Clinical and pathophysiological implications of a bicuspid aortic valve.
Explore the source record for details and available documents.
Adult↗
Biomedical subjects
Richard D Weisel
Publications and source records attributed to Richard D Weisel.
A self-fulfilling prophecy: C-reactive protein attenuates nitric oxide production and inhibits angiogenesis.
BACKGROUND: Given the central importance of nitric oxide (NO) in the development and clinical course of cardiovascular diseases, we sought to determine whether the powerful predictive value of C-reactive protein (CRP) might be explained through an effect on NO production. METHODS AND RESULTS: Endothelial cells (ECs) were incubated with recombinant CRP (0 to 100 microg/mL, 24 hours), and NO and cyclic guanosine monophosphate (cGMP) production was assessed. The effects of CRP on endothelial NO synthase (eNOS) protein, mRNA expression, and mRNA stability were also examined. In a separate study, the effects of CRP (25 microg/mL) on EC cell survival, apoptosis, and in vitro angiogenesis were evaluated. Incubation of ECs with CRP resulted in a significant inhibition of basal and stimulated NO release, with concomitant reductions in cGMP production. CRP caused a marked downregulation of eNOS mRNA and protein expression. Actinomycin D studies suggested that eNOS downregulation was related to decreased mRNA stability. In conjunction with a decrease in NO production, CRP inhibited both basal and vascular endothelial growth factor-stimulated angiogenesis as assessed by EC migration and capillary-like tube formation. CRP did not induce EC survival but did, however, promote apoptosis in a NO-dependent fashion. CONCLUSIONS: CRP, at concentrations known to predict adverse vascular events, directly quenches the production of the NO, in part, through posttranscriptional effect on eNOS mRNA stability. Diminished NO bioactivity, in turn, inhibits angiogenesis, an important compensatory mechanism in chronic ischemia. Through decreasing NO synthesis, CRP may facilitate the development of diverse cardiovascular diseases. Risk reduction strategies designed to lower plasma CRP may be effective by improving NO bioavailability.
Apoptosis↗
Fundamentals of reperfusion injury for the clinical cardiologist.
Explore the source record for details and available documents.
Aged↗
Endothelin antagonism and interleukin-6 inhibition attenuate the proatherogenic effects of C-reactive protein.
BACKGROUND: C-reactive protein (CRP) has been suggested to actively participate in the development of atherosclerosis. In the present study, we examined the role of the potent endothelium-derived vasoactive factor endothelin-1 (ET-1) and the inflammatory cytokine interleukin-6 (IL-6) as mediators of CRP-induced proatherogenic processes. METHODS AND RESULTS: Saphenous vein endothelial cells (HSVECs) were incubated with human recombinant CRP (25 microg/mL, 24 hours) and the expression of vascular cell adhesion molecule (VCAM-1), intracellular adhesion molecule (ICAM-1), and monocyte chemoattractant chemokine-1 was determined. The effects of CRP on LDL uptake were assessed in macrophages using immunofluorescent labeling of CD32 and CD14. In each study, the effect of endothelin antagonism (bosentan) and IL-6 inhibition (monoclonal anti-IL-6 antibodies) was examined. The effects of CRP on the secretion of ET-1 and IL-6 from HSVECs were also evaluated. Incubation of HSVECs with recombinant human CRP resulted in a marked increase in ICAM-1 and VCAM-1 expression (P<0.001). Likewise, CRP caused a significant increase in monocyte chemoattractant chemokine-1 production, a key mediator of leukocyte transmigration (P<0.001). CRP caused a marked and sustained increase in native LDL uptake by macrophages (P<0.05). These proatherosclerotic effects of CRP were mediated, in part, via increased secretion of ET-1 and IL-6 (P<0.01) and were attenuated by both bosentan and IL-6 antagonism (P<0.01). CONCLUSIONS: CRP actively promotes a proatherosclerotic and proinflammatory phenotype. These effects are mediated, in part, via the production of ET-1 and IL-6 and are attenuated by mixed ET(A/B) receptor antagonism and IL-6 inhibition. Bosentan may be useful in decreasing CRP-mediated vascular disease.
Antibodies↗
Cell transplantation in non-ischemic dilated cardiomyopathy. A novel biological approach for ventricular restoration.
OBJECTIVE: With a rising incidence, dilated cardiomyopathy (DCM) is regarded as a major health care concern. Although both medical therapy and novel surgical treatments have been applied to treat DCM, the effects of preventing left ventricular (LV) dilatation are limited, and the mortality rate associated with the disease remains high. Thus novel management strategies for improved treatment of DCM are awaited. METHODS: Researchers have found that, in models of regional ventricular dysfunction, transplanted cells induced a profound biological phenomenon that restored contractile function and prevented ventricular dilatation. We have investigated muscle cell transplantation in hamsters with DCM, and have found that heart cells and smooth muscle cells survived in the host myocardium after transplantation, which suppressed LV dilatation and wall thinning, and preserved heart function. Our current studies are focusing on the clinical applicability of these encouraging early findings by evaluating the optimal cell types, the timing of transplantation, and cryopreservation as cell storage. Concurrently, we are investigating the influence of cell transplantation on myocardial remodeling in order to outline the mechanism of benefit afforded by donor cell engraftment. We believe that the timing of cell transplantation with respect to the progression of the underlying disease is critical in preventing ventricular thinning, dilation and preserving cardiac function. CONCLUSIONS: This novel approach can be a clinically applicable biological therapy for patients with progressive DCM. More studies to uncover the specific molecular and cellular effects of cell transplantation on the host myocardium are necessary for future clinical application.
Animals↗
The characterization and purification of a human transcription factor modulating the glutathione peroxidase gene in response to oxygen tension.
An oxygen responsive transcription factor regulating human glutathione peroxidase gene (GPx) through two oxygen responsive elements (ORE I and ORE2) has been purified and characterized by sequence-specific DNA affinity chromatography. The DNA binding activity, termed Oxygen Responsive Element Binding Protein (OREBP), was partially represented by a 77 kD polypeptide (p70) possessing a blocked N-terminus. The p70 subunit co-eluted with an 86 kD subunit (p80) from affinity columns. N-terminal sequencing analysis of the 86 kD component revealed that this protein represented the larger member of the Ku antigen complex. The identity of the purified 77 kD subunit was determined by Western blot analysis using an antibody directed against the p70 protein. In addition to binding the GPx-ORE, the OREBP was itself regulated by oxygen tension. It was found that the abundance of the ORE binding activity was decreased in cells maintained at low oxygen tension (40 mm Hg). Anti-Ku-antibodies specifically supershifted the OREBP-ORE DNA complex. These observations further add to the numerous nuclear roles of the Ku-transcription factor.
Antibodies↗
Regional overexpression of insulin-like growth factor-I and transforming growth factor-beta1 in the myocardium of patients with hypertrophic obstructive cardiomyopathy.
OBJECTIVE: Hypertrophic obstructive cardiomyopathy has been proposed to be the result of gene mutations of contractile proteins. However, we have previously shown significant elevation of insulin-like growth factor-I (IGF-I) and transforming growth factor-beta1 (TGF-beta1) at the messenger RNA, protein, and receptor levels in patients with hypertrophic obstructive cardiomyopathy when compared with myocardium from patients without this disorder. We hypothesized that this growth factor overexpression is a regional phenomenon. To test this hypothesis, we compared levels of IGF-I and TGF-beta1 in hypertrophic and nonhypertrophic myocardium within the same group of patients with hypertrophic obstructive cardiomyopathy. METHODS: Two biopsy specimens were obtained from each patient undergoing septal myectomy for severely symptomatic hypertrophic obstructive cardiomyopathy, from hypertrophied septum and from nonhypertrophied myocardium (8 patients in total). Clinical data were prospectively recorded. Messenger RNA levels for growth factor were quantified by means of multiplex reverse transcriptase-polymerase chain reaction, expressed as a densitometric ratio of growth factor/glyceraldehyde-3-phosphate dehydrogenase. Protein levels were quantified by means of chemiluminescent slot blot analysis. Growth factor proteins were used to generate a standard curve. RESULTS: IGF-I messenger RNA and protein levels in hypertrophic myocardium were 2.6 and 2.9 times greater, respectively, than in nonhypertrophic myocardium of the same patients (both P <.01). TGF-beta 1 messenger RNA and protein levels in the hypertrophic myocardium were 2.5 and 2.8 times greater, respectively, than the levels in the nonhypertrophied myocardium (both P <.01). There was a significant correlation between the IGF-I protein ratio (hypertrophic/nonhypertrophic myocardium) and the inducible left ventricular outflow tract gradients measured at cardiac catheterization (r = 0.77, P =.025). CONCLUSIONS: Myocardial overexpression of IGF-I and TGF-beta1 is a regional phenomenon in patients with hypertrophic obstructive cardiomyopathy and is likely involved in the pathogenesis of the disorder.
Cardiomyopathy, Hypertrophic↗
Improved heart function with myogenesis and angiogenesis after autologous porcine bone marrow stromal cell transplantation.
OBJECTIVE: The study evaluated the utility of transplanting bone marrow stromal cells in a porcine myocardial infarction model. METHODS: A myocardial infarction was created by occluding the distal left anterior descending artery in pigs with coils and Gelfoam sponge. Sternal bone marrow was aspirated, and stromal cells were cultured and induced to differentiate to a myogenic phenotype with 5-azacytidine. Four weeks after coronary artery occlusion, sestamibi technetium single-photon emission computed tomographic scans were performed, and then either a graft of 100 x 10(6) bone marrow stromal cells (n = 5, 30% labeled with bromodeoxyuridine) or culture medium (n = 6) was injected into the infarct region. Four weeks later the tomographic scans were repeated and cardiac function was assessed with pressure and volume measurements. Morphologic and histologic characteristics of the heart were also studied. RESULTS: Histologic examination found bromodeoxyuridine-labeled cells within the infarct region in islands that had sarcomeres and Z-bands and stained positively for cardiac specific troponin I. The bone marrow stromal cell transplant sites had a greater (P <.05) capillary density than did the control sites. The tomographic scans showed that the hearts with the cell transplants had increases in stroke volume, regional perfusion, and wall motion (P <.05 for all groups) relative to the control hearts. The pressure-volume analysis showed improvement (P <.05) in end-systolic elastance and preload recruitable stroke work in the transplantation group relative to the control group. The left ventricular chamber size was smaller (P <.05) and the scar thickness was greater (P <.05) in the hearts with transplanted cells than in the control hearts (P =.06). CONCLUSION: 5-Azacytidine-treated bone marrow stromal cells transplanted into the myocardial infarct region formed islands of cardiac-like tissue, induced angiogenesis, prevented thinning and dilatation of the infarct region, and improved regional and global contractile function.
Animals↗
The insulin cardioplegia trial: myocardial protection for urgent coronary artery bypass grafting.
BACKGROUND: Small, nonrandomized clinical trials have demonstrated a beneficial effect of solutions containing insulin and glucose on the recovery of myocardial metabolism and ventricular function after cardioplegic arrest and reperfusion. However, no large, blinded, randomized study has yet determined the effects of insulin-enhanced cardioplegia on clinical outcomes after coronary artery bypass grafting. METHODS: The Insulin Cardioplegia Trial was designed to evaluate the clinical impact of insulin-enhanced cardioplegia on patients at high risk undergoing isolated coronary artery bypass grafting for unstable angina. A total of 1127 patients were randomly assigned at operation to receive cardioplegic solution supplemented with 10 IU/L insulin (n = 557) or placebo (n = 570). All personnel with direct patient contact were blinded to randomization group. RESULTS: Overall operative mortality was 2.2%, with no significant differences between groups. The prevalences of postoperative low output syndrome (insulin 10.4%, placebo 9.7%, P =.7) and enzymatic myocardial infarction (insulin 21.0%, placebo 18.8%, P =.3) were not different between groups. The primary composite outcome of low output syndrome and/or enzymatic myocardial infarction revealed no difference between groups (insulin 30.0%, placebo 26.3%, P =.2). CONCLUSIONS: Despite encouraging results from smaller, nonrandomized studies, the Insulin Cardioplegia Trial failed to demonstrate a clinical benefit of insulin-enhanced cardioplegic solution for patients undergoing high-risk isolated coronary artery bypass grafting.
Adult↗
Novel cardioprotective effects of tetrahydrobiopterin after anoxia and reoxygenation: Identifying cellular targets for pharmacologic manipulation.
OBJECTIVES: Contemporary cardioprotective strategies to prevent perioperative ischemia-reperfusion injury have focused on the l-arginine nitric oxide pathway. Tetrahydrobiopterin is an absolute cofactor required for the enzyme nitric oxide synthase and is thus a critical determinant of nitric oxide production. We hypothesized that ischemia-reperfusion results in diminished levels of tetrahydrobiopterin, which might represent a key cellular defect underlying endothelial and myocyte dysfunction after ischemia-reperfusion. To this aim, we examined the effects of tetrahydrobiopterin supplementation in (1) an in vivo experimental model of global ischemia-reperfusion and (2) an in vitro human ventricular heart cell model of simulated ischemia-reperfusion. Measures of endothelial function, oxidant production, cell survival, and cardiac function were used to assess outcome. METHODS: In study 1 Wistar rats were divided into one of 2 groups (n = 10 per group). One group received tetrahydrobiopterin (25 mg x kg(-1) x d(-1) for 7 days), and the other group served as the control group. Hearts were subjected to 30 minutes of ischemia followed by 30 minutes of reperfusion, and left ventricular developed pressure, left ventricular systolic pressure, and left ventricular end-diastolic pressure were determined by using the modified Langendorff technique. In study 2 we quantitated myocardial malondialdehyde, a marker of lipid peroxidation, in ventricular tissues from both groups of animals using butanol phase extraction and spectrophotometric analysis. In study 3 coronary vascular responses were determined in vascular segments of the left coronary artery in both groups of animals after ischemia-reperfusion. Endothelium-dependent and endothelium-independent vasodilatation to acetylcholine and sodium nitroprusside, respectively, were compared between groups. In study 4, using a human ventricular heart cell model of simulated ischemia-reperfusion, we studied the effects of tetrahydrobiopterin (20 micromol/L) on cellular injury (as assessed by means of trypan blue uptake). RESULTS: After ischemia-reperfusion, myocardial dysfunction was evidenced by a decrease in left ventricular developed pressure and an increase in left ventricular end-diastolic pressure (P =.01 compared with baseline). Hearts from tetrahydrobiopterin-treated rats exhibited protection against ischemia-reperfusion injury (left ventricular developed pressure: 74 +/- 4 vs control 42 +/- 8 mm Hg, P =.01; left ventricular end-diastolic pressure: 12 +/- 3 vs 34 +/- 7 mm Hg, P =.01). Furthermore, tetrahydrobiopterin treatment attenuated the rise in malondialdehyde levels after ischemia-reperfusion (P =.01). After reperfusion, coronary endothelial function to acetylcholine was attenuated (P =.003 vs sham-treated mice), whereas responses to sodium nitroprusside remained unchanged. Tetrahydrobiopterin-treated rats exhibited an improvement in acetylcholine-mediated vasorelaxation (P =.01 vs ischemia-reperfusion group). Cellular injury, as assessed by means of trypan blue uptake, was higher in human ventricular heart cells subjected to simulated ischemia-reperfusion; this effect was prevented with tetrahydrobiopterin treatment (P =.001). CONCLUSIONS: Supplemental tetrahydrobiopterin provides a novel cardioprotective effect on left ventricular function, endothelial-vascular reactivity, oxidative damage, and cardiomyocyte injury after ischemia-reperfusion injury and might represent an important cellular target for future operative myocardial protection strategies.
Adolescent↗
Increased endothelin-1 production in diabetic patients after cardioplegic arrest and reperfusion impairs coronary vascular reactivity: reversal by means of endothelin antagonism.
OBJECTIVES: Evidence has accrued to suggest that diabetic patients face an increased risk of ischemic events and low output syndrome and might mount an inordinate response to ischemia and reperfusion. Because hyperglycemia is a potent stimulus for endothelin-1 production, we hypothesized that increased production, action, or both of endothelin-1 in diabetes might represent an important mediator of endothelial dysfunction in patients with that disease. To this aim, we compared the effects of cardioplegic arrest and reperfusion on coronary sinus effluent endothelin-1 levels and atrial arteriolar vascular responses in diabetic and case-matched nondiabetic patients undergoing coronary artery bypass grafting. METHODS: In study 1 coronary sinus effluent endothelin-1 levels were assessed at baseline and at 1 and 10 minutes after reperfusion in 13 diabetic and 12 nondiabetic patients matched for age, ejection fraction, Parsonnet score, and crossclamp time. In study 2 vascular responses of atrial arterioles subjected to perioperative ischemia-reperfusion were evaluated with videomicroscopy. Atrial microvessels (from appendages) were obtained before and after removal of the aortic crossclamp, and vascular responses to exogenously administered endothelin-1 (10(-10) mol/L) and substance P (10(-8) mol/L) were studied in the presence or absence of BQ-123, an endothelin A receptor antagonist. RESULTS: Diabetic patients elaborated more endothelin-1 at 1 and 10 minutes after reperfusion (P =.01). Endothelin-1-mediated vasoconstriction was similar in diabetic and nondiabetic atrial microvessels before cardioplegic arrest and cardiopulmonary bypass. After cardiopulmonary bypass and reperfusion, endothelin-1-mediated vasoconstriction was enhanced in both groups; however, this response was greater in microvessels from diabetic patients (P =.02). BQ-123, the endothelin A antagonist, attenuated the effects of bypass and reperfusion on endothelin-1-mediated vasoconstriction in both groups (P =.01). Substance P-mediated vasodilatation was similar in diabetic and nondiabetic atrial microvessels before bypass. After bypass and reperfusion, substance P-mediated vasodilatation was diminished in both groups; however, this response was more pronounced in the diabetic group (P =.003). BQ-123 coincubation restored substance P-mediated vasodilatation in both groups. CONCLUSIONS: We determined the following: (1) the coronary effluent release of endothelin-1 is higher in diabetic than in nondiabetic patients after cardiopulmonary bypass and reperfusion; (2) diabetic coronary microvessels respond to bypass and reperfusion with greater endothelin-1-mediated vasoconstriction and diminished nitric oxide-mediated vasodilatation; and (3) these effects are attenuated by endothelin antagonism. Endothelin-1 might be an important mediator of ischemia-reperfusion injury in patients with diabetes. Furthermore, use of endothelin receptor antagonists might be a novel strategy for improving the resistance of the diabetic heart to cardioplegic arrest and reperfusion.
Aged↗
Hyperglycemia exaggerates ischemia-reperfusion-induced cardiomyocyte injury: reversal with endothelin antagonism.
OBJECTIVES: We have previously demonstrated an importance of endothelin-1 in diabetic patients undergoing bypass surgery. Recent evidence suggests that cardiomyocytes might also produce endothelin-1, which might directly impair myocyte contractility by increasing intracellular calcium levels. Because hyperglycemia is a potent stimulus of endothelin-1 production, we hypothesized that increased production, action, or both of endothelin-1 might be a mediator of direct cardiomyocyte injury in diabetes. Therefore we studied the effects of endothelin receptor blockers (BQ-123 and bosentan) on hyperglycemia-induced endothelin-1 production and cellular injury after ischemia-reperfusion. METHODS: Using a human ventricular heart cell model of simulated ischemia-reperfusion, we studied the effects of normoglycemia (5 mmol/L, 48 hours) and hyperglycemia (25 mmol/L, 48 hours) on cellular injury and endothelin-1 production. Furthermore, the effects of selective endothelin-A and mixed endothelin-A/B receptor antagonism (with BQ-123 and bosentan, respectively) were evaluated. RESULTS: Cellular injury, as assessed by means of trypan blue uptake, was higher in human ventricular heart cells subjected to hyperglycemia and simulated ischemia-reperfusion injury (P =.01); this effect was prevented with both BQ-123 and bosentan (P =.01). In addition, heart cells from the hyperglycemic group elaborated more endothelin-1 after ischemia-reperfusion (P =.02). CONCLUSIONS: Endothelin-1 production and cellular injury were greater in human ventricular heart cells subjected to hyperglycemic conditions and simulated ischemia-reperfusion. These effects are mediated by endothelin-A receptors because both BQ-123 and bosentan exerted similar degrees of protection. Endothelin receptor blockade is a novel strategy to improve the resistance of the diabetic heart to cardioplegic arrest and reperfusion.
Antihypertensive Agents↗
Aortic valve malformations and pulmonary autograft root dilatation.
Explore the source record for details and available documents.
Aorta↗
Histologic changes of nonbiodegradable and biodegradable biomaterials used to repair right ventricular heart defects in rats.
OBJECTIVES: Nonbiodegradable synthetic materials have been widely used to repair cardiac defects. Material-related failures, however, such as lack of growth, thrombosis, and infection, do occur. Because a biodegradable scaffold can be replaced by the patient's own cells and will be treated as a foreign body for a limited period, we compared four biodegradable materials (gelatin, polyglycolic acid (PGA), and copolymer made of epsilon-caprolactone and l-lactic acid reinforced with a poly-l-lactide knitted [KN-PCLA] or woven fabric [WV-PCLA]) with a nonbiodegradable polytetrafluoroethylene (PTFE) material. An animal heart model was tested that simulates the in vivo clinical condition to which a synthetic material would be used. METHODS: The five patches were used to repair transmural defects surgically created in the right ventricular outflow tracts of adult rat hearts (n = 5, each patch group). The PTFE patch group served as a control group. At 8 weeks after implantation, the biomaterials were excised. Patch size, patch thickness, infiltrated cell number, extracellular matrix composition, and patch degradation were evaluated. RESULTS: The PTFE patch itself did not change in size except for increasing in thickness because of fibroblast and collagen coverage of both its surfaces. Host cells did not migrate into the PTFE biomaterial. In contrast, cells migrated into the biodegrading gelatin, PGA, and KN-PCLA and WV-PCLA scaffolds. Cellular ingrowth per unit patch area was highest in the KN-PCLA patch. The KN-PCLA patch increased modestly in size and thinness. The WV-PCNA patch did not change in size or thickness. Fibroblasts and collagen were the dominant cellular infiltrate and extracellular matrix formed in the biodegrading scaffolds. The in vivo rates of biomaterial degradation, thinning, and expansion were material specific. All the subendocardial patch surfaces were covered with endothelial cells. No thrombi were seen. CONCLUSIONS: The unique, spongy matrix structure of the PCLA patch favored cell colonization relative to the other patches. The strong, durable outer poly-l-lactide fabric layers in these patches offered physical, biocompatible, and bioresorbable advantages relative to the other biodegradable materials studied. Host cells migrated into all the biomaterials. The cells secreted matrix and formed tissue, which was endothelialized on the endocardial surface. The biomaterial degradation rates and the tissue formation rates were material related. The PCLA grafts hold promise to become a suitable patch for surgical repair.
Absorbable Implants↗
L-arginine protects human heart cells from low-volume anoxia and reoxygenation.
Protective effects of L-arginine were evaluated in a human ventricular heart cell model of low-volume anoxia and reoxygenation independent of alternate cell types. Cell cultures were subjected to 90 min of low-volume anoxia and 30 min of reoxygenation. L-Arginine (0-5.0 mM) was administered during the preanoxic period or the reoxygenation phase. Nitric oxide (NO) production, NO synthase (NOS) activity, cGMP levels, and cellular injury were assessed. To evaluate the effects of the L-arginine on cell signaling, the effects of the NOS antagonist N(G)-nitro-L-arginine methyl ester, NO donor S-nitroso-N-acetyl-penicillamine, guanylate cyclase inhibitor methylene blue, cGMP analog 8-bromo-cGMP, and ATP-sensitive K+ channel antagonist glibenclamide were examined. Our data indicate that low-volume anoxia and reoxygenation increased NOS activity and facilitated the conversion of L-arginine to NO, which provided protection against cellular injury in a dose-dependent fashion. In addition, L-arginine cardioprotection was achieved by the activation of guanylate cyclase, leading to increased cGMP levels in human heart cells. This action involves a glibenclamide-sensitive, NO-cGMP-dependent pathway.
Arginine↗
Smooth muscle cells transplantation is better than heart cells transplantation for improvement of heart function in dilated cardiomyopathy.
Muscle cell transplantation may delay or prevent cardiac dilation in dilated cardiomyopathy. The present study was designed to compare the effects of the heart function of smooth muscle cell (SMCs) auto-transplantation and heart cell (CMs) allo-transplantation in dilated cardiomyopathic hamsters, and to determine which cells are better for cell transplantation. CMs and SMCs were isolated from BIO 53.58 hamsters, and cultured for transplantation. CMs, SMCs (4 X 10(6) cells each) or culture medium were transplanted into 17 weeks old BIO 53.58 hamsters to achieve CM transplantation (CMTx), SMC transplantation (SMCTx), and controls (Con) (N=10 each). Cyclosporine (5 mg/Kg) was administered subcutaneously to CMTx. Healthy hamsters (sham, N=6) were used to compare heart functions. Four weeks after transplantation, heart function was evaluated in all groups using a Langendorff perfusion apparatus. Histology demonstrated severe focal myocardial necrosis in the dilated cardiomyopathic hearts. CMTx and SMCTx formed huge muscle tissue in the dilated myocardium. Sham, SMCTx, and CMTx had a better heart function than Con (p < 0.01), and SMCTx had a better peak systolic pressure (p < 0.05) and developed pressure (p < 0.05) than CMTx at any balloon volume. However, sham and SMCTx were not statistically different. SMCTx and CMTx formed muscle tissue and produced better heart function in the cardiomyopathic hearts, and SMCTx showed better systolic and developed pressures than CMTx, even though they were similar in other functions. Significantly, SMCTx had heart functions, which were similar to those of healthy hamster's hearts.
Animals↗
Coenzyme Q(10) and congestive heart failure: what is the verdict?
Explore the source record for details and available documents.
Animals↗