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Biomedical subjects

G D Buckberg

Publications and source records attributed to G D Buckberg.

At least 37 records · Page 2Linked to original sources
PubMed2001

Left ventricular remodeling and functional mitral regurgitation: mechanisms and therapy.

Myocardial damage that results in dysfunction and remodeling changes left ventricular shape and size. Mitral competence requires the functional integrity of all components of the mitral apparatus. Progressive remodeling ultimately leads to geometric distortion of multiple elements of the mitral apparatus, resulting in functional mitral regurgitation (MR). In this article, we examine the mechanisms of functional MR in the remodeled ventricle. Surgical treatment should aim to correct all abnormalities of the mitral apparatus. These include (1) revascularization of viable myocardium, (2) reduction of ventricular volume and restoration of shape, (3) realignment of papillary muscles, and (4) reduction of annular orifice size.

Humans↗
PubMed2001

Surgical anterior ventricular endocardial restoration (SAVER) for dilated ischemic cardiomyopathy.

Anterior infarction changes ventricular shape and volume. Akinesia is most commonly observed after early reperfusion. Dyskinesia develops in the absence of reperfusion. Both produce heart failure by dysfunction of the remote muscle. Traditional surgery deals with dyskinesia. This study evaluates surgical anterior ventricular endocardial restoration (SAVER), an operation that excludes the apical and septal scar in both akinesia and dyskinesia. A new international group of cardiologists and surgeons from 13 centers, the RESTORE Group) investigated SAVER in ischemic cardiomyopathy following anterior infarction. From January 1998 to July 2000, 662 patients underwent surgery. Early and 3-year outcomes were investigated. Concomitant procedures included coronary artery bypass grafting (CABG) in 92%, mitral repair in 22%, and mitral replacement in 3%. Hospital mortality was 7.7%. Mortality among 606 patients with SAVER and CABG alone was 4.9%. It was 8.1% among 147 patients who underwent concomitant mitral valve repair. Few patients required IABPs (8.4%), LVADs (0.4%), or ECMO (0.6%). Postoperatively, ejection fraction increased from 29.7% +/- 11.3% to 40.0% +/- 12.3% and left ventricular end systolic volume decreased from 96 +/- 63 to 62 +/- 39 mL/m(2) (P <. 05). At 3 years, the survival rate was 89.4% +/- 1.3%. Survival was lower among those with preoperative volume >80 mL/m(2) compared with volume < or = 80 mL/m(2) (83.5% +/- 3.3% v 94.5% +/- 2.0%). Freedom from readmission to hospital for heart failure was at 88.7% at 3 years and was not related to preoperative volume. SAVER is a safe and effective procedure for treating the remodeled dilated anterior ventricle following anterior myocardial infarction.

Adult↗
PubMed2000

Batista procedure: elliptical modeling against spherical distention.

OBJECTIVE: Batista's cardio-reduction of mass and diameter changes the geometry of the left ventricle (LV). This in vivo study explores the LV changing from spherical distention to elliptic modeling. METHODS: Nineteen pigs were connected to cardio-pulmonary bypass (CPB), five of them without cardiac alteration (controls). The LV of the other fourteen pigs was incised between the left anterior descending and the circumflex arteries. Myocardial protection with the beating open method was used. In seven pigs, the LV incision was closed by direct suture to assess the surgical trauma of the Batista procedure (incision). In the other seven pigs a pericardial patch was placed for spherical distention of the LV as a model of heart failure (sphericalization). Patch removal and LV closure restored the normal cardiac geometry (elliptical modeling). Ventricular function was evaluated with Frank-Starling curves (stroke work index, SWI), with endsystolic elastance (EES) and diastolic compliance (beta(-1)) by impedance catheter, and with ejection fraction (EF) by transesophageal echocardiogram. Data were recorded after ventriculotomy, after sphericalization and after elliptical modeling (before and 30 min after discontinuation of CPB). RESULTS: CPB did not significantly alter controls' hemodynamic. Ventriculotomy decreased cardiac function (as % vs. post CPB-controls: SWI* 63 +/- 4; EES 93 +/- 2; beta(-1)* 86 +/- 5). Sphericalization additionally impaired the function (as % vs. ventriculotomy: SWI* 57 +/- 4; EES* 60 +/- 7; beta(-1)* 45 +/- 8). The elliptical modeling greatly improved ventricular performance (as % vs. sphericalization: SWI** 156 +/- 5; EES** 162 +/- 8; beta(-1)** 177 +/- 7; EF** 216 +/- 5) (P < 0.05 for Student's unpaired* and paired** t-test). CONCLUSIONS: Spherical distention of the left ventricular dimensions causes cardiac decompensation. The surgical trauma of the Batista procedure impairs the LV performance. However, the spherically distended LV benefits from Batista's cardio-reduction by elliptical modeling.

Animals↗
PubMed1999

Superiority of magnesium cardioplegia in neonatal myocardial protection.

BACKGROUND: We have shown that magnesium can offset the detrimental effects of normocalcemic cardioplegia in hypoxic neonatal hearts. It is not known, however, whether magnesium offers any additional benefit when used in conjunction with hypocalcemic cardioplegia. METHODS: Twenty neonatal piglets underwent 60 minutes of ventilator hypoxia (FiO2 8% to 10%) followed by 20 minutes of normothermic ischemia on cardiopulmonary bypass (hypoxic-ischemic stress). They then underwent 70 minutes of multidose blood cardioplegic arrest. Five (Group 1), received a hypocalcemic (Ca+2 0.2 to 0.4 mM/L) cardiologic solution without magnesium, whereas in 10, magnesium was added at either a low dose (5 to 6 mEq/L, Group 2) or high dose (10 to 12 mEq/L, Group 3). In the last 5 (Group 4), magnesium (10 to 12 mEq/L) was added to a normocalcemic cardioplegic solution. Function was assessed using pressure volume loops and expressed as percentage of control. RESULTS: Compared to hypocalcemia cardioplegic solution without magnesium (Group 1), both high- and low-dose magnesium enrichment (Groups 2 and 3) improved myocardial protection resulting in complete return of systolic (40% vs 101% vs 102%) (p < 0.001 vs Groups 2 and 3) and global myocardial function (39% vs 102% vs 101%) (p < 0.001 vs Groups 2 and 3), and reduced diastolic stiffness (267% vs 158% vs 154%) (p < 0.001 vs Groups 2 and 3). Conversely, even high-dose magnesium supplementation could not offset the detrimental effects of normocalcemic cardioplegia resulting in depressed systolic (End Systolic Elastance [EES] 41%+/-1%) (p < 0.001 vs Groups 2 and 3) and global myocardial function (40%+/-1%) (p < 0.001 vs Groups 2 and 3), and a marked rise in diastolic stiffness (258%+/-5%) (p < 0.001 vs Groups 2 and 3). Hypocalcemic magnesium cardioplegia has now been used successfully in 247 adult and pediatric patients. CONCLUSIONS: Magnesium enrichment of hypocalcemic cardioplegic solutions improves myocardial protection resulting in complete functional preservation. However, magnesium cannot prevent the detrimental effects of normocalcemic cardioplegia when the heart is severely stressed. This study, therefore, strongly supports using both a hypocalcemic cardioplegic solution and magnesium supplementation as their benefits are additive.

Adenosine Diphosphate↗
PubMed1999

Hypocalcemia in piglets reduces cardiac and pulmonary vascular disturbance after hypoxemia and reoxygenation during cardiopulmonary bypass.

BACKGROUND: Placing cyanotic newborns on cardiopulmonary bypass (CPB) and performing abrupt reoxygenation affects myocardial performance. This study tests the hypothesis that hypocalcemia is beneficial in this circumstance of reoxygenation. METHODS: Twenty-one newborn piglets (anesthetized, open-chests) were placed for one hour on CPB. Seven piglets under normoxic and normocalcemic conditions were the controls. The other piglets underwent hypoxemia and subsequent reoxygenation, for periods of 30 minutes each, under normo-calcemic (Normo-Ca++, n= 7) or hypocalcemic conditions (Hypo-Ca++, n=7). Thirty minutes after discontinuation of CPB, the hemodynamic function was assessed taking into account stroke work indices (SWI), end systolic elastance (EES), pulmonary vascular resistance index (PVRI), cardiac release of conjugated dienes (CD) and creatine phosphokinase (CK), and myocardial oxygen consumption (MVO2). These parameters were expressed as a percentage of the pre-CPB value. The endogenous antioxidant reserve capacity (AORC) of ventricular wall specimens was determined by in-vitro lipid peroxidation forming malondealdehyde (nmol MDA/g protein). RESULTS: After one hour of CPB the cardiac performance returned to normal range without any functional or metabolic disturbance. The normocalcemic condition resulted in a hardly impaired cardiac performance (42%**SWI; 67%**EES), an augmented PVRI (more than 4-fold**), and highly elevated release of CD and CK (3-fold** each). The Normo-Ca++ group's MVO2 (95 +/- 14%) was unaltered. The hypocalcemic condition improved the myocardial function to near control value (85% SWI; 91 % EES) and attenuated the augmentation of the PVRI (n.s. vs. Control group) down to 64% of the Normo-Ca++ group's level. The release of CD and CK in the Hypo-Ca++ group (both n. s. vs. Control group) only minimally increased. The Hypo-Ca++ group's MVO2 improved (137+/-8%*). The MDA formation was worse (344+/-38**) in the Normo-Ca++ group, but unaltered in the Hypo-Ca++ group (203+/-9; n.s. vs. Control group (218+/-20)). * =p<0.05 vs. Controls and Normo-Ca++, ** =p<0.05 vs. Controls and Hypo-Ca++, using ANOVA. CONCLUSIONS: Hypocalcemia during hypoxemia and subsequent reoxygenation highly attenuates myocardial and pulmonary vascular disturbance in newborn piglets. This condition of low blood calcium protects cardiac function and metabolism as well as the pulmonary vascular tone due to diminished myocyte membrane damage, reduced cellular membrane lipid peroxydation, and improved endogenous antioxidant reserve capacity.

Animals↗
PubMed1998

Delayed cardioplegic reoxygenation reduces reoxygenation injury in cyanotic immature hearts.

BACKGROUND: Hypoxemic developing hearts are susceptible to oxygen-mediated damage that occurs after reintroduction of molecular oxygen. This unintended hypoxemic/reoxygenation injury leads to lipid peroxidation and membrane damage and may contribute to postoperative cardiac dysfunction. Biochemical and functional status are improved by delaying reoxygenation on cardiopulmonary bypass (CPB) until cardioplegic arrest. METHODS: Six immature piglets (3 to 5 kg) without hypoxemia underwent 30 minutes of cardioplegic arrest during 1 hour of CPB. Fourteen others underwent 2 hours of hypoxemia on ventilator before reoxygenation on CPB. Reflecting our clinical routine, 9 were reoxygenated on CPB for 5 minutes followed by 30 minutes of cardioplegic arrest and 25 minutes of reperfusion. The other 5 were put on hypoxemic CPB for 5 minutes, before being reoxygenated during cardioplegic arrest for 30 minutes followed by 25 minutes of reperfusion. RESULTS: Cardioplegic arrest (no hypoxemia group) caused no functional or biochemical changes. In contrast, by preceding hypoxemia with subsequent reoxygenation on CPB (no treatment group) we found 39.5% decrease in antioxidant reserve capacity, 1,212% increase in myocardial conjugated diene production, significant increase in coronary sinus blood conjugated dienes, and an 81% reduction of left ventricular contractility, all of which were statistically significant (p < 0.05) when compared with the no hypoxemia group. Conversely, delaying reoxygenation until cardioplegic arrest (treatment group) resulted in 33.1% improvement in antioxidant reserve capacity, 91.7% less conjugated diene production, lower coronary sinus blood conjugated diene levels, and a 95% improved contractility, all of which were significant (p < 0.05) when compared with the no treatment group. CONCLUSIONS: A reoxygenation injury associated with lipid peroxidation and decreased postbypass contractility occurs in cyanotic immature hearts when reoxygenated on CPB. Delaying reoxygenation until cardioplegic arrest by starting CPB with ambient partial pressure of oxygen results in significantly improved myocardial status.

Animals↗
PubMed1998

Prevention of ischemic damage using controlled limb reperfusion.

Following prolonged limb ischemia, a reperfusion injury may occur with the reintroduction of unmodified blood, resulting in tissue loss and, in severe cases, limb loss. We have shown that the reperfusion injury in the heart can be minimized by using controlled reperfusion with a substrate-enriched cardioplegia solution prior to restoring normal blood flow. This article describes two clinical cases in which we used controlled reperfusion in an ischemic limb to prevent limb loss. It demonstrates that a controlled, substrate-enhanced, hypocalcemic, leukodepleted, modified blood reperfusate solution can minimize limb reperfusion damage and improve functional recovery. This preliminary experience is presented to familiarize surgeons with this form of treatment and to describe the solutions and method of administration that can be used to avoid the devastating complications of severe limb ischemia.

Aged↗
PubMed1997

Endothelial stunning and myocyte recovery after reperfusion of jeopardized muscle: a role of L-arginine blood cardioplegia.

Ischemia and reperfusion may damage myocytes and endothelium in jeopardized hearts. This study tested whether (1) endothelial dysfunction (reduced nitric oxide release) exists despite good contractile performance and (2) supplementation of blood cardioplegic solution with nitric oxide precursor L-arginine augments nitric oxide and restores endothelial function. Among 30 Yorkshire-Duroc pigs, 6 received standard glutamate/aspartate blood cardioplegic solution without global ischemia. Twenty-four underwent 20 minutes of 37 degrees C global ischemia. Six received normal blood reperfusion. In 18, the aortic clamp remained in place 30 more minutes and all received 3 infusions of blood cardioplegic solution. In 6, the blood cardioplegic solution was unaltered; in 6, the blood cardioplegic solution contained L-arginine (a nitric oxide precursor) at 2 mmol/L; in 6, the blood cardioplegic solution contained the nitric oxide synthase inhibitor L-nitro arginine methyl ester (L-NAME) at 1 mmol/L. Complete contractile and endothelial recovery occurred without ischemia. In jeopardized hearts, complete systolic recovery followed infusion of blood cardioplegic solution and of blood cardioplegic solution plus L-arginine. Conversely, contractility recovered approximately 40% after infusion of normal blood and blood cardioplegic solution plus L-NAME. Postischemic nitric oxide production fell 50% in the groups that received blood cardioplegic solution and blood cardioplegic solution plus L-NAME but was increased in the group that received blood cardioplegic solution L-arginine. In vivo endothelium-dependent vasodilator responses to acetylcholine recovered 75% +/- 5% of baseline in the blood cardioplegic solution plus L-arginine group, but less than 20% of baseline in other jeopardized hearts. Endothelium-independent smooth muscle responses to sodium nitroprusside were relatively unaltered. Myeloperoxidase activity (neutrophil accumulation) was similar in the blood cardioplegic solution (without ischemia) and blood cardioplegic solution plus L-arginine groups (0.01 +/- 0.002 vs 0.013 +/- 0.003 microgram/gm tissue). Myeloperoxidase activity was raised substantially to 0.033 +/- 0.002 microgram/gm after exposure to normal blood and to 0.025 +/- 0.003 microgram/gm after infusion of blood cardioplegic solution and was highest at 0.053 +/- 0.01 microgram/gm with exposure to blood cardioplegic solution plus L-NAME in jeopardized hearts. The discrepancy between contractile recovery and endothelial dysfunction in jeopardized muscle can be reversed by adding L-arginine to blood cardioplegic solution.

Animals↗
PubMed1997

Prevention of reoxygenation injury in hypoxaemic immature hearts by priming the extracorporeal circuit with antioxidants.

This study tests the hypothesis that abrupt reoxygenation of cyanotic immature hearts when starting cardiopulmonary bypass produces an unintended reoxygenation injury that: (i) nullifies the cardioprotective effects of blood cardioplegia; and (ii) is avoidable by adding the antioxidants, N-(2-mercaptopropionyl)-glycine (MPG) plus catalase to the cardiopulmonary bypass prime. Twenty immature piglets (aged 2-3 weeks) underwent 30 min of blood cardioplegic arrest (BCP) with standard clinical blood cardioplegia (hypocalcaemic, alkalotic, hyperosmolar, substrate-enriched). Six piglets remained normoxaemic (BCP). Fourteen others were made hypoxic (PO2 20-30 mmHg) for up to 2 h by lowering ventilator FiO2 (5-7%) before undergoing reoxygenation on cardiopulmonary bypass at PO2 400 mmHg. In eight animals, the pump prime was not supplemented with antioxidants (Reox + BCP), whereas MPG (80 mg/kg) and catalase (CAT; 5 mg/kg) were added to the pump prime in the other six (MPG/CAT). Myocardial function (end-systolic elastance, conductance catheter), oxidant damage (myocardial conjugated diene production), oxygen consumption and antioxidant reserve capacity were evaluated. Blood cardioplegic arrest caused no functional or biochemical changes in controls without preceding hypoxia. In contrast, hypoxia and reoxygenation in animals undergoing the same blood cardioplegic protocol (Reox + BCP) caused profound myocardial dysfunction, as end-systolic elastance recovered only to 21(2)% (P < 0.05 versus control) of baseline values. Additionally, it reduced antioxidant reserve capacity (malondialdehyde, MDA at 4.0 mM of t-BHP: 1342(59) (P < 0.05 versus control) versus 788(53) mmol/g protein), and led to significantly greater production of conjugated dienes during warm induction (42(4.4) (P < 0.05 versus control) versus 3.3(1.4) A233 nm/100 g per min) and reperfusion (22(2.7) (P < 0.005 versus control) versus 2(0.6) A233 nm/100 g per min). Conversely, supplementation of MPG plus catalase to the pump prime reduced lipid peroxidation (conjugated diene production during warm induction: 22.3(7) A233 nm/100 g per min P < 0.05 versus Reox + BCP), restored antioxidant reserve capacity (MDA at 4.0 M of t-BHP: 975(139) mmol/g protein P < 0.05 versus Reox + BCP) and allowed almost complete functional recovery (80(8)%). Abrupt reoxygenation of hypoxaemic immature hearts on cardiopulmonary bypass causes oxidant damage, nullifies the cardioprotective effects of blood cardioplegia, and leads to reduced myocardial contractility. Antioxidant supplementation of the cardiopulmonary bypass prime avoids these detrimental effects, and results in improved biochemical and functional status.

Animals↗
PubMed1997

Nitric-oxide-induced reoxygenation injury in the cyanotic immature heart is prevented by controlling oxygen content during initial reoxygenation.

Reintroduction of high levels of molecular oxygen after a hypoxic period is followed by a burst of nitric oxide (NO), peroxynitrite, and oxygen free radicals (OFR), which are highly cytotoxic. This study indicates that hyperoxic reoxygenation of cyanotic immature hearts on cardiopulmonary bypass (CPB) induces a reoxygenation injury and that, by reducing NO and OFR production during institution of CPB with subsequent reoxygenation under blood cardioplegic arrest, this oxygen-related damage can be avoided and biochemical and functional status improved. Of 25 immature piglets (3-5 kg, two to three weeks old), 6 underwent one hour of CPB including thirty minutes of aortic clamping with substrate-enriched modified blood cardioplegia (hypocalcemic, alkalotic, and hyperosmolar; warm induction-cold replenishment-warm reperfusion) without preceding hypoxia (controls). Nineteen others were made hypoxic (arterial [Po2] 20-30 mmHg) for up to two hours by lowering the fraction of inspired oxygen (FIO2) on ventilator. These hypoxic piglets were then reoxygenated on CPB at different Po2 levels (hyperoxic, normoxic, or hypoxic) for five minutes, followed by the aforementioned blood cardioplegic (BCP) arrest regimen. Myocardial conjugated diene (CD) production as a marker of lipid peroxidation, and NO production, determined as its spontaneous oxidation products, nitrite (NO2-) and nitrate (NO3-), were assessed during blood cardioplegic induction, and antioxidant reserve capacity was determined by incubating myocardium in the oxidant t-butylhydroperoxide (t-BHP). Myocardial function was evaluated from end-systolic elastance (Ees, conductance catheter). Blood cardioplegic arrest caused no functional or biochemical changes in normoxic control immature piglets. In contrast, brief reoxygenation at PO2 > 400 mmHg, followed by BCP-arrest (hyperoxic) resulted in marked CD production (42 +/- 4 vs 3 +/- 1 A233 nm/minute/100 g; P < 0.05), and NO production (4500 +/- 500 vs 450 +/- 32 mmol/minute/100 g; P < 0.05) during blood cardioplegic induction, reduced antioxidant reserve capacity (malondialdehyde [MDA] at 4.0 mM of t-BHP: 1342 +/- 59 vs 958 +/- 50 nM/g protein; P < 0.05), and caused profound myocardial dysfunction; Ees recovered only 21 +/- 2% (vs 104 +/- 7; P < 0.05), despite the blood cardioplegic regimen shown to be cardioprotective in control normoxic piglets. Conversely, controlling initial PO2 to normoxic (100 mmHg) or hypoxic (20-30 mmHg) levels reduced lipid peroxidation (CD production 16 +/- 2, 2 +/- 1 A233nm/minute/100 g) and NO production (1264 +/- 736, 270 +/- 182 mmol/minute/100 g), restored antioxidant reserve capacity (MDA at 4.0 mM of t-BHP: 940 +/- 95, 982 +/- 88 nM/g protein), and allowed significant functional recovery (58 +/- 11% and 83 +/- 8%), in a PO2-dependent fashion. The authors conclude that reoxygenation of hypoxemic immature hearts by initiating hyperoxic CPB causes oxidant-related damage characterized by lipid peroxidation, enhanced NO production, and reduced antioxidants, leading to functional depression that nullifies the cardioprotective effects of blood cardioplegia. These detrimental effects can be reduced in a PO2-dependent fashion by controlling initial PO2 on CPB and subsequent reoxygenation during blood cardioplegic arrest.

Animals↗
PubMed1996

Pulmonary vasoconstriction due to impaired nitric oxide production after cardiopulmonary bypass.

BACKGROUND: Pulmonary hypertension is a serious complication after cardiopulmonary bypass (CPB). This study tests the hypothesis that CPB provokes oxidant-mediated pulmonary endothelial dysfunction, leading to reduced nitric oxide (NO) production and pulmonary vasoconstriction. METHODS: Twelve piglets underwent 2 hours of CPB. In 6 of them, CPB prime was supplemented with N-mercaptopropionylglycine and catalase, whereas the others were not treated. Left and right ventricular function were evaluated from end-systolic elastance and Starling analysis. Pulmonary vascular resistance and transpulmonary NO production (measuring NO2-, NO3-) were determined to assess pulmonary endothelial function. RESULTS: Cardiopulmonary bypass caused a significant increase in pulmonary vascular resistance (83 +/- 12 to 212 +/- 30 dynes.cm-5.s kg-1, p < 0.05), associated with a reduction of NO production (8.8 +/- 1.4 to 2.5 +/- 0.5 mumol/min, p < 0.05) and depressed right ventricular function (56 +/- 12% of control), whereas N-mercaptopropionylglycine and catalase added to the CPB allowed a substantial improvement of these deleterious effects of CPB. CONCLUSIONS: Cardiopulmonary bypass impairs pulmonary NO production, resulting in pulmonary vasoconstriction and right ventricular dysfunction, which can be reduced by antioxidants. These findings imply the validity of NO inhalation therapy for postoperative pulmonary hypertension as a supplementation of endogenous endothelium-derived relaxing factor.

Animals↗