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Biomedical subjects

S Levitsky

Publications and source records attributed to S Levitsky.

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

Physiological and cellular mechanisms of myocardial protection.

BACKGROUND: Despite 40 years of clinically successful open heart surgery, cardiac surgeons continue to seek the ideal myoprotective strategy to minimize perioperative myocardial damage and maximize clinical outcome. Although crude measures, such as length of hospital stay or operative mortality rate, may provide useful administrative data, the ultimate outcome measure of significance to the patient is the lack of operatively induced myocellular injury. METHODS: An ideal biological marker would thus quantitate the number of viable and functioning myocytes remaining postoperatively. The purpose of the present review was to develop the theoretical framework for modern approaches to intraoperative myocardial protection when considering the fundamental principles of physiological and cellular ischemic mechanisms. RESULTS AND CONCLUSIONS: It is hoped that this review provides insight into the implementation of these fundamental concepts developed at the University of Illinois and applied in our present experiences in advanced myocardial muscle mechanics and molecular biology.

Animals↗
PubMed1996

Developmental differences in cytosolic calcium accumulation associated with surgically induced global ischemia: optimization of cardioplegic protection and mechanism of action.

OBJECTIVE: The effect of cardioplegic solutions with high concentrations of potassium or magnesium (or both) on cytosolic calcium accumulation was investigated with fura-2 in isolated perfused mature (n = 24) and aged (n = 24) rabbit hearts. METHODS: We compared cytosolic calcium accumulation before ischemia (control), during 30 minutes of ischemia and 30 minutes of reperfusion under global ischemia, or after treatment with potassium (20 mmol/L), magnesium (20 mmol/L), or both. RESULTS: Cytosolic calcium accumulation was increased during global ischemia in the mature heart (from 178.7 +/- 24.2 in the control group to 393.6 +/- 25.5 nmol/L; p < 0.005) and in the aged heart (from 187.4 +/- 18.7 in the control group to 501.0 +/- 46.1 nmol/L; p < 0.005). Potassium reduced cytosolic calcium accumulation during ischemia in both the mature and aged hearts (300.9 +/- 23.2 and 365.2 +/- 27.7 nmol/L, respectively; p < 0.05 vs global ischemia). Magnesium and potassium/magnesium completely controlled cytosolic calcium accumulation in the mature heart (198.7 +/- 27.5 nmol/L; p < 0.01 vs global ischemia and p < 0.05 vs potassium: 182.3 +/- 22.7 nmol/L; p < 0.05 vs global ischemia and potassium, respectively). Magnesium and potassium/magnesium attenuated cytosolic calcium accumulation in the aged heart (261.3 +/- 26.7, 262.3 +/- 25.2 nmol/L, respectively; p < 0.01 vs global ischemia). These changes in cytosolic calcium accumulation correlated with improved post-ischemic ventricular function. To investigate the mechanism(s) of magnesium-supplemented cardioplegic inhibition of cytosolic calcium accumulation, we performed parallel studies (n = 43) using nifedipine, ryanodine, and dimethylthiourea. Nifedipine with or without ryanodine reduced cytosolic calcium accumulation. Dimethylthiourea did not alter cytosolic calcium accumulation during global ischemia. Our results suggest that cytosolic calcium accumulation during global ischemia was mainly increased via the sarcolemmal 1-type calcium channel and the sarcoplasmic reticulum calcium-release channel. The modulating action of potassium/magnesium cardioplegia on cytosolic calcium accumulation during ischemia would appear to act through the inhibition of the myocardial 1-type calcium channel and the sarcoplasmic reticulum calcium-release channel. CONCLUSION: Senescent cardiac dysfunction correlates with increased ischemia-induced cytosolic calcium accumulation. Magnesium-supplemented potassium cardioplegia ameliorates this age-related phenomenon at normothermia and may have important implications in myocardial protection in the elderly population.

Aging↗
PubMed1995

Magnesium cardioplegia enhances mRNA levels and the maximal velocity of cytochrome oxidase I in the senescent myocardium during global ischemia.

BACKGROUND: The aged myocardium accumulates significantly more cytosolic calcium [Ca2+]i during ischemia, and functional recovery is more severely compromised as compared with the mature heart. Cardioplegia ameliorates these phenomena. The mechanism by which increased calcium accumulation reduces functional recovery in the senescent myocardium is unknown, but it has been suggested that futile calcium cycling in the mitochondria leading to depletion of ATP stores during normothermic global ischemia may be involved. METHODS AND RESULTS: To investigate the effect of cardioplegia on mitochondrial calcium ([Ca2+]mt) accumulation and the expression of cytochrome oxidase I (COX I) during global ischemia, mitochondria were isolated from mature (age, 15 to 20 weeks) and aged (age > 130 weeks) rabbit hearts after Langendorff perfusion. Five perfused heart groups were investigated: 30 minutes of global ischemia without treatment (control), with potassium (K, 20 mmol/L), magnesium (Mg, 20 mmol/L), or potassium and magnesium (K/Mg) cardioplegia. No significant difference in [Ca2+]mt was evident in mature hearts with any protocol. In aged hearts, [Ca2+]mt was increased in global ischemia but was ameliorated with Mg and K/Mg cardioplegia. COX I mRNA levels in aged hearts were lower in both control and global ischemia but were increased with cardioplegia. Maximal velocities for COX I were significantly increased with Mg cardioplegia both in the mature and the aged myocardium. CONCLUSIONS: K and/or Mg cardioplegia ameliorates [Ca2+]mt accumulation in aged hearts during normothermic global ischemia and increases COX I mRNA levels to a level not significantly different from that found in mature hearts.

Aging↗
PubMed1995

Does cardiopulmonary bypass alone elicit myoprotective preconditioning?

BACKGROUND: Brief episodes of ischemia can precondition myocardium. Ischemic preconditioning (PC) has been proposed as an adjuvant method of improving myocardial protection during cardiac surgery. It is unknown whether CPB without an episode of ischemia generates the PC response. METHODS AND RESULTS: To prove that PC occurs in sheep, groups 1 (non-CPB control) and 2 (non-CPB ischemic PC, three 5-minute episodes of normothermic regional ischemia) were studied. Groups 3 (CPB alone), 4 (CPB-alpha receptor blockade, phentolamine 5 mg/kg), and 5 (CPB-adenosine receptor blockade, 8-sulfophenyltheophylline 5 mg/kg) were placed on CPB for 30 minutes and subsequently weaned. All groups underwent 60 minutes of normothermic regional ischemia and 150 minutes of reperfusion. The area at risk (AR) was delineated by Monastryl blue pigment, whereas the infarct size (IS) was determine by tetrazolium staining. Body mass, left ventricular mass, and AR were not different between groups. Ischemic PC was demonstrated in this ovine model by a 54% reduction of IS relative to AR (group 1 versus group 2, P < .01). CPB alone produced a similar percentage IS reduction without ischemia (group 3 versus group 1, P < .01) that was prevented by either alpha-adrenergic receptor (group 4 versus group 3, P < .01) or adenosine receptor (group 5 versus group 3, P < .01) blockade. CONCLUSIONS: CPB alone appears sufficient to elicit the PC response important for myocardial protection during cardiac surgery. These data suggest that myocardial alpha-adrenergic receptor and adenosine receptor stimulation are involve in initiating CPB-induced PC.

Animals↗
PubMed1995

Pressure and volume loading of the right ventricle have opposite effects on left ventricular ejection fraction.

BACKGROUND: Left ventricular ejection fraction has been reported to be depressed in patients with right ventricular volume overload (RVVO) due to Ebstein's anomaly and uncomplicated atrial septal defect, whereas it is usually preserved in right ventricular pressure overload (RVPO) due to congenital pulmonic stenosis. In the present study, we examined the hypothesis that the differential timing of active displacement of the ventricular septum into the left ventricle in RVPO (end systole) and RVVO (end diastole) results in opposite effects of RVPO and RVVO on left ventricular ejection fraction. METHODS AND RESULTS: Ten patients with severe tricuspid regurgitation after tricuspid valve resection for endocarditis and 10 patients with primary pulmonary hypertension were studied as models of isolated RVVO and RVPO, respectively. Left ventricular ejection fraction, end-diastolic volume, and regional systolic shortening were measured with the use of echocardiographic techniques in these 20 patients and 10 healthy control subjects. In RVPO, despite marked underfilling of the left ventricle relative to the healthy control subjects (end-diastolic volume, 48 +/- 26 versus 77 +/- 20 mL; P < .02), left ventricular ejection fraction was similar to that of the control subjects (56 +/- 5% versus 60 +/- 4%; P = .07) and only 1 of 10 RVPO patients had an ejection fraction of less than 50%. In contrast, in RVVO the left ventricle was volume replete (end-diastolic volume, 84 +/- 26 versus 77 +/- 20 mL; P = NS), but left ventricular ejection fraction was significantly depressed (51 +/- 4% versus 60 +/- 4%, P < .001) compared with the control subjects, and 4 of 10 RVVO patients had an ejection fraction of less than 50%. Analysis of systolic fractional shortening along two perpendicular short-axis diameters and the mutually orthogonal long axis demonstrated isolated augmentation of fractional shortening in the ventricular septal-to-posterolateral free wall dimension in RVPO (47.4 +/- 13.7% versus 34.2 +/- 13.1%, P < .05) and isolated depression of fractional shortening along that same dimension in RVVO (13.7 +/- 11.8% versus 34.2 +/- 13.1%, P < .001) compared with the control subjects. CONCLUSIONS: End-systolic leftward ventricular septal shift in RVPO results in isolated augmentation of systolic shortening in the septal-to-free wall dimension, whereas end-diastolic leftward ventricular septal shift in RVVO results in isolated reduction in systolic shortening in the septal-to-free wall dimension. As a result, despite relative underfilling of the left ventricle in RVPO, resting left ventricular ejection fraction is preserved, whereas ejection fraction is depressed for the volume-replete left ventricle of patients with RVVO.

Adolescent↗
PubMed1995

Does aprotinin increase the myocardial damage in the setting of ischemia and preconditioning?

BACKGROUND: Aprotinin reduces postoperative bleeding in cardiac operations, but its association with perioperative myocardial infarction remains controversial. Ischemic preconditioning is a novel method of myocardial protection. METHODS: To answer whether aprotinin increases postischemic myocardial damage and also to characterize the effect of aprotinin on ischemic preconditioning, four groups of sheep were fully heparinized to keep activated clotting time readings greater than 750 seconds and subjected to 60 minutes of normothermic regional ischemia (diagonal artery occlusion) with 3 hours of reperfusion. Group I was the control with no treatment, group II received aprotinin (1 million KIU load followed by 250,000 KIU/h), group III underwent ischemic preconditioning (three 5-minute intervals of ischemia and reperfusion) before prolonged 1-hour ischemia, and group IV underwent similar ischemic preconditioning and received aprotinin. Area at risk was delineated by monastryl blue pigment, and infarction size by tetrazolium staining. RESULTS: The ratios of weight of area at risk to left ventricular weight and left ventricular weight to body weight were constant between groups. Infarction size to area at risk ratio data demonstrated that aprotinin increases infarction size by 60% (infarction size to area at risk ratio from 52% +/- 10% to 84% +/- 10% for I versus II; p < 0.001). Aprotinin also attenuates the protective effect of ischemic preconditioning (infarction size to area at risk ratio from 25% +/- 4% to 41% +/- 6%; p < 0.001). CONCLUSIONS: In the setting of ischemia, aprotinin increases myocardial damage. If, however, the heart is provided with protective preconditioning, then the deleterious effect of aprotinin may be neutralized. From these data we suggest that aprotinin should not be used routinely in cardiac operations unless extensive blood loss is anticipated, such as in redo open heart operations.

Animals↗
PubMed1995

Myocardial mitochondrial calcium accumulation modulates nuclear calcium accumulation and DNA fragmentation.

BACKGROUND: Previously, we have shown that normothermic global ischemia increases cytosolic calcium accumulation in both the mature and aged heart. Increased nuclear and mitochondrial calcium accumulation was shown to occur in the aged but not the mature heart, and these age-related differences were associated with increased DNA fragmentation and decreased cellular viability only in the aged heart. METHODS: To investigate the relationship between increased mitochondrial and nuclear calcium and DNA fragmentation, mature and aged rabbit hearts were subjected to normothermic global ischemia with and without the addition of ruthenium red to block mitochondrial calcium influx. Cytosolic calcium accumulation was measured in a parallel experiment using fura-2. RESULTS: Ruthenium red ameliorated mitochondrial calcium accumulation and was associated with both decreased DNA fragmentation and decreased nuclear calcium accumulation. CONCLUSIONS: Nuclear calcium accumulation was correlated with increased mitochondrial calcium accumulation but not increased cytosolic calcium accumulation in the aged heart. Modulation of mitochondrion "futile calcium cycling" may be of significance in the modulation of ischemic myocardial injury.

Aging↗
PubMed1995

The rapid expression of myocardial hsp 70 mRNA and the heat shock 70 kDa protein can be achieved after only a brief period of retrograde hyperthermic perfusion.

The induction of heat shock proteins in the myocardium has been suggested as a possible intervention to allow for enhanced cardioprotection. We have postulated that a brief period of retrograde hyperthermic perfusion would be sufficient to induce Hsp 70 mRNA and protein accumulation. To investigate this hypothesis, rat hearts (n = 45) were perfused at 37 degrees C for 30 min, then perfused for 15 min at 42 degrees C, and allowed to recover at 37 degrees C for 120 min. Control hearts (n = 23) were perfused at 37 degrees C continuously. Northern analysis indicated that in hearts treated with a brief period of retrograde hyperthermic perfusion Hsp 70 mRNA levels were increased 2.85 +/- 0.02-fold (P < 0.01) by 10 min, 4.88 +/- 0.94-fold (P < 0.01) by 15 min, 9.19 +/- 0.62-fold (P < 0.001) by 30 min, 9.4 +/- 0.52-fold (P < 0.001) by 60 min, 9.45 +/- 0.57-fold (P < 0.001) by 90 min and 9.66 +/- 0.99-fold (P < 0.001) by 120 min of normothermic recovery as compared to control hearts. Western analysis revealed that the heat inducible Hsp 72 kDa protein was increased 2.37 +/- 0.45-fold (P < 0.01) at 60 min, 2.53 +/- 0.25-fold (P < 0.01) at 90 min, and 2.7 +/- 0.6&-fold (P < 0.01) at 120 min when compared to control hearts. Our results indicate that the induction of the heat shock protein Hsp 70 can be rapidly achieved through retrograde hyperthermic perfusion of the myocardium.

Animals↗
PubMed1995

Blood cardioplegia in the senescent heart.

As an increasingly aged population undergoes cardiac surgery, myocardial protective strategies must address the fundamental differences between adult and senescent myocardium. In a test of the hypothesis that senescent myocardium is less tolerant of cardioplegic arrest, adult (0.5 to 1.0 years) and senescent (6 to 9 years) sheep underwent 55 minutes of hypothermic blood cardioplegic arrest. A 5-minute dose of terminal warm blood cardioplegic solution was administered followed by 30 minutes of vented reperfusion. Left ventricular volume was monitored by means of sonomicrometric crystals in three orthogonal planes. Myocardial function was assessed with the preload recruitable stroke work relationship. Diastolic function was assessed with two techniques: the "stiffness" coefficient (beta), derived from the exponential end-diastolic pressure-volume relationship, and the time constant of isovolumic left ventricular pressure decay (tau). Data were acquired before arrest and after the reperfusion period. Contractility in the adult hearts was well preserved (preload recruitable stroke work: 63.7 +/- 6.1 versus 56.8 +/- 4.1 mJ/beat per milliliter per 100 gm, prearrest versus postarrest, p = not significant). In contrast, senescent heart contractility was poorly preserved (56.8 +/- 4.1 versus 35.4 +/- 4.2 mJ/beat per milliliter per 100 gm, p < 0.025). Early diastolic relaxation (tau) was prolonged in the adult hearts (42.5 +/- 3.3 versus 48.8 +/- 3.5 msec prearrest versus postarrest, p < 0.05), whereas the senescent hearts were essentially unchanged (49.3 +/- 3.1 versus 52.3 +/- 4.5 msec. p = 0.35). Myocardial stiffness (beta) was unchanged in both groups. When compared with adult hearts, contractility in senescent hearts is poorly preserved after cold blood cardioplegic arrest. Active diastolic relaxation, however, is more prolonged in adult hearts. Passive diastolic properties are unchanged in both groups. Because there are specific age-related differences in tolerance to cardioplegic arrest, extrapolation of myocardial protective strategies from studies in adult hearts to elderly patients may not be appropriate.

Aging↗
PubMed1995

Limitations of R-average as an index of left ventricular isovolumic relaxation.

Freeman et al. (1993) have recently introduced a new index measuring isovolumic relaxation in the in situ left ventricle. This index, called the R-average, shows less variability than the traditionally used monoexponential time constant (tau), and could therefore represent an alternative measure of isovolumic relaxation during different physiological or pathophysiological interventions. However, the R-average represents the average pressure fall during isovolumic relaxation (isovolumic pressure fall divided by the isovolumic time period), and is therefore highly influenced by the end-systolic pressure level. The present study was done in order to assess whether small increments in loading conditions would alter the R-average without changes in the isovolumic relaxation period or the monoexponential pressure decay tau. We used a right heart bypass porcine model, and end-systolic pressure was altered between 92 and 140 mmHg by pre-loading (servo-pump) or after-loading (phenylephrine) in spontaneously beating and paced hearts. During loading, we found a significant increase in the R-average and a close correlation (r = 0.72 - 0.99) between R-average and en-systolic pressure. However, no alterations were found in the duration of the isovolumic relaxation time period or monoexponential pressure decay (tau) during these loading conditions. In our view, the R-average indicates the systolic loading level for the ventricle, but does not necessarily reflect alterations in the process of active relaxation.

Animals↗
PubMed1995

Heat-shock gene expression in alcoholic liver disease in the rat is related to the severity of liver injury and lipid peroxidation.

To evaluate the relationship between heat-shock gene expression and the severity of pathologic liver injury and lipid peroxidation in experimental alcoholic liver disease, we used the intragastric-feeding rat model. Six groups of male Wistar rats weighing between 225 and 250 g were fed liquid diets containing different dietary fats (saturated fat, corn oil, and fish oil) and ethanol or dextrose for 1 month. Pathologic injury, mRNA and protein levels of HSP70, microsomal conjugated dienes, and hydrogen peroxide were evaluated at sacrifice. Fish oil-ethanol fed rats developed the most severe injury, while the saturated fat-ethanol group showed no liver injury. The highest levels of HSP70 mRNA were seen in the fish oil-ethanol group. There was no difference in HSP70 protein levels between the groups. The levels of HSP70 mRNA correlated significantly with microsomal conjugated dienes (r = 0.87, P < 0.01) and hydrogen peroxide (r = 0.90, P < 0.01). Increased centrilobular HSP70 expression was seen in rats showing liver injury. The close relationship seen between oxidant stress and HSP70 mRNA but not protein suggest that the binding of HSP70 protein to other damaged proteins reduces free HSP70 protein leading to increased HSP70 expression. HSP70 expression may also be a cellular adaptive response to ethanol-induced oxidative stress.

Animals↗
PubMed1995

Effect of type of dietary fat and ethanol on antioxidant enzyme mRNA induction in rat liver.

We carried out a study to relate the effect of the type of dietary fat and ethanol on antioxidant enzyme mRNA levels in liver in the intragastric feeding rat model. Different types of dietary fat were administered [saturated fat (SE), corn oil (CE) and fish oil (FE)] with ethanol to induce varying severities of liver injury. Ethanol-fed rats were pair-fed with dextrose-fed controls that received isocaloric amounts of dextrose. All animals were killed at 1 month and the following studies were carried out: evaluation of severity of pathologic liver injury, mRNA quantitation for catalase, glutathione peroxidase (GPx), and manganese superoxide dismutase (MnSOD), microsomal conjugated dienes, and hydrogen peroxide. SE animals had no liver injury, FE animals had severe liver injury, and CE animals had moderate liver injury. Ethanol induced GPx mRNA in all dietary groups, with the highest levels seen in the FE group. The pattern of catalase mRNA induction was similar to that of GPx mRNA. In contrast, MnSOD mRNA was decreased compared to controls in animals that developed pathologic liver injury, i.e., CE and FE groups. A positive correlation was seen between conjugated diene levels and GPx mRNA (r = 0.88, P < 0.01) and catalase mRNA. The similar slopes for the relationship between conjugated dienes and catalase in the fish oil and non-fish oil groups indicate that the same degree of lipid peroxidation increases catalase mRNA to a greater degree in fish oil-fed rats. A positive correlation was also seen between catalase mRNA and H2O2 (r = 0.95, P < 0.001).

Animals↗
PubMed1994

Magnesium cardioplegia reduces cytosolic and nuclear calcium and DNA fragmentation in the senescent myocardium.

Previous reports have indicated that the senescent myocardium is less tolerant to surgically induced ischemia and that diminished functional recovery is associated with alterations in cytosolic calcium ([Ca2+]i) accumulation. Recently, increased [Ca2+]i has been suggested to alter nuclear calcium ([Ca2+]n) accumulation. To investigate the relation between [Ca2+]i and [Ca2+]n, we subjected mature and aged rabbit hearts to normothermic global ischemia, either without treatment or after treatment with potassium cardioplegia, magnesium cardioplegia, or a combination of potassium and magnesium cardioplegia. The relation between altered [Ca2+]n and DNA fragmentation was also investigated. Our results indicate that [Ca2+]i was increased during 30 minutes of normothermic global ischemia without treatment in both the mature and aged hearts (p < 0.05). Accumulation of [Ca2+]i during global ischemia was reduced with the use of potassium, magnesium, and a combination of potassium and magnesium cardioplegia (p < 0.05 versus untreated ischemia) in both the mature and aged hearts. Levels of [Ca2+]n were unaffected by global ischemia or cardioplegia in the mature myocardium; however, in the aged myocardium, [Ca2+]n was increased during global ischemia and with potassium cardioplegia and was associated with increased nuclear DNA fragmentation (p < 0.05). The use of magnesium and a combination of potassium and magnesium cardioplegia attenuated [Ca2+]n accumulation and nuclear DNA fragmentation (p < 0.05). Control of [Ca2+]i and [Ca2+]n was associated with enhanced functional recovery during reperfusion. These results indicate that during normothermic ischemia, there is increased [Ca2+]i and [Ca2+]n in the aged myocardium, and increased [Ca2+]n is associated with increased nuclear DNA fragmentation.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1994

Ischemia-dependent efficacy of phosphodiesterase inhibition.

To evaluate the inotropic efficacy of phosphodiesterase inhibition in hearts with and without ischemic injury, 27 sheep were evaluated sonomicrometrically during incremental volume loading on right heart bypass. Contractility was assessed with the preload recruitable stroke work relationship. Active relaxation rate was estimated using the time constant of isovolumic pressure decay (tau). For nonischemic assessment, groups 1 and 2 (n = 6 each) underwent 45 minutes of vented perfusion after which milrinone was administered to group 1; group 2 served as nonischemic controls. There was no detectable increase in preload recruitable stroke work or decrement in tau after milrinone administration. Groups 3 and 4 underwent 15 minutes of 37 degrees C ischemia (aortic cross-clamping) followed by 30 minutes of vented reperfusion. Milrinone was then administered to group 3 (n = 7); group 4 (n = 8) served as ischemically injured controls. Inotropic and lusitropic effects were present (group 3 preload recruitable stroke work: 35.4 +/- 5.8 mJ.beat-1.100 g-1.mL-1 before milrinone to 49.5 +/- 4.4 mJ.beat-1.100 g-1.mL-1 after milrinone [p < 0.05]; group 3 tau: 51.8 +/- 5.5 ms before milrinone to 32.2 +/- 2.5 ms after milrinone [p < 0.02]). Although milrinone restored contractility and increased the rate of active relaxation in the postischemic hearts, there was no detectable inotropic effect in nonischemic hearts. In this model, milrinone augments contractility and relaxation in postischemic myocardium but offers little inotropic benefit in non-ischemically injured hearts.

Animals↗
PubMed1994

Perfusion deficits with retrograde warm blood cardioplegia.

Prior studies of cold retrograde cardioplegia have demonstrated the existence of regional deficits in perfusate delivery. To address the hypothesis that these deficits persist with the use of warm perfusate, cardioplegic arrest was induced in 7 swine hearts with retrograde warm blood cardioplegia. Regional perfusion was assessed with the simultaneous infusion of colored 10-microns microspheres. The percentage microsphere recovery (regional microsphere count/total number of microspheres counted x 100) was greatest in the anterior (43% +/- 4%) and lateral (35% +/- 6%) left ventricle. The microsphere recoveries in the posterior left ventricle (7% +/- 1%) and anterior septum (14% +/- 4%) were intermediate, and were statistically lower than those in the anterior left ventricle (p < 0.01). The lateral right ventricle (0.6% +/- 0.2%) and the posterior septum (1.4% +/- 0.9%) exhibited minimal perfusion versus that in the anterior left ventricle (p < 0.01). Less than 1% of the infused microspheres were recovered in the aortic root; 67% were recovered in the right ventricle and are presumed to have bypassed the microcirculation as nonnutritive flow. These data demonstrate that cold retrograde perfusion patterns persist during retrograde warm blood cardioplegia. Limited perfusion of the right ventricle and the posterior septum as well as a large nonnutritive flow were also noted. These perfusion deficits in metabolically active arrested hearts may limit myopreservation at low cardioplegia flow rates.

Animals↗
PubMed1994

Perfusion and cardioplegia.

The focus of the reports reviewed in the last year has shifted to "outcomes," perhaps in response to the pressures of national health care reform. With regards to the extracorporeal circulation requisite for complex cardiac repair, emphasis is placed on anticoagulation management, blood use and its systemic effects, cognitive outcome after cardiac operations, and the requirement and effects of intra-aortic balloon pumping on weaning from bypass. Additionally, interest in the systemic effects of prolonged warm perfusion consequent to the novel myocardial management strategy of warm cardioplegia is evident. Advances in cardioplegia have shifted predominantly toward additives, with specific emphasis on modulating inflammation, enhancing the metabolic substrate, and limiting toxic oxygen free radical injury and the ischemia-induced accumulation of cations.

Acute-Phase Reaction↗
PubMed1994

Myocardial cytosolic calcium accumulation during ischemia/reperfusion: the effects of aging and cardioplegia.

Cytosolic calcium in the myocardium is rapidly accumulated during ischemia and has been correlated with the attenuation of functional recovery in the myocardium. The aged myocardium is more sensitive to ischemia and accumulates significantly more cytosolic calcium than either the newborn or the mature myocardium. Modification of the age-related propensity to increased cytosolic calcium accumulation may be achieved through the use of magnesium or potassium/magnesium cardioplegia. Improved postischemic ventricular function obtained with magnesium or potassium/magnesium cardioplegia may have important implications in the reduction of myocardial morbidity and mortality.

Adult↗