Can we distinguish clinically hibernation from stunning and does it matter?
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Blood Flow Velocity↗
Biomedical subjects
C Ceconi
Publications and source records attributed to C Ceconi.
Metabolic adaptation during a sequence of no-flow and low-flow ischemia. A possible trigger for hibernation.
BACKGROUND: Myocardial hibernation is an adaptive phenomenon occurring in patients with a history of acute ischemia followed by prolonged hypoperfusion. METHODS AND RESULTS: We investigated, in isolated rabbit heart, whether a brief episode of global ischemia followed by hypoperfusion maintains viability. Four groups were studied; group 1,300 minutes of aerobia; group 2,240 minutes of total ischemia and 60 minutes of reperfusion; group 3, 10 minutes of total ischemia, 230 minutes of hypoperfusion (90% coronary flow reduction), and 60 minutes of reperfusion; and group 4, 240 minutes of hypoperfusion followed by reperfusion. In group 3, viability was maintained. Ten minutes of ischemia caused quiescence, a fall in interstitial pH (from 7.2 +/- 0.01 to 6.1 +/- 0.8), creatine phosphate (CP), and ATP (from 54.5 +/- 5.0 and 25.0 +/- 1.9 to 5.0 +/- 1.1 and 15.3 +/- 2.5 mumol/g dry wt, P < .01). Subsequent hypoperfusion failed to restore contraction and pH but improved CP (from 5.0 +/- 1.1 to 20.1 +/- 3.4, P < .01). Reperfusion restored pH, developed pressure (to 92.3%), and NAD/NADH and caused a washout of lactate and creatine phosphokinase with no alterations of mitochondrial function or oxidative stress. In group 4, hypoperfusion resulted in progressive damage. pH fell to 6.2 +/- 0.7, diastolic pressure increased to 34 +/- 5.6 mm Hg, CP and ATP became depressed, and oxidative stress occurred. Reperfusion partially restored cardiac metabolism and function (47%). CONCLUSIONS: A brief episode of total ischemia without intermittent reperfusion maintains viability despite prolonged hypoperfusion. This could be mediated by metabolic adaptation, preconditioning, or both.
Adaptation, Physiological↗
Aorta and skeletal muscle NO synthase expression in experimental heart failure.
Nitric oxide (NO), the free radical that accounts for the biological activity of endothelium-derived relaxing factor, is synthesized from L-arginine by NO synthase (NOS). There is evidence that NO availability is reduced in the peripheral vasculature of patients with congestive heart failure (CHF). The aim of this study was to investigate the expression of NOS in the descending aorta and in the skeletal muscles of rats subjected to heart failure. The alkaloid, monocrotaline, was used to induce pulmonary hypertension and cardiac failure in rats. The expression of both the constitutive (ecNOS) and the inducible (iNOS) isoforms of the enzyme was assessed by Western blot analysis. In CHF animals, the ecNOS location in the aorta is altered: the endothelial protein expression is substantially reduced (from 0.083 +/- 0.012 to 0.003 +/- 0.004 OD/microgram total proteins, P < 0.001) whereas the expression of ecNOS in the smooth muscle is increased (from 0.024 +/- 0.004 to 0.059 +/- 0.009 OD/ microgram total proteins, P < 0.01). The total aortic ecNOS is diminished in CHF respect to control animals (0.062 +/- 0.009 v 0.107 +/- 0.013 OD/microgram total proteins, P < 0.01). On the contrary, no difference in ecNOS protein expression was observed in the extensor digitorum longus and soleus muscles. Furthermore, iNOS was not detected in any of the tissues considered. In conclusion, experimental CHF causes a re-setting of the ecNOS protein expression in the descending aorta but not in skeletal muscles. The reduced abundance of ecNOS in the aortic endothelium is consistent with the impairment of the vasodilating function reported in patients with CHF.
Animals↗
Skeletal muscle metabolism in experimental heart failure.
We studied peripheral skeletal muscle metabolism in monocrotaline-treated rats. Two distinct groups emerged: a percentage of the animals developed ventricular hypertrophy, with no signs of heart failure (compensated group), whilst others, besides ventricular hypertrophy, developed the syndrome of congestive heart failure (CFH group). Oxidative metabolism and redox cellular state were expressed in terms of creatine phosphate, purine (ATP, ADP and AMP) and pyridine (NAD and NADH) nucleotides tissue content. Skeletal muscles with different metabolism were studied: (a) Soleus (oxidative), (b) extensor digitorium longus (glycolytic) and tibialis anterior (oxidative and glycolytic). The results showed that in CFH animals a decreased high-energy phosphates content occurs in the soleus and extensor digitorum longus, but not in the tibialis anterior. In the soleus. ATP declined from 20.31 +/- 2.5 of control group to 9.55 +/- 0.61 mumol/g dry wt. while in the extensor digitorum longus ATP declined from 30.92 +/- 2.68 to 22.7 +/- 1.54 mumol/g dry wt. In both these muscles, a shift of NAD/NADH couple towards oxidation was also observed (from 26.58 +/- 3.34 to 6.95 +/- 0.97 and from 18.88 +/- 3.43 to 10.57 +/- 1.61, respectively). These alterations were more evident in the aerobic soleus muscle. On the contrary, no major changes occurred in skeletal muscle metabolism of compensated animals. The results show that: (1) a decrease in muscle high-energy phosphates occurs in CFH; (2) this is accompanied by a decrease of NAD/NADH couple suggesting an impairment in oxygen utilization or availability.
Adenosine Diphosphate↗
Is stunning an important component of preconditioning?
We tested the hypothesis that stunning following a brief period of ischaemia is a component of cardioprotection afforded by preconditioning in an in vitro model of global normothermic ischaemia. Isolated Langendorff-perfused rat hearts, after 120-150 min of aerobic perfusion, were divided into four groups. Groups 1 and 2 constituted the aerobic and ischaemic controls. The other hearts were preconditioned by two 2-min ischaemia/reperfusion cycles. Two ischaemic preconditioning protocols were used, the only difference being prolongation of the reperfusion cycle from 5 (group 3) to 20 min (group 4) before the onset of severe ischaemic insult. Mechanical function, energetic metabolism and the rate of enzyme release were followed throughout. In group 3, myocardial function remained significantly downregulated before the onset of severe ischaemia. This resulted in cardiac protection as evidenced by enhanced recovery of systolic pressure (37.7 +/- 3.6 v 61.9 +/- 5.7 mmHg for groups 2 and 3, respectively; P < 0.02), reduced rise in diastolic pressure (55.8 +/- 5.9 v 34.3 +/- 5.2 mmHg; P < 0.02), reduced creatine kinase (CK) release (957.3 +/- 175.7 v 541.5 +/- 85.9 mU/min/gww; P < 0.05) and higher contents of high-energy phosphate at the end of ischaemia [3.6 +/- 0.3 v 25.3 +/- 2.9 mumol/gdw for creatine phosphate (CP), P < 0.001] as well as after reperfusion (16.8 +/- 2.4 v 31.4 +/- 1.8 for CP, P < 0.01, and 3.9 +/- 0.5 v 6.2 +/- 0.8 mumol/gdw for ATP, P < 0.05). When severe ischaemia was started only after complete recovery of mechanical function (group 4), no protection was observed. Our data suggest that a decrease in mechanical function or stunning occurring after the short period of ischaemia causes ATP sparing and constitutes an additional mechanism of preconditioning cardioprotection in vitro.
Animals↗
Effects of felodipine on the ischemic heart: insight into the mechanism of cytoprotection.
To assess whether the administration of felodipine protects the myocardium in a dose-dependent manner against ischemia and reperfusion, isolated rabbit hearts were infused with three different concentrations of felodipine: 10(-10), 10(-9), and 10(-8) M. Diastolic and developed pressures were monitored; coronary effluent was collected and assayed for CPK activity and for noradrenaline concentration; mitochondria were harvested and assayed for respiratory activity; and ATP production and calcium content and tissue concentration of ATP, creatine phosphate (CP), and calcium were determined. The occurrence of oxidative stress during ischemia and reperfusion was also monitored in terms of tissue content and release of reduced (GSH) and oxidized (GSSG) glutathione. Treatment with felodipine at 10(-10) and 10(-9) M had no effect on the hearts when perfused under aerobic conditions, whilst the higher dose reduced developed pressure from 57.7 +/- 2.6 to 30.0 +/- 2.6 mmHg (p < 0.01). On reperfusion treated hearts recovered better than the untreated hearts with respect to left ventricular performance, replenishment of ATP and CP stores, and mitochondrial function. Recovery of developed pressure was 100% at 10(-8) M, 55% at 10(-9) M, and 46% at 10(-10) M. The reperfusion-induced tissue and mitochondrial calcium overload, release of CPK and noradrenaline, and oxidative stress were also significantly reduced. The effects of felodipine were dose dependent. Felodipine inhibited the initial rate of ATP-driven calcium uptake but failed to affect the initial rate of mitochondrial calcium transport. It is concluded that felodipine infusion provides dose-dependent protection of the heart against ischemia and reperfusion. Because this protection also occurred at 10(-9) M and 10(-10) M in the absence of a negative inotropic effect during normoxia and of a coronary dilatory effect during ischaemia, it cannot be attributed to an energy-sparing effect or to improvement in oxygen delivery. From our data we can envisage two other major mechanisms-(1) membrane protection and (2) reduction in oxygen toxicity. The ATP-sparing effect occurring at 10(-8) M is likely to be responsible for the further protection.
Adenosine Triphosphate↗
Activation of the neuroendocrine response in heart failure: adaptive or maladaptive process?
Congestive heart failure is a clinical syndrome in which the capacity of the heart to maintain cardiac output is impaired. As a consequence, blood pressure is threatened and endocrine and paracrine mechanisms are activated to preserve circulatory homeostasis and to maintain blood pressure. At terminal stages, a complex multiorgan syndrome develops with severe pump failure, intense systemic vasoconstriction, and avid water and sodium retention. Increasing evidence points to humoral circulating or locally synthesized substances as one of the causes of the terminal consequences of heart failure. Therefore, the hypothesis that the syndrome of heart failure is, at least in part, a humoral disease has developed and is obtaining scientific credibility. Consequently, the neuroendocrine response to heart failure is no longer viewed as a compensatory beneficial mechanism. Instead, we have learned through the years that pharmacological treatment aimed at reducing the effect of the neuroendocrine response is indeed clinically and prognostically advantageous for the patient.
Adaptation, Physiological↗
Cardioprotective effect of angiotensin-converting enzyme inhibitors in patients with coronary artery disease.
Clinical and experiments study with angiotensin-converting enzyme (ACE) inhibitors suggest that these agents may improve coronary artery disease by acting at multiple sites in the series of events leading to end-stage heart disease. These agents reduce blood pressure, improve prognosis and symptoms in patients with severe heart failure and in patients after acute myocardial infarction with left ventricular dysfunction. They are useful in the early, acute phase of myocardial infarction. More recently, ACE inhibitors have been shown to reduce in vitro vascular hypertrophy, to attenuate arteriosclerosis, and to maintain endothelium function. Whether these effects occur at clinical levels is still uncertain. The exciting clinical data have led to the proposal that alteration of ACE activity, particularly in tissue, is an important factor in development and progression of CAD. The ACE system is complex, with endocrine, paracrine, and autocrine effects. ACE is present in cardiac and vascular tissue. Therefore, the beneficial effects of ACE inhibitors can be classified as "cardio" and "vasculo" protective. This article summarizes a number of independent and complementary mechanisms pointing to a role of ACE and ACE inhibition in coronary artery disease.
Angiotensin-Converting Enzyme Inhibitors↗
Continuous versus intermittent warm blood cardioplegia: functional and energetics changes.
BACKGROUND: The aim of this study was to compare the protective effects of continuous warm blood cardioplegia (CWBC) and intermittent warm blood cardioplegia (IWBC) in an experimental model of blood-perfused, isolated rabbit heart. METHODS: In the CWBC group, cardiac arrest was induced by continuous infusion of blood cardioplegia (10 mEq/L KCl) followed by 30 minutes of reperfusion with blood. In the IWBC group, after 5 minutes of perfusion with blood cardioplegia (10 mEq/L KCl), coronary flow was abolished for 10 minutes, followed by reperfusion with blood cardioplegia for 5 minutes. This sequence was repeated three times for a total period of 45 minutes. Finally the hearts were reperfused for 30 minutes with blood. RESULTS: Infusion of potassium induced a marked increase in coronary perfusion pressure (from 50 +/- 3 to 98 +/- 1 mm Hg; p < 0.01), which remained elevated throughout in the CWBC group, whereas in the IWBC group, it dropped to 0 during each no-flow period. In both groups, cardioplegia resulted in a significant reduction in oxygen consumption (from 5.5 +/- 0.2 to 0.6 +/- 0.03 mL O2.min-1.100 g-1 wet wt; p < 0.01). During CWBC, glucose extraction was significantly reduced (from 152 +/- 10 to 64 +/- 18 micrograms.min-1.g-1 wet wt; p < 0.01). Free fatty acid uptake and creatine kinase and lactate release were not affected. During IWBC, in contrast, a transient but significant release of creatine kinase (from 643 +/- 254 to 2,234 +/- 296 mU.min-1.g-1 wet wt; p < 0.01) and lactate (from 63 +/- 22 to 374 +/- 32 micrograms.min-1.g-1 wet wt; p < 0.01) occurred after each period of ischemia. Despite these metabolic differences, both cardioplegic procedures allowed a prompt and complete recovery of mechanical function and tissue content of high-energy phosphates. CONCLUSIONS: Both CWBC and IWBC exert optimal protection in the isolated blood perfused rabbit heart. Thus, IWBC can be safely used to improve visualization of the surgical field.
Adenine Nucleotides↗
Left ventricular dysfunction due to the new ischemic outcomes: stunning and hibernation.
Several potential manifestations and outcomes are associated with myocardial ischemia and reperfusion. When ischemia is severe and prolonged, irreversible damage occurs and there is no recovery of contractile function. When ischemia is less severe or shorter in duration, recovery of contraction may occur instantaneously or more commonly, after considerable delay, which is the condition recognized as "stunned myocardium." Stunning is defined as a transient left ventricular dysfunction that persists after reperfusion despite the absence of irreversible damage and restoration of normal or near-normal coronary flow. Oxidative stress and alteration of calcium homeostasis during reperfusion are the probable causes of stunning. Clinically, stunning may occur after acute infarction, successful thrombolysis, unstable angina, angioplasty, resolution of coronary spasm, open-heart surgery, or transplantation. It can be treated with interventions aimed at prevention or reversal. When ischemia is prolonged but less severe, myocytes may remain viable but exhibit depressed contraction. Under these conditions, reperfusion restores normal contractile performance. This type of ischemia, leading to a reversible, chronic left ventricular dysfunction, has been termed "hibernating myocardium." The intrinsic mechanisms of this condition are unknown. Clinically, it is very important to diagnose hibernation because reperfusion of the hibernating myocardium by angioplasty or heart surgery restores contraction, and this correlates with long-term survival. A number of methods are available to access the hibernating myocardium. These include cardiac imaging techniques that evaluate myocardial viability, such as positron emission tomography and thallium myocardial imaging, or methods that evaluate contractile reserve, such as low-dose dobutamine echocardiography. Interestingly, reperfusion of patients with end-stage ischemic cardiomyopathy and hibernating myocardium can be considered an alternative to transplantation.
Cardiomyopathies↗
Neuroendocrine response to standing and mild exercise in patients with untreated severe congestive heart failure and chronic constrictive pericarditis.
OBJECTIVES: Plasma hormones at rest in patients with untreated severe congestive cardiac failure are similar to those occurring during heavy exercise in healthy people. This study examines the hypothesis that the neuroendocrine effects of exercise are modified in untreated congestive cardiac failure. DESIGN: The effect of lying, standing, upright exercise, and recovery on several plasma hormones was measured in healthy controls and 2 groups of patients with severe untreated heart failure. The level of exercise was the same in all groups and low enough to be within the capacity of patients with severe failure. PATIENTS: There were 12 healthy controls, 9 patients with untreated severe congestive cardiac failure caused by myocardial disease, and 12 patients with untreated constrictive pericarditis. SETTING: A tertiary referral centre in North India. RESULTS: Heart rate, noradrenaline, renin activity, aldosterone, cortisol, growth hormone and atrial natriuretic peptide (ANP) were higher in the 2 groups of patients than in the healthy controls during both rest and exercise (P < 0.01 for both comparisons). In general, the effects of this mild degree of exercise were no greater than those of standing. The increase in heart rate during exercise was greater in the group with constrictive pericarditis than in the controls (P = 0.04) and (non-significantly) in congestive heart failure. Apart from these differences the pattern of responses to standing and exercise was similar in the three groups. CONCLUSIONS: While there was evidence of a broad neuroendocrine activation in patients with congestive cardiac failure, the only abnormal increase during exercise (of marginal significance) was found for renin activity in those with myocardial disease. In patients with untreated congestive failure, a substantially normal endocrine response to exercise was superimposed on abnormal resting concentrations.
Adult↗
Right heart failure chronically stimulates heat shock protein 72 in heart and liver but not in other tissues.
OBJECTIVES: During cardiac failure several ontogenically developed adaptional mechanisms are activated. Among these, heat-shock proteins (HSP) are expressed in response to stress. The aim of the present study was to investigate the HSP72 protein expression in lungs, liver, cardiac and skeletal muscles during congestive heart failure (CHF). METHODS: CHF was induced in Sprague-Dawley rats by a single intraperitoneal injection of monocrotaline (50 mg/kg). Two groups of animals emerged: a CHF group (n = 10) with right ventricular hypertrophy, pleural and peritoneal effusions, and an Hypertrophy group (n = 12) with right ventricular hypertrophy without CHF. The data for each group were compared with those of control (saline infused) age-matched rats. Lungs, liver, right and left ventricles, soleus, extensor digitorum longus and tibialis anterior muscles were excised and analyzed for HSP72 concentration by Western blot analysis using a specific monoclonal antibody. Noradrenaline levels in the heart were also measured using HPLC. RESULTS: The CHF group showed: (1) reduced right (0.460 +/- 0.090 vs 0.830 +/- 0.070 nmol/ventricle, P < 0.01) and left (1.10 +/- 0.09 vs 2.10 +/- 0.130 nmol/ventricle, P < 0.001) ventricular content of noradrenaline compared to the control; (2) significant activation of HSP72 concentration in right and left ventricles (39.4 +/- 1.6 vs 5 +/- 0.9% and 13 +/- 1.2 vs 3.5 +/- 0.6%, P < 0.001 both) and in the liver (39.8 +/- 11 vs 6 +/- 2%, P < 0.001); (3) no modification in HSP72 concentration in lungs and all of the peripheral muscles considered. The Hypertrophy group showed: (1) unchanged total noradrenaline tissue content as compared to the control; and (2) unmodified HSP72 concentration in all tissues analyzed. CONCLUSIONS: The present study demonstrates that CHF, but not compensatory hypertrophy, is a specific stimulus for chronic HSP72 induction in the heart and liver. On the contrary, CHF does not affect HSP in lungs and peripheral muscles. HSP 72 induction represents an intracellular marker of stress reaction which can persist chronically.
Animals↗
In vitro administration of ergothioneine failed to protect isolated ischaemic and reperfused rabbit heart.
Ergothioneine, a natural thiol-containing molecule, has recently been proposed to protect the heart against damage caused by ischaemia and reperfusion. We investigated the possibility that ergothioneine can have a role in maintaining the myocardial thiol/disulfide balance and consequently also a protective effect against ischaemic and reperfusion injury. We used isolated Langendorff-perfused rabbit hearts subjected to 45 min global and total ischaemia followed by 30 min reperfusion at baseline coronary flow (22 ml/min). Ergothioneine was delivered at 10(-5) M and 10(-4) M 60 min before ischaemia and during reperfusion. Myocardial damage was determined in terms of mechanical function, creatine kinase (CK) and lactate release, energy phosphate stores and the occurrence of oxidative stress. In our experimental conditions the treatment was unable to prevent myocardial damage. Ergothioneine, independently from the dosage used, failed to: (i) increase recovery of developed pressure upon reperfusion (14.4 +/- 2.3 mmHg in control hearts vs. 10.3 +/- 2.9 and 12.5 +/- 2.3 mmHg in 10(-5) M and 10(-4) M ergothioneine treated hearts, respectively); (ii) decrease the rise in diastolic pressure (44.3 +/- 4.4 mmHg in control hearts vs. 49.8 +/- 5.8 and 48.0 +/- 7.7 mmHg in treated hearts); (iii) decrease the release of CK and lactate; (iv) increase the levels of adenosine triphosphate (ATP) and creatine phosphate (CP) in tissue upon reperfusion; (v) maintain ratio between oxidized and reduced forms of adenine nucleotide coenzyme, as index of aerobic metabolism; (vi) prevent the decline of reduced glutathione (GSH), or the accumulation of oxidized glutathione (GSSG) as an index of oxidative stress.
Adenine Nucleotides↗
Intermittent v continuous ischemia decelerates adenylate breakdown and prevents norepinephrine release in reperfused rabbit heart.
Myocardium tolerates intermittent ischemia followed by short reperfusions better than continuous ischemia of the same duration. We attempted to delineate the differential mechanism(s) involved in intermittent v continuous ischemia. Isolated, paced rabbit hearts were perfused at 22 ml/min. Coronary flow was stopped intermittently 12 x for 2 or 4 min, with 3-min reperfusions (total reperfusion period: 36 min). In two other groups, flow was stopped continuously for 24 or 36 min followed by a flat 36-min reperfusion. Following the first intermittent 2-min ischemia, adenosine efflux increased ninefold; in all subsequent ischemia/reperfusion cycles, adenosine and total purine releases were substantially less despite identical heart rates, coronary flows and ischemic periods. The rate-pressure product prior to the intermittent ischemias exhibited exponential correlations with total purine efflux during the 3 min of reperfusion. When intermittent ischemia was extended to 4 min, the initial attenuation of ATP breakdown during the prior 2-min occlusions was overcome, but during subsequent 4-min ischemia/reperfusion cycles, ATP breakdown was again attenuated relative to the first 4-min ischemia. After the prolonged continuous ischemias, purine efflux was up to 6 x higher than with intermittent ischemias of the same total time of zero flow. Lactate release and hence cellular H+ export after intermittent ischemias remained consistently elevated, but following the continuous ischemia of 36 min, release of lactate, and thus H+, was subsequentially decreased. Glycogen mobilization occurred regardless of the ischemia's nature, but it was markedly enhanced during continuous ischemias, where no fall in proglycogen levels occurred. Similarly, myocardial norepinephrine release increased substantially only during the prolonged continuous ischemias. Thus short intermittent ischemia attenuates cardiac adenylate degradation and glycogen mobilization; such ischemic insult also provides for better lactate and H+ washouts immediately upon reperfusion. Another beneficial effect of intermittent ischemia was the near-complete absence of free interstitial norepinephrine, which exacerbates myocardial ischemic insults. In addition, the exponential correlations between preischemic rate-pressure product and postischemic purine release suggest that preischemic energy demand may determine ATP breakdown in ischemic rabbit myocardium.
Adenine Nucleotides↗
Oxidative stress during reperfusion of human hearts: potential sources of oxygen free radicals.
OBJECTIVE: The aim was to examine the role of neutrophil activation in the genesis of oxidative stress during the early phases of reperfusion after ischaemia in patients subjected to aortocoronary bypass grafting. METHODS: Ten selected patients were studied. All had normal ejection fraction and normal left ventricular end diastolic pressures before operation. Each patient required at least three grafts, so that the duration of aortic crossclamping exceeded 30 min, the minimum ischaemic period required to detect oxidative stress upon reperfusion. Oxidative stress was assessed by measuring the formation and release of oxidised glutathione (GSSG) in the coronary sinus 1 min before and 3 min after the start of the cardiopulmonary bypass, and then 1, 5, 10, and 20 min after removal of the aortic clamp, and again 5 and 10 min after the end of the cardiopulmonary bypass. The arterial-coronary sinus difference for neutrophils, elastase-alpha 1 protease complex (elastase), and creatine phosphokinase was also monitored at the same intervals. RESULTS: Before clamping GSSG was undetectable in arterial and coronary sinus blood. There was no significant arterial-coronary sinus difference for neutrophils or elastase [53(SEM 66) cell.ml-1 and 1.10(2.49) micrograms.litre-1, respectively[. Five minutes after re-establishment of coronary blood flow, there was both a release of GSSG into the coronary sinus [arterial-coronary sinus difference: 11(2.6) nmol.dl-1] and an accumulation of neutrophils in the heart [arterial-coronary sinus difference: 262(33), P < 0.01 cell.ml-1], whereas no elastase release from the heart was measured [arterial-coronary sinus difference 7.6(4.46) microgram.litre-1, NS]. The arterial levels of elastase increased progressively during the operation from 48(5) microgram.litre-1 (preclamping) to 405(62) microgram.litre-1, P < 0.01 (end of the cardiopulmonary bypass). CONCLUSIONS: These data indicate that, in man, neutrophils do accumulate in the myocardium during early reperfusion. However, they are not activated when oxidative stress occurs. It is unlikely that the neutrophil localisation in the heart has pathological significance in the production of oxygen free radicals during early reperfusion. Free radical accumulation in the coronary vessels may contribute to disorders of coronary flow associated with reperfusion.
Coronary Artery Bypass↗
Extraction and assay of creatine phosphate, purine, and pyridine nucleotides in cardiac tissue by reversed-phase high-performance liquid chromatography.
The levels of creatine phosphate, purine, and pyridine nucleotides in tissues provide important information on energetic and oxidative cellular states. Nevertheless, technical, theoretical, and methodological difficulties in extraction and quantification procedures have so far limited our understanding of the exact role that these substances play in metabolic processes which take place in cells. The objective of our study was to find an easy and rapid method for extracting, separating, and quantifying creatine phosphate, purine, and pyridine nucleotides in solid tissues. We adapted the classic acid-extraction procedure with HClO4 for purine and oxidized pyridine nucleotides and then developed a new alkaline extraction with phenol in a phosphate buffer solution (pH 7.8) for reduced pyridine nucleotides. Biopsies of myocardial tissue were frozen and ground at -180 degrees C using the appropriate extraction procedure. The separation and quantification of the metabolites were performed using a reversed-phase 3-microns Supelchem C18 column, with the addition of tetrabutylammonium as an ion-pair agent to the buffer solution, by ultraviolet detection. The recovery of the external and internal standards always exceeded 90%. The autooxidation or interconversion processes were almost insignificant for each reduced form. This technique allowed us to avoid complex enzymatic procedures and difficulties in the selective assay of pyridine nucleotides with chemiluminescence and surface spectroscopy.
Chromatography, High Pressure Liquid↗
Evidence against malondialdehyde bound to cellular constituents in phospholipid peroxidation.
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Animals↗
Lipid peroxidation in normal pregnancy and preeclampsia.
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Blood Pressure↗