two equal groups according to the core temperature during cardiopulmonary bypass: warm (33.4 +/- 0.3 degrees C) or cold (27.1 +/- 0.4 degrees C, P < .0001 versus warm). Arterial blood samples were collected before, during, and 30 minutes after bypass and processed for the expression of L-selectin and beta 2-integrins (CD11a, CD11b, and CD11c) with flow cytometry. Warm bypass was associated with an early and sustained upregulation of CD11b. In contrast, hypothermia resulted in a strikingly less pronounced CD11b upregulation during bypass. However, CD11b expression sharply increased thereafter so that 30 minutes after bypass, it was no longer significantly different between the two groups. Changes in CD11c expression grossly paralleled those described for CD11b. Neither CD11a nor L-selectin changed significantly from baseline values in either group. CONCLUSIONS: Clinical cardiopulmonary bypass is associated with a marked upregulation of the neutrophil CD11b and CD11c integrins. Hypothermia delays but does not prevent the increased expression of these adhesion molecules, which could consequently represent logical targets for interventions designed to blunt the neutrophil-mediated component of bypass-induced inflammatory tissue damage.

Cardiopulmonary Bypass↗
PubMed1995

In vivo regulation of muscle glycogen synthase and the control of glycogen synthesis.

The activity of glycogen synthase (GSase; EC 2.4.1.11) is regulated by covalent phosphorylation. Because of this regulation, GSase has generally been considered to control the rate of glycogen synthesis. This hypothesis is examined in light of recent in vivo NMR experiments on rat and human muscle and is found to be quantitatively inconsistent with the data under conditions of glycogen synthesis. Our first experiments showed that muscle glycogen synthesis was slower in non-insulin-dependent diabetics compared to normals and that their defect was in the glucose transporter/hexokinase (GT/HK) part of the pathway. From these and other in vivo NMR results a quantitative model is proposed in which the GT/HK steps control the rate of glycogen synthesis in normal humans and rat muscle. The flux through GSase is regulated to match the proximal steps by "feed forward" to glucose 6-phosphate, which is a positive allosteric effector of all forms of GSase. Recent in vivo NMR experiments specifically designed to test the model are analyzed by metabolic control theory and it is shown quantitatively that the GT/HK step controls the rate of glycogen synthesis. Preliminary evidence favors the transporter step. Several conclusions are significant: (i) glucose transport/hexokinase controls the glycogen synthesis flux; (ii) the role of covalent phosphorylation of GSase is to adapt the activity of the enzyme to the flux and to control the metabolite levels not the flux; (iii) the quantitative data needed for inferring and testing the present model of flux control depended upon advances of in vivo NMR methods that accurately measured the concentration of glucose 6-phosphate and the rate of glycogen synthesis.

Allosteric Regulation↗
PubMed1995

1H NMR determination of lactate 13C-enrichment in skeletal muscle: using a double quantum filter for the simultaneous editing of 13C-coupled and 13C-uncoupled methyl protons resonance.

1H NMR simultaneous editing of 13C-coupled and 13C-uncoupled methyl protons resonance, using the selection of double quantum coherences by a gradient pulse, was analyzed in vitro and demonstrated in situ on the hindlimb of an exercised rat model postmortem. In vitro calibration showed agreement with theoretical analysis. High-resolution NMR of muscle extract confirmed the accuracy of the lactate 13C-enrichment calculated using the in situ NMR data and the calibration factor obtained in vitro.

Animals↗
PubMed1995

Preconditioning with potassium channel openers. A new concept for enhancing cardioplegic protection?

Ischemic preconditioning defines an adaptive endogenous mechanism in which a brief episode of reversible ischemia renders the heart more resistant to a subsequent period of sustained ischemia. Because the cardioprotective effects of ischemic preconditioning might be mediated by an activation of adenosine triphosphate-sensitive potassium channels, this study was designed to assess whether these effects could be duplicated by the preischemic administration of a potassium channel opener. Fifty isolated isovolumic buffer-perfused rat hearts underwent 45 minutes of normothermic potassium arrest followed by 1 hour of reperfusion. They were divided into five equal groups that differed with regard to the preconditioning regimen: Group 1 hearts were left untreated and served a controls; in group 2, preconditioning was achieved with 5 minutes of total global ischemia followed by 5 minutes of buffer reperfusion before cardioplegic arrest; in group 3, the preconditioning stimulus consisted of a 5-minute infusion of the potassium channel opener nicorandil (10 mumol/L) followed by 5 minutes of drug-free buffer perfusion before arrest; group 4 hearts underwent a similar protocol except that the infusion of nicorandil was preceded by that of the potassium channel blocker glibenclamide (10 mumol/L); group 5 hearts were ischemically preconditioned like those of group 2 except that the no-flow preconditioning period was also preceded by a 5-minute infusion of glibenclamide (50 mumol/L). The results demonstrate that ischemic preconditioning significantly improved contractility and reduced contracture during reperfusion, as compared with results in control hearts. These protective effects were duplicated by pretreatment with nicorandil but were abolished when the drug was antagonized by a prior infusion of glibenclamide. Likewise, the glibenclamide-induced blockade of potassium channels largely blunted the beneficial effects of ischemic preconditioning. These data suggest that opening of adenosine triphosphate-sensitive potassium channels substantially contributes to preconditioning-induced cardiac protection in a surgically relevant model of global ischemia and, consequently, that the use of potassium channel openers like nicorandil could be an effective means of enhancing cardioplegic protection.

Animals↗
PubMed1995

[Does temperature in extracorporeal circulation affect neutrophil-endothelium interactions?].

The increasing interest in "warm" aerobic cardioplegia requires a critical reevaluation of the systemic effects of the associated normothermic cardiopulmonary bypass (CPB). As activated neutrophils seem to be essential mediators of the inflammatory response to CPB via the cytotoxicity of the products that are released during their adhesion to endothelial cells, the authors undertook a study of the influence of temperature on the interaction between the neutrophils and the endothelium in 95 patients undergoing warm (31-33.5 degrees C, n = 49) and cold (26-27 degrees C, n = 46) CPB surgery. Blood sampling was performed before, during and after CPB. The following markers of neutrophil-endocardium interaction were analysed: complement activation (C3a), cytokine production (tumor necrosis factor alpha, interleukines 1, 6 and 8, and interleukin-1 receptor antagonist); endothelial expression of cytokine-dependent [intercellular adhesion molecule (ICAM)] and cytokine-independent (P-selectin) adhesion molecules (P-selectin); expression of cytokine molecules on the surface of polynuclear neutrophils (CD11a, CD11b, CD11c); and finally, endothelial adhesion and transendothelial migration of neutrophils (interleukin 8 and elastase). The results showed that, irrespective of temperature, CPB was associated with changes strongly suggestive of phenomena of transendothelial adhesion and migration. Moreover, normothermia increased the intensity of the inflammatory response as shown by increased cytokine production, earlier expression of neutrophil adhesion molecules and increased elastase production.

Aged↗
PubMed1994

Functional magnetic resonance imaging of human prefrontal cortex activation during a spatial working memory task.

High-speed magnetic resonance (MR) imaging was used to detect activation in the human prefrontal cortex induced by a spatial working memory task modeled on those used to elucidate neuronal circuits in nonhuman primates. Subjects were required to judge whether the location occupied by the current stimulus had been occupied previously over a sequence of 14 or 15 stimuli presented in various locations. Control tasks were similar in all essential respects, except that the subject's task was to detect when one of the stimuli presented was colored red (color detection) or when a dot briefly appeared within the stimulus (dot detection). In all tasks, two to three target events occurred randomly. The MR signal increased in an area of the middle frontal gyrus corresponding to Brodmann's area 46 in all eight subjects performing the spatial working memory task. Right hemisphere activation was greater and more consistent than left. The MR signal change occurred within 6-9 sec of task onset and declined within a similar period after task completion. An increase in MR signal was also noted in the control tasks, but the magnitude of change was less than that recorded in the working memory task. These differences were replicated when testing was repeated in five of the original subjects. The localization of spatial working memory function in humans to a circumscribed area of the middle frontal gyrus supports the compartmentalization of working memory functions in the human prefrontal cortex and the localization of spatial memory processes to comparable areas in humans and nonhuman primates.

Color Perception↗
PubMed1994

Proton NMR observation of glycogen in vivo.

Our previous solution studies of the proton relaxation properties of glycogen H1 have shown significant dipolar cross-relaxation with intra-ring H2 and inter-ring H4' protons characterized by a correlation time tau c = 2.7 x 10(-9) s. This leads to a significant negative Nuclear Overhauser Enhancement (NOE) of glycogen H1 following either transient or steady state perturbations of the longitudinal magnetization of dipolar coupled protons, especially H2 and H4'. Here we use the NOE to edit selectively the H1 resonance of glycogen in the rat liver in vivo using a surface coil probe. The approach shows the possibility of measuring glycogen in vivo with high sensitivity using 1H NMR.

Animals↗
PubMed1994

Retrograde warm blood cardioplegia preserves hypertrophied myocardium: a clinical study.

The ability of retrograde warm blood cardioplegia to preserve hypertrophied myocardium remains controversial. This two-part study was undertaken to address this question in patients subjected to aortic valve replacement for calcified aortic valve stenosis complicated with echocardiographically defined left ventricular hypertrophy. Part 1 was designed to assess the intraoperative patterns of myocardial oxidative metabolism in 20 patients in whom the severity of left ventricular hypertrophy was reflected by a mean (+/- standard error of the mean) myocardial mass index of 213 +/- 15 g/m2. After antegrade arrest, warm blood cardioplegia was continuously given through the coronary sinus at a flow rate of 200 +/- 5 mL/min. The use of a low-dilution cardioplegia delivery technique enabled us to keep hematocrit at 25.6% +/- 0.9% and the core temperature was allowed to drift to 32.7 +/- 0.2 degrees C. At the end of the arrest period, blood samples were simultaneously taken from inflow (coronary sinus catheter) and outflow (left coronary ostium) cardioplegia and assayed for blood gases, oxygen content and saturation and lactate. Part II was designed to compare the clinical outcomes of these 20 warm patients with those of 20 case-matched patients in whom a conventional hypothermic myocardial protection technique was used. The results of part I show that after an average arrest period of 72 +/- 4 minutes, the residual oxygen demand was still high as reflected by a percent oxygen extraction of 34.8% +/- 4.1%. This demand, however, was adequately met by the supply, as demonstrated by (1) the absence of transmyocardial acid production, (2) a negligible release (outflow minus inflow) of lactate (0.28 +/- 0.1 mmol/L), and (3) a high residual oxygen saturation (65.7% +/- 3.8%) in outflow cardioplegia. The results of part II show that the clinical outcomes of warm patients were overall good and not different from those of the cold group. We conclude that retrograde warm blood cardioplegia can adequately preserve hypertrophied myocardium by keeping its metabolism predominantly aerobic during aortic cross-clamping provided that measures are taken to optimize the determinants of the oxygen demand/supply ratio throughout. These measures include avoidance of left ventricular distention, immediate ablation of any recurring activity during arrest, maintenance of high retrograde flow rates, limitation of hemodilution, and uninterrupted mode of cardioplegia delivery.

Acids↗
PubMed1994

Experimental evaluation of Celsior, a new heart preservation solution.

An original heart preservation solution (Celsior) has been developed, the formulation of which has been designed to fulfil two major objectives: (1) to combine the general principles of hypothermic organ preservation with those specific for the myocardium, and (2) to offer the possibility of being used not only as a storage medium but also as a perfusion fluid during initial donor heart arrest, poststorage graft reimplantation and early reperfusion. The major principles addressed by the Celsior formulation include (1) prevention of cell swelling (by mannitol and lactobionate), (2) prevention of by the Celsior formulation include (1) prevention of cell swelling (by mannitol and lactobionate), (2) prevention of oxygen-derived free radical injury (by reduced glutathione, histidine and mannitol), and (3) prevention of contracture by enhancement of energy production (glutamate) and limitation of calcium overload (high magnesium content, slight degree of acidosis). Two experimental preparations were used: The isolated isovolumic buffer-perfused rat heart model and the heterotopic rabbit heart transplantation model. In isolated heart experiments, hearts were arrested with and stored in Celsior for 5 h at 4 degrees C and subsequently reperfused for 1 h. A similar protocol was used in the transplantation experiments except that the total ischemic time was approximately 1 1/2 h longer (corresponding to 6 h of storage followed by the 25 additional minutes of cold ischemia required for graft implantation.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdomen↗
PubMed1994

In vivo regulation of rat muscle glycogen resynthesis after intense exercise.

Time courses of the glycogen synthesis rate and of the glucose 6-phosphate (G-6-P) concentration after an electrically induced exercise were followed in the anesthetized rat gastrocnemius by in vivo 13C and 31P nuclear magnetic resonance (NMR) spectroscopy, respectively. The ratio of glycogen synthase I to glycogen synthase I and D (I/I+D) and allosteric activation by G-6-P were also studied in vitro on muscles sampled at rest and 10 min (early recovery) and 100 min (late recovery) after exercise. From early recovery to late recovery, the in vivo glycogen synthesis rate dropped from 0.46 +/- 0.06 to 0.11 +/- 0.04 mmol.kg wet tissue-1.min-1, the G-6-P concentration from 0.83 +/- 0.08 to 0.32 +/- 0.05 mmol/kg wet tissue, and I/I+D from 83 +/- 4 to 47 +/- 1%. The combination of the changes in G-6-P concentration and in I/I+D quantitatively describes the fourfold decrease in glycogen synthesis rate from early to late recovery. These results demonstrate that phosphorylation, determining glycogen synthase I/I+D, and allosteric control of glycogen synthase by G-6-P contribute approximately equally to the regulation of the postexercise in vivo glycogen synthesis rate.

Animals↗
PubMed1994

Does normothermia during cardiopulmonary bypass increase neutrophil-endothelium interactions?

BACKGROUND: The use of warm blood cardioplegia is usually associated with that of warm cardiopulmonary bypass (CPB). Little is known, however, about the effect of temperature during bypass on neutrophil-endothelium interactions, which are currently considered a key component of the inflammatory response to CPB. METHODS AND RESULTS: Twenty-five patients operated on under CPB were studied. Core temperature during bypass was kept normothermic (33.5 degrees C to 37 degrees C) in 14 and lowered to 28 degrees C to 30 degrees C in the 11 remaining patients. The two groups were otherwise comparable. Arterial blood samples were collected before CPB and 30 minutes, 4 hours, and 24 hours thereafter. Samples were assayed for interleukin-1 receptor antagonist (IL-1ra), soluble intercellular adhesion molecule 1 (sICAM-1), and elastase, which are markers of cytokine production, cytokine-upregulated endothelial ligands for neutrophil adhesion molecules, and degranulation secondary to adhesion of neutrophils to endothelial cells, respectively. IL-1ra levels (mean +/- SEM) peaked 4 hours after bypass and were significantly higher in the warm group (87,926 +/- 24,067 versus 18,090 +/- 5798 mg/L, P < .02). Peak values of sICAM-1, which occurred 24 hours after bypass, were correspondingly higher in warm patients (414 +/- 74 versus 298 +/- 23 micrograms/L in cold patients). In keeping with these data, warm patients released significantly more elastase at both the 30-minute (703 +/- 101 versus 349 +/- 55 micrograms/L, P < .01) and 4-hour (627 +/- 116 versus 324 +/- 31 micrograms/L, P < .03) post-CPB study points. CONCLUSIONS: Temperature profoundly affects neutrophil-endothelium interactions, which leads one to question the use of systemic normothermia in patients at higher risk of suffering from postbypass inflammation-mediated organ damage.

Body Temperature↗
PubMed1994

Metabolic and functional evidence that retrograde warm blood cardioplegia does not injure the right ventricle in human beings.

BACKGROUND: Retrograde warm blood cardioplegia is now recognized as an effective method of myocardial protection, but concerns persist about its ability to adequately preserve the right ventricle. METHODS AND RESULTS: A total of 75 patients in whom warm blood cardioplegia was continuously given through the coronary sinus were included in this three-part study. Part 1, which involved 30 patients undergoing coronary artery bypass grafting operations, was designed to assess whether the right ventricle incurred a greater degree of anaerobic metabolism than the left ventricle during warm arrest. Immediately before aortic unclamping, antegrade perfusion was resumed and, within 1 minute of washout, blood samples were simultaneously taken from the right ventricle and coronary sinus and assayed for lactate. There was no significant difference in lactate concentrations between the two sampling sites (right ventricle, 2.53 +/- 0.1 mmol/L; coronary sinus, 2.47 +/- 0.1 mmol/L). Part 2 focused on recovery of function. A complete set of postoperative hemodynamic measurements was obtained in 15 among the 30 patients enrolled in part 1 and compared with that obtained in 15 case-matched patients who received conventional cold antegrade crystalloid cardioplegia. Postoperative right ventricular stroke work index was not significantly different between the two groups (retrograde warm, 4.6 +/- 0.2 g.m-1.m-2; antegrade cold, 4.8 +/- 0.2 g.m-1.m-2). Part 3 was also targeted at functional end points but in 30 additional patients undergoing reoperative mitral valve replacement and consequently deemed to be at higher risk of right ventricular ischemia. Fifteen patients who received retrograde warm cardioplegia were compared with 15 case-matched control subjects in whom antegrade cold crystalloid cardioplegia was used. In keeping with data of part 3, postoperative right ventricular stroke work index was not significantly different between the two groups (retrograde warm, 6.9 +/- 0.4 g.m-1.m-2; antegrade cold, 7.7 +/- 0.5 g.m-1.m-2), nor was there a difference in clinical outcomes or biological recoveries of hepatic function. CONCLUSIONS: Inadequate protection of the right ventricle associated with the use of retrograde warm blood cardioplegia does not appear to be a clinically founded concern since this technique preserves right ventricular function to the same extent as conventional antegrade cold cardioplegia does.

Aged↗
PubMed1994

A potential mechanism of vasodilation after warm heart surgery. The temperature-dependent release of cytokines.

Peripheral vasodilation is a common feature of warm heart surgery and creates clinical concerns when pressor agents become necessary because of the potential for some of these drugs to adversely affect flow through newly engrafted arterial and venous bypass conduits. The possible role of a temperature-dependent production of cytokines in the pathogenesis of this vasodilation was investigated in a two-part study. In part I, lipopolysaccharide-activated peritoneal rabbit macrophages (5 x 10(6)/ml) were incubated at 30 degrees or 37 degrees C up to 9 hours and the concentration of tumor necrosis factor released in the supernatant was serially measured by a bioassay. Tumor necrosis factor production was found to increase over time for each of the two temperatures of incubation but was significantly higher throughout the observation period in normothermic experiments than in those done at 30 degrees C. Part II was a prospective clinical study involving 30 patients who underwent either cold (core temperature 28 degrees to 30 degrees C, n = 15) or warm (37 degrees C, n = 15) cardiopulmonary bypass and in whom serum levels of tumor necrosis factor alpha, interleukin-1 beta, and interleukin-6 were measured by enzyme-linked immunosorbent assays at 2, 4, 10, and 24 hours after bypass. Cytokine levels were found to be consistently higher in patients having normothermic bypass. Differences between the two groups were significant 2 hours after bypass for tumor necrosis factor alpha and interleukin-6 (p < 0.02 and p = 0.0001, respectively) and 4 and 10 hours after bypass for interleukin-1 beta (p < 0.01 and p < 0.04, respectively). The incidence of vasodilation necessitating vasopressor support was twofold higher in the normothermic group (six patients versus three in the hypothermic group). Taken as a whole, patients supported by pressor agents had significantly higher cytokine levels after bypass than those who did not require pressor therapy. Our results suggest that vasodilation occurring with warm heart operation is, at least partly, mediated by a temperature-dependent release of cytokines. Vasodilation might therefore be mitigated by simply allowing the core temperature to drift during bypass. Our recent clinical experience suggests that this "tepid" heart surgery (32 degrees to 34 degrees C) effectively blunts most of the vasodilatory response to strictly normothermic bypass without compromising maintenance of myocardial aerobiosis during arrest.

Animals↗
PubMed1993

In vivo 31P NMR measurement of glucose-6-phosphate in the rat muscle after exercise.

Comparison of 31P NMR spectra of the rat gastrocnemius, obtained in vivo and from PCA extracts, after electrically induced contractions, demonstrates that glucose-6-phosphate (G6P) is the major metabolite in the low-field part of the PME spectral region. In vivo 31P NMR can thus be used to measure the muscle G6P concentration after exercise.

Animals↗