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Biomedical subjects

R M Engelman

Publications and source records attributed to R M Engelman.

At least 37 records · Page 2Linked to original sources
PubMed1999

The 'primeless pump': a novel technique for intraoperative blood conservation.

PURPOSE: Hemodilution during cardiopulmonary bypass may lead to anemia requiring intraoperative transfusions. Prime removal from the cardiopulmonary bypass circuit was used to limit dilution and intraoperative transfusions. METHODS: The technique of prime removal consists of arterial and then venous side evacuation of crystalloid prior to cardiopulmonary bypass. The effectiveness of this technique, to maintain a higher hematocrit and reduce intraoperative transfusions, was studied prospectively in two consecutive groups of patients undergoing coronary revascularization (controls versus primeless). RESULTS: Intraoperative hematocrits were significantly higher (P < 0.0001) and transfusions lower (4%) in the primeless versus the control group (19%) (P = 0.003). Prime removal is of particular benefit in anemic (hematocrit < or = 35%) and/or small patients (body surface area < or = 2 m2). CONCLUSION: The technique of prime removal is simple, safe and cost-effective, reducing intraoperative transfusions, especially in small and/or anemic patients. It could be part of blood conservation strategies in most adult cardiac operations.

Aged↗
PubMed1999

Cardioprotection of red wine: role of polyphenolic antioxidants.

Epidemiological studies suggest that the consumption of wine, particularly of red wine, reduces the incidence of mortality and morbidity from coronary heart disease. This has given rise to what is now popularly termed the "French paradox". The cardioprotective effect has been attributed to antioxidants present in the polyphenol fraction of red wine. Grapes contain a variety of antioxidants, including resveratrol, catechin, epicatechin and proanthocyanidins. Of these, resveratrol is present mainly in grape skin while proanthocyanidin is present in the seeds. In this report, we provide evidence that red wine extract as well as resveratrol and proanthocyanidins are equally effective in reducing myocardial ischemic reperfusion injury, which suggests that these red wine polyphenolic antioxidants play a crucial role in cardioprotection.

Antioxidants↗
PubMed1998

Coordinated role of vasoactive intestinal peptide and nitric oxide in cardioprotection.

The present study sought to examine the interrelationship between nitric oxide (NO) and vasoactive intestinal peptide (VIP) in myocardial protection. Isolated rat hearts were perfused for 15 min with buffer only (Group I); 0.3 mM VIP (Group II); 3 mM L-arginine (a precursor of NO) (Group III); VIP and aminoguanidine (iNOS blocker) (Group IV); or L-arginine plus VIP 10-28 (VIP inhibitor) (Group V). Each heart was then made globally ischemic for 30 min followed by 2 h reperfusion. Both VIP and NO were found to provide cardioprotection during ischemia and reperfusion. However, the beneficial effects of VIP and NO were reduced by inhibition of NO and VIP, respectively, suggesting that cardioprotection by VIP is modulated by NO and vice versa. The results of this study suggested a coordinated regulation by cardioprotection by NO and VIP.

Animals↗
PubMed1998

Presence of angiographic coronary collaterals predicts myocardial recovery after coronary bypass surgery in patients with severe left ventricular dysfunction.

BACKGROUND: Patients with coronary artery disease and left ventricular dysfunction (LVD) may have areas of hibernating myocardium that improve functionally after revascularization. Coronary collateral circulation may sustain ischemic, dysfunctional myocardium and favor myocardial recovery after revascularization. We evaluated the effect of angiographic coronary collaterals on myocardial functional recovery after coronary bypass graft (CABG) surgery in a group of patients with severe LVD. METHODS AND RESULTS: Forty-one patients with multivessel coronary artery disease and advanced LVD (left ventricular ejection fraction [LVEF] 25 +/- 5%) undergoing CABG were identified from a prospective database. Preoperative coronary angiograms were evaluated for collaterals, which were graded according to Rentrop's classification (0 to 3), and a collateral index was calculated (collateral sum divided by 3). Preoperative and postoperative radionuclide ventriculograms provided global LVEF and regional ejection fractions. Of 123 regions evaluated, 120 were dysfunctional at baseline. Virtually all (122 of 123) regions were subtended by an artery with > or = 70% stenosis that was bypassed. Thirty-eight (81%) of 47 dysfunctional regions with grade 2 or 3 collaterals improved regional ejection fraction after surgery versus 38 (52%) of 73 dysfunctional regions with grade 0 or 1 collaterals (P = 0.0018). Global LVEF was 34 +/- 10% after surgery (P < 0.001 versus before surgery). Among patients with a global LVEF increase > or = 10%, collateral index was 1.81 versus 0.83 in those with an LVEF increase < 10% (P = 0.005). CONCLUSIONS: In this population of patients with coronary artery disease with severe LVD, the presence of angiographic grade 2 or 3 collaterals predicted recovery of regional and global myocardial function after CABG.

Aged↗
PubMed1998

Influence of the preoperative signal-averaged electrocardiogram on left ventricular function after coronary artery bypass graft surgery in patients with left ventricular dysfunction. The CABG Patch Trial.

Patients with ischemic left ventricular (LV) dysfunction often have an improved survival and life quality after coronary artery bypass grafting (CABG), in part due to an improvement in LV function. A lack of LV ejection fraction (EF) improvement postoperatively portends a worse prognosis. Recently, an abnormal preoperative signal-averaged electrocardiogram (SAECG) in patients with a severely depressed LV ejection fraction undergoing elective CABG was shown to be associated with a higher early and late postoperative mortality. The present study evaluated patients with severe LV dysfunction to identify any relation between an abnormal preoperative SAECG and postoperative changes in LV function after successful CABG. Forty-five patients with LV dysfunction (LVEF <0.36) scheduled for elective CABG underwent preoperative SAECG and both pre- and postoperative LVEF determinations using radionuclide scans. Thirty-one patients in the group had an abnormal preoperative SAECG and 14 patients had a normal preoperative SAECG. Baseline patient characteristics were similar in both groups and the mean preoperative LVEF was 0.26. Overall, LVEF improved 31% postoperatively with a significantly greater benefit noted in the group with a normal baseline SAECG (14.9+/-5.7-point vs 4.8+/-8.5-point increase, p <0.001). All patients whose LVEF did not improve or worsened postoperatively had an abnormal preoperative SAECG. No SAECG measure was altered significantly by the operation. A preoperative SAECG provides information on the postoperative functional recovery of ischemic myocardium.

Aged↗
PubMed1998

Echocardiography allows safer venous cannulation during excision of large right atrial masses.

BACKGROUND: Excision of large right atrial masses requires bicaval cannulation and cardiopulmonary bypass. Safe venous cannulation can be accomplished only by knowing the exact intracavitary location and extension of the mass to avoid fragmentation. Transthoracic echocardiography and intraoperative transesophageal echocardiography, although helpful, cannot always define the exact intracavitary relationships of the tumor. METHODS: We have used both intraoperative transesophageal and epicardial echocardiography to guide venous cannulation in 4 patients with large right atrial masses. Both echo images are used by the surgeon to select the exact site and method of cannulation to avoid fragmentation of the mass. Epicardial echocardiography complemented the images obtained by transesophageal echocardiography. RESULTS: The technique of combined transesophageal and epicardial echocardiography allowed safe venous cannulation in all 4 patients. Each of the right atrial masses was safely excised using case-specific cannulation techniques guided by the echocardiographic images. CONCLUSIONS: We propose the routine use of both intraoperative transesophageal and epicardial echocardiography in guiding venous cannulation for safe excision of large right atrial masses.

Adult↗
PubMed1998

A cost-effective retractor and heart stabilizer for minimal-access coronary bypass.

Exposure for internal mammary artery harvesting and immobilization of the coronary artery during the performance of minimally invasive direct coronary artery bypass grafting requires the use of appropriate retractors and instruments. We have successfully used existing retractors and instruments, modified for such use, which are reusable and cost effective. The use of such a retractor and cardiac stabilizer is described.

Anastomosis, Surgical↗
PubMed1998

Preconditioning of rat heart with monophosphoryl lipid A: a role for nitric oxide.

Preconditioning with monophosphoryl lipid A (MLA) protects rabbit hearts from prolonged ischemic reperfusion injury by a mechanism involving inducible nitric oxide synthase (iNOS) activation. This study was undertaken to determine whether MLA also could precondition rat hearts in a similar manner. Rats were injected with two different doses of MLA (300 microg/kg or 450 microg/kg i.v.) or vehicle (control), and after 24 hr the animals were sacrificed for preparation of isolated perfused rat hearts. Hearts were then perfused by working mode, and then made ischemic for 30 min followed by 30 min of reperfusion. Another group of hearts were treated simultaneously with a nitric oxide (NO) blocker, L-nitro-arginine-methyl-ester (L-NAME) (10 mg/kg) and MLA (450 microg/kg). For arrhythmia studies, 12 hearts were used in each group (total, 48 hearts). Cardiac functions were examined in a separate group of 24 hearts (n = 6/group). MLA-treated hearts (either dose) were tolerant to ischemic reperfusion injury as evidenced by improved postischemic ventricular recovery [coronary flow (ml/min) 19.1 +/- 0.8 (300 microg/kg MLA), 22.6 +/- 1.0 (450 microg/kg MLA) vs. 15.9 +/- 0.7 (control); aortic flow (ml/min) 20.7 +/- 1.8 (300 microg/kg MLA), 25.8 +/- 1.4 (450 microg/kg MLA) vs. 11. 0 +/- 0.8 (control); left ventricular developed pressure (kPa) 13.3 +/- 0.6 (300 microg/kg MLA), 14.6 +/- 0.2 (450 microg/kg MLA) vs. 10. 3 +/- 0.7 (control)]. Incidences of ventricular fibrillation and ventricular tachycardia were decreased compared with the control group only in the 450 microg/kg dose of MLA-treated hearts (92% to 33%). Pretreatment of the hearts with L-NAME inhibited the preconditioning effect of MLA. To examine the induction of the iNOS expression, RNAs were extracted from the control and MLA-treated hearts (after 2, 4,6, 8, 12 and 24 hr of treatment) and Northern blot analyses were performed with a specific cDNA probe for iNOS. A single band of approximately 4.6 kb corresponding to iNOS mRNA was detected after 4 hr of MLA treatment, whereas the maximal iNOS expression was found between 6 and 8 hr of MLA treatment. The results of this study demonstrated that MLA induced the expression of iNOS and protected the myocardium from ischemic reperfusion injury which is blocked by an inhibitor of NO synthesis, which suggests a role of NO in MLA-mediated cardioprotection.

Adjuvants, Immunologic↗
PubMed1998

Ischemic preconditioning attenuates apoptotic cell death associated with ischemia/reperfusion.

Apoptosis or programmed cell death is a genetically controlled response for cells to commit suicide and is associated with DNA fragmentation or laddering. The common inducers of apoptosis include oxygen free radicals/oxidative stress and Ca2+ which are also implicated in the pathogenesis of myocardial ischemic reperfusion injury. To examine whether ischemic reperfusion injury is mediated by apoptotic cell death, isolated perfused rat hearts were subjected to 15, 30 or 60 min of ischemia as well as 15 min of ischemia followed by 30, 60, 90 or 120 min of reperfusion. At the end of each experiment, the heart was processed for the evaluation of apoptosis and DNA laddering. Apoptosis was studied by visualizing the apoptotic cardiomyocytes by direct fluorescence detection of digoxigenin-labeled genomic DNA using APOPTAG in situ apoptosis detection kit. DNA laddering was evaluated by subjecting the DNA obtained from the hearts to 1.8% agarose gel electrophoresis and photographed under UV illumination. The results of our study revealed apoptotic cells only in the 90 and 120 min reperfused hearts as demonstrated by the intense fluorescence of the immunostained digoxigenin-labeled genomic DNA when observed under fluorescence microscopy. None of the ischemic hearts showed any evidence of apoptosis. These results were corroborated with the findings of DNA fragmentation which showed increased ladders of DNA bands in the same reperfused hearts representing integer multiples of the internucleosomal DNA length (about 180 bp). The presence of apoptotic cells and DNA fragmentation in the myocardium were completely abolished by subjecting the myocardium to repeated short-term ischemia and reperfusion which also reduced the ischemic reperfusion injury as evidenced by better recovery of left ventricular performance in the preconditioned myocardium. The results of this study indicate that reperfusion of ischemic heart, but not ischemia, induces apoptotic cell death and DNA fragmentation which can be inhibited by myocardial adaptation to ischemia.

Adaptation, Physiological↗
PubMed1997

Glutathione peroxidase knockout mice are susceptible to myocardial ischemia reperfusion injury.

BACKGROUND: To test our hypothesis that intracellular antioxidant enzymes constitute a cellular defense against acute stress, we studied myocardial ischemia reperfusion injury in the setting of reduced level of glutathione peroxidase using GSHPx-1 gene knockout mice. METHODS: Knockout mice were developed by disrupting the coding sequence of GSHPx-1 gene after inserting a neomycin resistance gene derived from pMCIpol A into the EcoRI site located in exon 2. Isolated perfused hearts were prepared from two groups of mice-knockout and nontransgenic controls. A 4-0 silk was attached to the apex of the heart which in turn was attached to a force transducer. Hearts were perfused by the Langendorff mode, and after 20 minutes of stabilization subjected to 30 minutes of ischemia followed by 2 hours of reperfusion. The force developed by the heart (DF) and the first derivative of DF (dF/dt) were recorded. Creatine kinase (CK) release was measured in the perfusate and the infarct size was measured at the end of each experiment. RESULTS: For both GSHPx-1 knockout and nontransgenic control groups, DF and dF/dt were significantly lower during early postischemic reperfusion compared with baseline, but these values were significantly higher for the control group than the knockout mice throughout most of the reperfusion period. CK release from the heart increased during reperfusion for both groups, but this increase was significantly lower for the control group. The infarct size was also smaller for the control mice as compared with knockouts. CONCLUSIONS: The results indicate that the knockout mice are more susceptible to ischemia reperfusion injury, suggesting the importance of GSHPx-1 gene in myocardial protection from ischemic reperfusion injury.

Animals↗
PubMed1996

Nitric oxide/carbon monoxide. A molecular switch for myocardial preservation during ischemia.

BACKGROUND: In heart, NO is produced from L-arginine catalyzed by NO synthase, and CO is formed during the conversion of bilirubin from heme by the action of heme oxygenase. NO, which exerts its biological actions through cGMP and heme, has recently been implicated in myocardial protection during ischemia and reperfusion. We hypothesized that the intracellular signaling by NO may be modulated by heme oxygenase. METHODS AND RESULTS: To test this hypothesis, isolated rat hearts were perfused for 10 minutes with one of the following: (1) buffer alone; (2) 3 mmol/L L-arginine, a precursor for NO; (3) 650 mumol/L zinc protoporphyrin, a heme oxygenase inhibitor; (4) 3 mmol/L L-arginine plus 650 mumol/L zinc protoporphyrin; (5) 15 mumol/L methylene blue, a cGMP inhibitor; or (6) 3 mmol/L L-arginine plus 15 mumol/L methylene blue. Hearts were then made ischemic for 30 minutes, followed by 30 minutes of reperfusion. L-Arginine afforded significant myocardial protection, as evidenced by increased developed pressure (DP) (53.3 +/- 4.3 versus 35.4 +/- 1.8 for control), dP/dtmax (2405 +/- 125 versus 1758 +/- 117 for control), aortic flow (23 +/- 1.5 versus 9.4 +/- 1.6 for control), and coronary flow (CF) (23.0 +/- 0.8 versus 19.0 +/- 1.6 for control) at the end of reperfusion. Protoporphyrin tended to reduce these values compared with L-arginine alone (DP, 27.5 +/- 1.4; dP/dtmax, 1400 +/- 78; CF, 17 +/- 0.5), suggesting a contribution of heme oxygenase in addition to NO for myocardial preservation. Increased mRNAs for the heme oxygenase were noticed in the ischemic reperfused myocardium. Contents of cGMP, the second messenger for NO signaling, increased in the L-arginine group (1.6 +/- 0.1 versus 1.1 +/- 0.1 for control) and were reduced by protoporphyrin. cGMP was completely inhibited by methylene blue, which also retarded postischemic myocardial functional recovery. Malonaldehyde formation, a presumptive marker for free radical generation, was decreased in the L-arginine group (0.053 +/- 0.003) compared with control (0.089 +/- 0.005) but was increased in the protoporphyrin group (0.09 +/- 0.003) compared with the L-arginine group. In vitro studies demonstrated that NO was able to reduce the reactive oxygen species produced by myoglobin, especially oxoferrylmyoglobin, which either are present in heart or are formed in high concentrations during the reperfusion of ischemic myocardium. CONCLUSIONS: The results suggest that NO contributes to myocardial preservation by both cGMP-dependent and cGMP-independent mechanisms, the former being modulated by CO signaling and the latter by virtue of its antioxidant action.

Animals↗
PubMed1996

Critical timing of nitric oxide supplementation in cardioplegic arrest and reperfusion.

BACKGROUND: It has been shown that increased nitric oxide (NO) generation is associated with improved myocardial preservation during ischemia/reperfusion. This study sought to determine the optimal timing for NO supplementation in the setting of cardioplegic arrest, regional ischemia, and reperfusion. METHODS AND RESULTS: Isolated working rat hearts were arrested with normothermic oxygenated potassium cardioplegia for 5 minutes, followed by 60 minutes of normothermic continuous cardioplegic administration with left anterior descending coronary artery (LAD) occlusion. The hearts were divided into four groups. Hearts in group 1 were ischemic/reperfused controls without L-arginine treatment. Hearts in group 2 were perfused with 3 mmol/L L-arginine for 5 minutes before cardioplegic arrest. Hearts in group 3 were perfused with 3 mmol/L L-arginine in the cardioplegia solution. Hearts in group 4 were perfused with 3 mmol/L L-arginine for 5 minutes only during initial reperfusion. Myocardial contractile function after 30 minutes of reperfusion was significantly better in group 2 compared with the other groups and was significantly lower in group 4 than group 1. Coronary flow, although decreased from base line in all groups at 30 minutes of reperfusion, was highest in group 2. The tissue accumulation of cGMP in groups 2 and 3 increased significantly after L-arginine infusion compared with the control group (group 1). In contrast, the LAD regional cGMP after reperfusion in group 4 was comparable to group 1 and significantly lower than groups 2 and 3, whereas the circumflex region cGMP in group 4 was significantly increased over group 1, comparable to groups 2 and 3. LDH release in groups 2 and 3 was significantly lower compared with groups 1 and 4. CONCLUSIONS: As assessed by myocardial function and LDH release, L-arginine is most beneficial when given before cardioplegic arrest, effective during cardioplegic arrest, and detrimental during reperfusion. This suggests that L-arginine given during reperfusion is deleterious to optimal recovery of myocardial function in this ischemic model and that the effect of NO generation in the ischemic/reperfused myocardium may be dependent on the condition of the endothelium.

Animals↗