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Biomedical subjects

S F Bolling

Publications and source records attributed to S F Bolling.

At least 109 records · Page 6Linked to original sources
PubMed1993

Wound complications and treatment of the infected implantable cardioverter defibrillator generator.

Since 1980, the automatic implantable cardioverter defibrillator (ICD) has evolved as effective therapy for prevention of sudden cardiac death following documented sustained ventricular tachycardia or fibrillation. During a 5-year period, 412 ICD devices were implanted at the University of Michigan Hospitals with a wound complication rate of 4.1%. In this group, there were 13 infections, 3 erosions of the generator pocket, and 1 wound hematoma. Of the 16 patients with infection or erosion, 12 patients were treated with a rectus abdominis muscle flap closure and 4 with ICD generator removal. In 83% (n = 12) of the muscle flap patients, the wound healed uneventfully. Preoperative chest CT scanning was found to be helpful in identifying probable infection of the epicardial leads. In these cases, all hardware had to be removed to achieve resolution of the infection. We concluded that rectus abdominis muscle flaps were helpful in salvaging infected or exposed ICD generators in the absence of infected epicardial leads.

Bacterial Infections↗
PubMed1993

Flavone improves functional recovery after ischemia in isolated reperfused rabbit hearts.

The effects of flavone (2-phenyl-1,4-benzopyrone), a modulator of the cytochrome P-450 monooxygenase system, on myocardial postischemic reperfusion recovery were examined in the present study. Left ventricular functional recovery was evaluated in isolated, crystalloid-perfused rabbit hearts after 2 hours of modestly hypothermic (34 degrees C) global ischemia. Four groups (n = 8 in each group) were studied and compared: a vehicle control group, a second group pretreated with flavone (8 x 10(-6) mol/L) before ischemia, a third group pretreated with flavone followed by SKF 525-A (1.7 x 10(-5) mol/L), an inhibitor of cytochrome P-450, and a fourth group pretreated with flavone followed by indomethacin (1 x 10(-6) mol/L), an inhibitor of cyclooxygenase. At 15, 30, and 45 minutes after reperfusion, recovery of left ventricular developed pressure in the control group averaged (mean +/- standard deviation) only 2.60% +/- 12.7%, 35.5% +/- 15.0%, and 42.9% +/- 13.5% of baseline, respectively. In the flavone-treated group, recovery was significantly better, averaging 67.7% +/- 10.7%, 73.9% +/- 9.3%, and 73.6% +/- 7.6% of baseline at the same time periods. Recovery of peak positive rate of pressure rise in the control group averaged 27.4% +/- 15.2%, 38.6% +/- 19.2%, and 45.4% +/- 18.6% of baseline at 15, 30, and 45 minutes of reperfusion, respectively. In the flavone-treated group recovery values were significantly higher, averaging 67.8% +/- 9.6%, 77.3% +/- 8.5%, and 77.0% +/- 9.0% of baseline. End-diastolic pressures were significantly lower in the flavone-treated group compared with the control group at all reperfusion time points. Myocardial oxygen consumption was significantly higher in the flavone-treated group at 30 and 45 minutes of reperfusion, as well. The improvement resulting from flavone infusion was abolished completely by SKF 525-A, providing support for the interpretation that the effects of flavone were mediated through the cytochrome P-450 system. The cyclooxygenase inhibitor indomethacin midly attenuated the effects of flavone pretreatment, suggesting that the effects of flavone were only minimally related to metabolites of cyclooxygenase. We conclude that pretreatment with flavone represents a promising approach to myocardial protection that may be due to modulation of the myocardial cytochrome P-450 system.

Animals↗
PubMed1992

Neutrophils are not necessary for ischemia-reperfusion lung injury.

The role of neutrophils (PMNs) in ischemia-reperfusion injury after lung transplantation is unclear. If PMNs are involved in ischemia-reperfusion injury in the intact rat, then PMNs should sequester in the injured lung and PMN-depleted rats should develop less injury. Group A rats were treated with a rabbit anti-rat PMN antibody causing profound neutropenia (less than 100 PMNs/microL) and group B with control serum (greater than 2,000 PMNs/microL). Rats were anesthetized and left lung ischemia was sustained for 90 or 180 minutes by clamping the bronchus and the pulmonary artery and vein. Lung injury was quantified by the accumulation of radiolabeled (125I) albumin in ischemic left and nonischemic right lungs (cpm per gram of lung/cpm per gram of blood). Ischemia caused significant lung injury (p less than 0.05) in both PMN-depleted (albumin leak index: 90 min, 0.208; 180 min, 0.218) and nondepleted (90 min, 0.222; 180 min, 0.241) animals compared with nonischemic controls (depleted: 90 min, 0.050; 180 min, 0.100; nondepleted: 90 min, 0.063; 180 min, 0.101); microscopy also demonstrated lung injury. The injury was not associated with PMN sequestration as shown by light microscopy. Thus, we conclude that PMNs are not necessary for ischemia-reperfusion injury and PMN-depletion does not attenuate ischemia-reperfusion injury.

Albumins↗
PubMed1992

Acadesine (AICA-riboside) improves postischemic cardiac recovery.

To test if acadesine (5-aminoimidazole-4-carboxamide riboside), a purine precursor, has cardioprotective effects, 16 dogs were placed on total cardiopulmonary bypass and subjected to global myocardial ischemia. Hemodynamic recovery was compared between a control (n = 8) group receiving standard cardioplegia and an acadesine (n = 8) group pretreated with intravenous acadesine (2.5 mg.kg-1.min-1 for 5 minutes, then 0.5 mg.kg-1.min-1) before ischemia, during ischemia, and until 10 minutes after removal of the aortic cross-clamp. Additionally, in the acadesine group the cardioplegia also contained 20 mumol/L acadesine. While the dogs were on cardiopulmonary bypass, global warm myocardial ischemia was induced by aortic cross-clamping for 5 minutes under normothermic conditions to simulate an angioplasty accident. Five minutes after aortic cross-clamping, hypothermic cardioplegia (30 mL/kg) was administered. The left anterior descending coronary artery was occluded before the first infusion of cardioplegia to simulate poor cardioplegia delivery that can occur during an emergency coronary artery bypass procedure after an angioplasty accident. The left anterior descending artery occlusion was released, and additional cardioplegia (15 mL/kg) infusions were made every 30 minutes thereafter during 120 minutes of cardioplegic ischemia. Thirty minutes after reperfusion, all animals in both groups were weaned from bypass and recovery data were obtained to compare with baseline preischemic values. There were no significant differences in heart rate, left atrial pressure, or systemic vascular resistance between groups after weaning from bypass. Peak developed pressure recovered to 79% +/- 19% (mean +/- standard deviation) of baseline in the acadesine group compared with 56% +/- 22% in the control group (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Aminoimidazole Carboxamide↗
PubMed1992

Amino acid substrate preloading and postischemic myocardial recovery.

During induced myocardial ischemia for cardiac surgery, myocardial stunning occurs and aerobic metabolism of glucose, fatty acids, and lactate is inhibited as anaerobic pathways predominate. Even following reperfusion, stunned myocardium uses oxygen and substrate inefficiently leading to poor functional recovery as less mechanical work is developed per oxygen utilized. Amino acids potentially can act as cardiac metabolic substrates during and after ischemia, utilizing the transamination of amino acids by the malate-aspartate shuttle to form high energy phosphates via the tricarboxylic acid cycle. We investigated if "preloading" hearts with a physiologic spectrum of amino acids could increase postischemic myocardial recovery. Isolated perfused rabbit hearts were subjected to 120 min of 34 degrees C cardioplegic ischemia. Hearts received cardioplegia alone as controls or were "preloaded" with a 0.05% amino acid perfusion for 30 min prior to cardioplegic ischemia. Following reperfusion, analysis of functional recovery revealed that contractility and cardiac efficiency were improved with amino acids substrate preloading. The mechanism of this may be due to uptake of amino acids prior to ischemia, which are later utilized for internal reparative work during ischemia and external contractile work after ischemia.

Amino Acids↗
PubMed1992

Prolongation of cardiac allograft survival in rats by anti-TNF and cyclosporine combination therapy.

Cyclosporine is well known to have many adverse side effects. However, while decreasing the dosage of CsA can reduce its toxicity, this also lowers its immunosuppressive effectiveness. Additionally, anti-tumor necrosis factor has been demonstrated to have immunosuppressive activity and been shown to prolong cardiac allograft survival. This current study therefore investigated the efficacy of a combined therapy of anti-TNF with low-dose CsA in a rat heterotopic cardiac transplant model utilizing Brown-Norway donors and Lewis recipients. Control transplant recipients received no immunotherapy. Experimental animals received single-dose anti-TNF intraperitoneally on posttransplant days 0, 3, or 5 and/or low-dose CsA (1.5 mg/kg/day) intramuscularly from days 0 to 14 after transplantation. Rejection was determined by the lack of contractions in the transplanted heart. No animal received any other form of immunosuppression. Graft survival was significantly prolonged with combination CsA and anti-TNF therapy, suggesting a synergistic effect against acute cardiac allograft rejection, possibly from CsA and anti-TNF interacting at different levels of the recipient immune response. This form of combination therapy may hold promise for future immunosuppressive techniques.

Animals↗
PubMed1992

The effect of intramyocardial pH on functional recovery in neonatal hearts receiving St. Thomas' Hospital cardioplegic solution during global ischemia.

The experiments in the present study were designed to address two issues: Is it possible to manipulate intramyocardial pH in neonatal hearts with different buffers in cardioplegic solution and, if so, do differences in intramyocardial pH during ischemia influence functional recovery? Isolated working hearts from 7- to 10-day-old rabbits underwent 60 minutes of cardioplegic arrest at 37 degrees C with cardioplegic washouts at the onset of ischemia and at 30 minutes. Hearts were reperfused with oxygenated physiologic saline solution (pH = 7.4), returned to the working mode for 30 minutes, and hemodynamic measurements were obtained to compare with baseline values. Intramyocardial pH was held constant during the ischemic interval by infusing cardioplegic solution containing different buffers: histidine (pK 6.0 at 37 degrees C), bicarbonate (pK 6.4), or tromethamine (pK 8.1). The intramyocardial pH was measured continuously with a Khuri glass electrode system (Vascular Technology, Inc., North Chelmsford, Mass.). Cardioplegic solutions buffered to pH values of 6.0 (histidine), 7.4 (bicarbonate), and 8.0 (tromethamine) were associated with ischemic intramyocardial pH values of 6.3 +/- 0.03, 7.02 +/- 0.05, and 7.88 +/- 0.06, respectively. Functional recovery was best in the acidic (histidine) and worst in the basic (tromethamine) groups. Recoveries of developed pressure, the rate of rise of pressure over time, and aortic flow were significantly better for each parameter in the bicarbonate-treated compared with the tromethamine-treated hearts (p less than 0.005). Recovery in the histidine group, however, was superior to that in both the bicarbonate-treated and the tromethamine-treated hearts (p less than 0.005). Regression analysis demonstrated that a significant inverse relationship existed between functional recovery and intramyocardial pH, supporting the conclusions that intramyocardial pH is an important determinant of functional recovery in the neonatal heart and that acidic conditions during normothermic ischemia optimize preservation of myocardial function.

Animals↗
PubMed1992

Enhanced myocardial protection during global ischemia with 5'-nucleotidase inhibitors.

Depletion of adenosine triphosphate precursors, such as myocardial adenosine, during global ischemia results in poor postischemic adenosine triphosphate repletion and functional recovery. Neonatal hearts may be more resistant to this deleterious effect of ischemia, because they are characterized by low 5'-nucleotidase activity, which may result in higher sustained endogenous myocardial adenosine triphosphate precursor levels during ischemia. Adult hearts, however, have high levels of 5'-nucleotidase activity leading to depleted precursors during ischemia and poor postischemic functional recovery. Augmenting myocardial adenosine exogenously during ischemia in adult hearts has a beneficial effect on recovery. The present study tested if preservation of nucleotide precursors, better adenosine triphosphate repletion, and enhanced postischemic myocardial recovery in adult hearts could be achieved with a "neonatal" strategy. Therefore 5'-nucleotidase inhibitors were administered to isolated, perfused adult rabbit hearts subjected to 120 minutes of ischemia (at 34 degrees C) to determine if this improved functional recovery. Hearts received St. Thomas' Hospital cardioplegic solution (control hearts) or cardioplegic solution containing 5'-nucleotidase inhibitors: pentoxifylline, thioinosine, [s-(p-nitrophenyl)-4-thioinosine], or thioinosine's dimethyl sulfoxide vehicle alone. After ischemia and reperfusion, recovery of systolic function, diastolic function, and myocardial oxygen consumption was significantly better with 5'-nucleotidase inhibition. No changes in coronary flow were noted. We speculate and are pursuing the theory that the mechanism of 5'-nucleotidase inhibition's favorable action is due to preventing the catabolism, transport, and loss of nucleotide precursors during ischemia, maintaining adenosine triphosphate precursor availability.

5'-Nucleotidase↗
PubMed1991

Reduction in medical care cost associated with radiofrequency catheter ablation of accessory pathways.

The cost of definitive therapy was compared in 25 patients who underwent radiofrequency catheter ablation of accessory pathways in 1990 and 25 patients who underwent surgical ablation of accessory pathways in 1989. In the radiofrequency group, 23 of 25 patients had a single accessory pathway and the remaining 2 patients each had 2 accessory pathways. In the surgical group, 20 patients had a single accessory pathway and 5 patients each had 2 accessory pathways. The success rate was 96% in each group. The mean duration of hospitalization was 3 +/- 1 days in the radiofrequency group and 9 +/- 4 days in the surgical group (p less than 0.0001). All the cost data are expressed in fiscal year 1990/1991 dollar values. The total cost of therapy in the radiofrequency group was $14,919 +/- $6,740 compared with $53,265 +/- $12,755 in the surgical group (p less than 0.0001). The cost of radiofrequency ablation consisted of a hospital charge of $7,753 +/- $3,472 and physician fees of $7,166 +/- $3,439. The hospital charge included charges for use of the electrophysiology laboratory, hospital stay, electrocardiograms, echocardiograms and blood studies. The cost of surgery consisted of a hospital charge of $37,708 +/- $10,179 and physician fees of $15,557 +/- $3,149. The hospital charge in the surgical group included the costs of a baseline electrophysiology study, in-hospital care and a follow-up office visit. In conclusion, radiofrequency catheter ablation of accessory pathways results in a dramatic reduction in the cost of definitive therapy in patients with the Wolff-Parkinson-White syndrome.

Adolescent↗
PubMed1991

Incidence of loss of consciousness during automatic implantable cardioverter-defibrillator shocks.

OBJECTIVE: To determine the incidence of loss of consciousness occurring in association with shocks delivered by automatic implantable cardioverter-defibrillators (AICD) in patients who had undergone implantation as treatment for ventricular tachycardia or ventricular fibrillation. DESIGN: Cohort study. SETTING: Two major tertiary medical care facilities. PATIENTS: A total of 180 patients who had undergone implantation of an AICD for treatment of ventricular tachycardia or ventricular fibrillation. INTERVENTION: Implantation of an AICD that delivered only high-energy shock. MEASUREMENTS: During a mean (+/- SD) follow-up period of 16 +/- 12 months, the incidence of loss of consciousness occurring in association with spontaneous AICD shocks was determined. Various clinical factors were analyzed to identify predictors of loss of consciousness that occurred during AICD shocks. MAIN RESULTS: Of the 180 patients who received an AICD, 106 patients (59%) experienced AICD shocks during follow-up. Sixteen of the 180 patients (9%) experienced loss of consciousness; 13 of these 16 patients had syncope and 3 died suddenly, in association with AICD shocks. The absence of syncope during one AICD shock did not always predict the absence of syncope during subsequent shocks. Syncope could not be predicted by age, sex, history of syncope, left ventricular function, type of underlying heart disease, electrophysiologic findings, rate of ventricular tachycardia, antiarrhythmic medications, and type of pulse generator implanted. CONCLUSIONS: Patients with sustained ventricular tachycardia or ventricular fibrillation who receive an AICD that delivers only high-energy shock therapy are at moderate risk for experiencing loss of consciousness during AICD shocks. No clinical variables were found to be predictors of syncope. Therefore, driving and other activities that require patients to be extra vigilant should not be assumed to be safe after implantation of an AICD that delivers only high-energy shock.

Adult↗
PubMed1991

Hemodynamics versus biopsy findings during cardiac transplant rejection.

Before the use of cyclosporine as the major component for immunosuppression after cardiac transplantation, rejection was accompanied by catastrophic hemodynamic decompensation. However, the hemodynamic changes that occur during rejection after cardiac transplantation in patients treated with cyclosporine have not been clearly described. Between July 1986 and October 1989, 89 adults underwent orthotopic heart transplantation at the University of Michigan Medical Center. All patients received triple-drug therapy immunosuppression consisting of steroids, cyclosporine, and azathioprine. Cardiac hemodynamics were measured and correlated with the histologic assessment of rejection. There have been ten deaths among these 89 patients for an overall survival of 89%. There were no deaths from rejection. One hundred fifty-three of the biopsy specimens were read as grade 0, 31 were grade 1, 75 were grade 2, 103 were grade 3, and 9 patients had grade 4 biopsy specimens. No hemodynamic differences were noted in patients with increasing grade of rejection. Five patients (5/9, 55%) with severe rejection (grade 4) had symptoms of congestive heart failure at the time of biopsy. These symptomatic grade 4 patients differed from asymptomatic grade 4 patients only in cardiac output (2.9 versus 5.2 L/min). Overall hemodynamic decompensation was not evident as rejection grade increased. Routine serial endomyocardial biopsies remain the procedure of choice in the diagnosis of rejection in the asymptomatic patient after cardiac transplantation as hemodynamics do not predict degree of rejection.

Adult↗
PubMed1991

Current treatment for Wolff-Parkinson-White syndrome: results and surgical implications.

From July 1986 to January 1991, 123 patients with Wolff-Parkinson-White syndrome underwent operation for ablation of aberrant conduction pathways. There were 85 male and 38 female patients ranging in age from 11 months to 68 years. Associated anomalies included Ebstein's anomaly, sudden death syndrome, coronary artery disease, cardiomyopathy, abdominal aortic aneurysm, neurofibromatosis, other arrhythmias, or other complex congenital heart disease. Forty-one patients had multiple accessory pathways. Operative results showed a 7% initial failure rate, which dropped to 3% after reoperation. One patient had undergone previous operation for Wolff-Parkinson-White syndrome at another institution. Procedures performed concomitantly included mitral or tricuspid valve repair or replacement (6), right ventricular conduit replacement, subaortic resection, Fontan repair, corrected transposition repair, coronary artery bypass, and placement of an automatic internal cardioverter defibrillator. There was no operative mortality. Late follow-up is 27 +/- 16 months, and complications included mitral regurgitation and myocardial infarction. By comparison, in the last 12 months 124 patients with the Wolff-Parkinson-White syndrome underwent catheter ablation using radiofrequency current. There were 9 patients with multiple pathways. One hundred twelve patients (90%) had all accessory atrioventricular connections ablated and have remained free of symptomatic tachycardia. There have been 12 failures (10%), of which 5 have had operation and 7 are being treated medically. Mean follow-up is 7 +/- 5 months, and complications included circumflex coronary artery occlusion, excessive bleeding, valve perforation, and cerebral vascular accident.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

ATP precursor depletion and postischemic myocardial recovery.

Although cardioplegia reduces myocardial metabolism during ischemia, adenosine triphosphate (ATP) depletion occurs, which may contribute to poor functional recovery after reperfusion. Augmenting myocardial adenosine during ischemia is successful in improving ATP repletion and myocardial recovery following ischemia. If adenosine is an important determinant of ischemic tolerance, then depletion or elimination of myocardial adenosine should lead to poor functional and metabolic recovery after ischemia. To test this hypothesis, isolated, perfused rabbit hearts were subjected to 120 min of 34 degrees C ischemia. Hearts received St. Thomas cardioplegia alone or cardioplegia containing 200 microM adenosine, or cardioplegia containing 15, 5, 2.5, or 0.025 micrograms/ml adenosine deaminase (ADA), which catalyzes the breakdown of adenosine to inosine, making adenosine unavailable as an ATP precursor. Functional recovery was determined and myocardial nucleotide levels were measured before, during, and after ischemia. Following ischemia and reperfusion, control hearts recovered to 51 +/- 3% of preischemic developed pressure (DP). There was significantly better recovery in adenosine-augmented hearts (68 +/- 7%), while ADA hearts had significantly worse recovery. Hearts treated with 0.025 microgram/ml ADA recovered to only 29 +/- 5% of DP and higher dose ADA hearts failed to demonstrate any recovery of systolic function. Furthermore, adenosine enhanced metabolic recovery, whereas ADA resulted in greatly depleted ATP and precursor reserves. Postischemic developed pressure closely paralleled the availability of myocardial adenosine, consistent with the hypothesis that myocardial adenosine levels at end ischemia and early reperfusion are important determinants of functional recovery after global ischemia.

Adenosine↗
PubMed1991

A randomized prospective comparison of MALG with OKT3 for rescue therapy of acute myocardial rejection.

A randomized prospective trial for rescue therapy from acute myocardial rejection was undertaken utilizing Minnesota antilymphoblastic globulin (n = 15) versus murine monoclonal anti-CD3 antibody therapy (OKT3) (n = 14). Patients included in the study had moderate rejection unresponsive to bolus high-dose steroid therapy, or moderate-to-severe rejection with hemodynamic instability. Analysis was performed using the t test and chi-square, significance was P less than 0.05. Patient age, sex, interval from transplant to treatment, and number of unresponsive patients vs. hemodynamically unstable patients were similar in both groups (P greater than 0.05). Initial resolution occurred in 9/15 MALG- vs. 14/14 OKT3-treated patients (P = 0.017). Secondary resolution following repeat treatment occurred in 5/6 remaining MALG patients, for a final resolution of 14/15 MALG vs. 14/14 OKT3 patients (P = NS). Rebound rejection was not significantly different (1/14 MALG vs. 4/13 OKT3). However, 7/14 OKT3-treated patients developed life-threatening infections (1 CMV pancreatitis, 2 CMV pneumonias, 1 systemic candidiasis, 3 CMV viremia) vs. 1/15 MALG-treated patients (CMV viremia) (P = 0.014). Death occurred in 4/14 OKT3- (infection) vs. 1/14 MALG- (rejection) treated patients (P = NS). There were no significant differences in the rate of resolution, rebound, infection, or outcome between unresponsive or hemodynamically unstable patients within either group. Although initial rescue is significantly better with OKT3, final resolution is the same in both groups. Since there was a significant incidence of life-threatening infections (7/14) leading to 4 deaths with OKT3 treatment, we recommend MALG for rescue therapy of refractory acute myocardial rejection if this immunosuppressive regimen is to be used.

Adult↗
PubMed1991

Effect of antiarrhythmic drug therapy on the incidence of shocks in patients who receive an implantable cardioverter defibrillator after a single episode of sustained ventricular tachycardia/fibrillation.

Seventy-four patients (16 women, 58 men, age 58 +/- 11 years, mean +/- standard deviation) who received an implantable cardioverter defibrillator (ICD) after experiencing a single episode of ventricular tachycardia or ventricular fibrillation were followed to determine if antiarrhythmic drug therapy affects the incidence of ICD discharges. Thirty-three patients (group A) were treated with an antiarrhythmic drug that was either untested or previously demonstrated during electropharmacological testing to be ineffective in suppressing the induction of ventricular tachycardia. Forty-one patients (group B) were not treated with an antiarrhythmic drug. There were no significant differences between the two groups in regards to age, sex, incidence of coronary artery disease, left ventricular function or the type of ICD pulse generator used. During a mean follow-up of 14 months for the entire cohort, 15 patients (46%) in group A and 18 patients (44%) in group B experienced at least one ICD shock. The time to the first appropriate shock (5 +/- 5 months in both groups) and the frequency of ICD shocks (0.3 +/- 0.2/month in group A vs 0.4 +/- 0.5/month in group B) were similar in both groups. The incidence of syncope at the time of ICD discharge was higher in group A than group B patients (31% vs 5%, P less than 0.05). In conclusion, antiarrhythmic drugs that are untested or have failed electropharmacological testing do not appear to reduce the probability of ICD discharge over a short-term (mean 14 months) follow-up in patients who have had only one clinical episode of VT/VF and may increase the risk of syncope during ICD discharge.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗
PubMed1991

Inhibition of cyclooxygenase metabolite production attenuates ischemia-reperfusion lung injury.

We investigated if cyclooxygenase metabolites of arachidonic acid were involved in ischemia-reperfusion lung injury by determining if inhibition of their production attenuated the injury. Isolated rat lungs were perfused with physiologic salt solution osmotically stabilized with Ficoll until circulating blood elements were not detected in lung effluent. Ischemia was induced by stopping ventilation and perfusion for 90 min. Lung ventilation and perfusion were then resumed. Ischemia-reperfusion resulted in the production of prostacyclin and thromboxane assessed by lung effluent and tissue measurements of their respective stable metabolites, 6-keto-PGF1 alpha thromboxane B2 (TxB2). In contrast, prostaglandin F2 alpha did not increase. Ischemia-reperfusion also caused lung injury as assessed by increased lung 125I-BSA accumulation compared with nonischemic control lungs. Addition of the cyclooxygenase inhibitors, indomethacin, or flubiprofen to the lung perfusate before and after ischemia inhibited lung injury as well as the production of 6-keto-PGF1 alpha and TxB2. Addition of a thromboxane synthetase inhibitor (U 63557A) reduced lung injury as well as TxB2 formation without affecting the production of 6-keto-PGF1 alpha. The attenuation of lung injury was not explained by direct H2O2 removal by indomethacin, flubiprofen, or U 63557A because the concentrations of the inhibitors used in the isolated lung experiments did not remove exogenously added H2O2 from buffer in vitro. We conclude that cyclooxygenase metabolites of arachidonic acid are involved in ischemia-reperfusion injury to isolated rat lungs.

6-Ketoprostaglandin F1 alpha↗
PubMed1991

Management of recurrent ventricular pseudoaneurysm.

A 49-year-old man suffered multiple recurrences of pseudoaneurysm following ventricular aneurysmectomy in which Teflon felt strips had been used to reinforce the closure. The pseudoaneurysm was secondary to infection of the cardiac suture line, caused by a pathogen resident in the multifilamented Teflon strips. The patient was treated successfully by removal of all residual foreign material and reinforcement of the suture line with an omental pedicle graft.

Journal Article↗