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Biomedical subjects

S F Bolling

Publications and source records attributed to S F Bolling.

At least 127 records · Page 7Linked to original sources
PubMed1991

Recovery of the neonatal heart after normothermic ischemia. Effect of oxygen and catalase.

The objective of this study was to determine the effect of oxygen and the oxygen radical-scavenging enzyme catalase on the neonatal rabbit heart exposed to global ischemia. The experiments were performed with an isolated neonatal (7 to 10 days of age) working heart model in which normothermic (37 degrees C) ischemia was produced for 60 minutes. Left ventricular developed pressure, ratio of change of ventricular pressure to change in time, and aortic flow were measured before ischemia and 30 minutes after reperfusing the hearts with physiologic saline solution. In the control group (ischemia only), developed pressure and ratio of change of ventricular pressure to change in time recovered to 27% +/- 3% (mean +/- standard error of the mean) and 24% +/- 7% of baseline; the hearts were incapable of ejecting (aortic flow = 0). Treatment of hearts before and after ischemia with catalase (150 units/ml of perfusate) was studied in a second group (control plus catalase), but functional recovery (developed pressure = 32% +/- 1%; ratio of change of ventricular pressure to change in time = 24% +/- 2%, and aortic flow = 0) was not significantly different from the control group. The effect of washout midway through the ischemic period with a low oxygen (oxygen concentration less than 35 mm Hg) solution was measured in a third group (hypoxic physiologic saline solution). Functional recovery (developed pressure = 13% +/- 3%; ratio of change of ventricular su pressure to change in time = 13% + 2%; aortic flow = 0) was not significantly different from the control and control plus catalase groups. In marked contrast were the effects of washout with an oxygenated (oxygen concentration greater than 500 mm Hg) solution (oxygenated physiologic saline solution) in which functional recovery (developed pressure = 78% +/- 3%; ratio of change of ventricular pressure to change in time = 80% +/- 3%; aortic flow = 39% +/- 9%) was significantly better than in the control, control plus catalase, and hypoxic physiologic saline solution groups. Use of modified St. Thomas' Hospital cardioplegic solution (cardioplegic solution group) during the ischemic period also resulted in substantial functional recovery (developed pressure = 80% +/- 3%; ratio of change of ventricular pressure to change in time = 78% +/- 5%; aortic flow = 64% +/- 7%) that did not differ significantly from that in the oxygenated physiologic saline solution group.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1990

The introduction of closed chest cardiac massage.

The introduction of closed chest cardiac massage by Dr William Kouwenhoven and associates has markedly changed the outcome of patients with cardiac arrest. The fortuitous discovery of the simple yet ingenious concept of closed cardiac massage has saved countless lives. In fact the manuscript published by Kouwenhoven and colleagues has been touted "to have resulted in saving more lives than any other medical manuscript during the past century." Although newer techniques and methods of cardiac resuscitation have been developed, their successes will be measured against the technique described by Kouwenhoven and colleagues.

Heart Massage↗
PubMed1990

The concentration of calcium in neonatal cardioplegia.

The optimal calcium concentration in cardioplegia for the newborn has not been determined. Therefore, the effect of 0, 0.6, 1.2, 1.8, and 2.4 mmol/L calcium in modified St. Thomas cardioplegia was evaluated in isolated working hearts of 7- to 10-day-old rabbits. Functional recovery was determined by comparing aortic flow, developed pressure, and first derivative of left ventricular pressure (dP/dt) before and after 1 hour of normothermic (37 degrees C) ischemia. As percentages of baseline values, recovery of developed pressure and dP/dt averaged 10% +/- 1% (mean +/- standard error of the mean) and 10% +/- 1% with 0 mmol/L, 46% +/- 7% and 44% +/- 8% with 0.6 mmol/L, 79% +/- 2% and 76% +/- 2% with 1.2 mmol/L, 67% +/- 2% and 61% +/- 5% with 1.8 mmol/L, and 65% +/- 5% and 65% +/- 7% with 2.4 mmol/L calcium, respectively. Significant improvement in recovery of developed pressure and dP/dt was detected when the calcium concentration was increased from 0 to 0.6 mmol/L and from 0.6 to 1.2 mmol/L, but the groups with 1.2, 1.8, and 2.4 mmol/L did not differ from one another significantly in terms of developed pressure and dP/dt recovery. There was no recovery of aortic flow when 0 mmol/L calcium was used; at calcium concentrations of 0.6, 1.2, 1.8, and 2.4 mmol/L, recovery of aortic flow averaged 16% +/- 7%, 63% +/- 10%, 23% +/- 10%, and 36% +/- 11% of baseline values, respectively. Recovery of aortic flow with 1.2 mmol/L calcium was significantly higher than at concentrations of 0.6 and 1.8 mmol/L.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Shone's anomaly: operative results and late outcome.

Shone's anomaly, a congenital cardiac malformation, consists of multiple levels of left heart obstruction including supravalvar mitral ring, parachute mitral valve, subaortic stenosis, and coarctation. The prognosis for patients with Shone's anomaly is poor. To assess operative results and late outcome, we reviewed the records of 30 consecutive patients seen with Shone's anomaly at our institution between 1966 and 1989. Anatomical diagnoses in these patients were supravalvar mitral ring (22 patients), mitral valve abnormalities including parachute mitral valve, fused chordae, or single papillary muscle (26 patients), subaortic gradients (26 patients), and coarctation (29 patients). Nineteen patients had all four lesions. Other common defects were bicuspid aortic valve (19 patients) and ventricular septal defect (20). Two patients were treated medically. The other 28 patients required 84 operative procedures with 18 patients undergoing more than one procedure. Operations included coarctation repair (28 patients), mitral valve repair or replacement (11), ventricular septal defect closure (8), subaortic resection (8), and complex left ventricular outflow tract reconstruction or bypass (4). Age at first operation ranged from 7 days to 7 years (median age, 3 months). There were no operative deaths at the first operation. However, mortality rose to 24% (4/17) after the second operation. All operative deaths were secondary to severe mitral valve disease. The survivors have been followed from 1 to 16 years (mean follow-up, 6 +/- 1 years). There were no late or sudden deaths. Morbidity has included stroke (1), gastrointestinal bleeding (2), permanent heart block (1), and persistent congestive heart failure (6).(ABSTRACT TRUNCATED AT 250 WORDS)

Aortic Coarctation↗
PubMed1990

Effect of ATP synthesis promoters on postischemic myocardial recovery.

The use of cardioplegia during surgically induced ischemia greatly reduces myocardial metabolic requirements. However, adenosine triphosphate (ATP) depletion may occur, resulting in poor functional recovery after ischemia. This study investigated if augmentation of intracellular ATP could be achieved by delivering known ATP synthesis promoters (adenosine and/or phosphate) during cardioplegic arrest, and whether this could enhance myocardial functional and metabolic recovery following ischemia. Isolated, perfused rabbit hearts were subjected to 120 min of hypothermic (34 degrees C) cardioplegia-induced ischemia. Controls received St. Thomas cardioplegia (CTL); remaining hearts received cardioplegia containing 200 microM adenosine (ADO), or 25 microM phosphate (PO4), or both ADO and PO4. Following ischemia and reperfusion, recovery of developed pressure (%DP) and postischemic diastolic stiffness was significantly better in adenosine hearts when compared with control or PO4 hearts. To determine if ADO or PO4 minimized depletion of ATP during ischemia or accelerated synthesis of ATP in the postischemic period, nucleotide levels were obtained before, during, and after ischemia. During ischemia, ATP fell equally in all groups, indicating that ADO and PO4 did not alter ischemia-induced depletion of ATP. However, intracellular adenosine was augmented during ischemia in adenosine-treated hearts. Consequently, during reperfusion, ADO and ADO/PO4 hearts had significantly enhanced ATP levels, suggesting that augmenting myocardial adenosine accelerated synthesis of ATP postischemia. The addition of phosphate, a stimulus for ATP synthesis, did not augment postischemic ATP. In fact, the beneficial effect of adenosine may have been decreased when phosphate was added to adenosine. In conclusion, adenosine but not PO4 augments intracellular ATP by allowing better metabolic repletion following ischemia, thereby improving postischemic myocardial functional recovery.

Adenosine↗
PubMed1990

Impaired myocardial function and oxygen utilization due to protamine sulfate in an isolated rabbit heart preparation.

The myocardial effects of protamine, with and without heparin, were documented in this investigation. Isolated rabbit hearts (n = 30) were retrograde perfused with Krebs-Ringers bicarbonate solution aerated with 95% O2/5% CO2 through the aortic root (37 C, 80 mmHg). Developed left ventricular blood pressure, heart rate, coronary artery flow, contractility as reflected by peak +dp/dt, oxygen extraction (a-vO2), and oxygen consumption (VO2) were measured at baseline and continuously throughout the experiment. Protamine (25 micrograms, 50 micrograms, and 250 micrograms per mL of perfusate) was circulated in the Krebs-Ringers buffer to hearts perfused without heparin (groups I, II, and III) or hearts perfused with heparin added to the buffer solution, 0.1 IU/1.0 microgram protamine (groups IV, V, and VI). Blood pressure 4 minutes after protamine was less in groups III (-23 mmHg) and VI (-28 mmHg) than in groups I (-6 mmHg), II (-18 mmHg), IV (-1 mmHg), and V (-7 mmHg). Heart rate changes (beats/minute) at 4 minutes revealed similar dose-dependent reductions (III and VI: -51, -55; II and V: -36, -36; and I and IV: -20, -16, respectively). Coronary artery flow at 4 minutes was slightly increased in groups III (9 mL/minute) and VI (15 mL/minute), but was relatively unchanged in the other groups. Decreases in contractility were apparent in all groups 4 minutes after protamine was started: group I, -14%; II, -16%; III, -30%; IV, -7%; V, -15%; and VI, -34%. Similarly declines in oxygen extraction and consumption were noted in all groups at the same time period and were greater in groups III (-53%, -44%) and VI (-55%, -49%) than in groups I (-25%, -26%), II (-15%, -12%), IV (-48%, -49%) and V (-15%, -18%), with p less than or equal to 0.05 or p less than or equal to 0.01 compared to baseline. Three of ten hearts exposed to high-dose protamine stopped beating after 5 minutes. This investigation establishes, for the first time, that protamine has dose- and time-specific adverse effects on cardiac contractility. In addition protamine decreases myocardial a-vO2 and VO2. These changes may contribute to certain adverse events accompanying the clinical administration of protamine.

Animals↗
PubMed1990

Neutrophils are not necessary for induction of ischemia-reperfusion lung injury.

Ischemia-reperfusion lung injury limits lung transplantation. Neutrophil activation and/or xanthine oxidase-mediated purine degradation may cause toxic oxygen metabolite production and lung injury. We investigated whether circulating blood elements are involved in the pathogenesis of ischemia-reperfusion lung injury. Isolated rat lungs were perfused with physiological salt solution (PSS) stabilized with Ficoll until circulating blood elements were not detected in the lung effluent. Lungs were then rendered ischemic by stopping ventilation and perfusion for 45 min at room temperature. Lung injury occurred and was quantitated by the accumulation of 125I-bovine serum albumin into lung parenchyma and alveolar lavage fluid during reperfusion. Lung injury occurred, in the absence of circulating blood elements, when ischemic lungs were reperfused with PSS-Ficoll solution alone. Reperfusion with whole blood or PSS-Ficoll supplemented with human or rat neutrophils did not increase lung injury. Furthermore, during lung ischemia, the presence of neutrophils did not enhance injury. Experiments using PSS-albumin perfusate and quantitating lung injury by permeability-surface area product yielded similar results. Microvascular pressures were not different and could not account for the results. Toxic O2 metabolites were involved in the injury because addition of erythrocytes or catalase to the perfusate attenuated the injury. Thus reperfusion after lung ischemia causes injury that is dependent on a nonneutrophil source of toxic O2 metabolites.

Animals↗
PubMed1990

Augmenting intracellular adenosine improves myocardial recovery.

The objective of this study was to determine if augmentation of myocardial adenosine levels during global ischemia improves functional recovery after reperfusion. Isolated adult rabbit hearts were subjected to 120 minutes of mildly hypothermic ischemia (34 degrees C) with modified St. Thomas' Hospital cardioplegic solution used to provide myocardial protection. Myocardial adenosine levels were augmented during ischemia by providing exogenous adenosine in the cardioplegic solution or by inhibiting adenosine degradation with 2-deoxycoformycin, a noncompetitive inhibitor of adenosine deaminase. Four groups of hearts were studied: (1) control (n = 23)--cardioplegia alone; (2) adenosine group (n = 10)--adenosine 200 mumol/L added to the cardioplegic solution; (3) 2-deoxycoformycin group (n = 8)--2-deoxycoformycin 1 mumol/L added to the cardioplegic solution; and (4) a combined adenosine/deoxycoformycin group (n = 10). Recovery of developed pressure 45 minutes after reperfusion in the control group averaged only 38% +/- 4% of baseline values. Significantly better recovery was evident in the adenosine (66% +/- 7%), deoxycoformycin (59% +/- 2%), and adenosine/deoxycoformycin (75% +/- 2%) groups. The slope of the relationship between end-diastolic pressure and volume was used as an index of diastolic stiffness. The slope averaged 85 +/- 2 mm Hg/ml in the control group 45 minutes after reperfusion, significantly higher than that in the adenosine (31 +/- 6), deoxycoformycin (75 +/- 5), and adenosine/deoxycoformycin (58 +/- 5) groups; this suggests better diastolic function in the adenosine-augmented groups. During ischemia, adenosine levels were significantly elevated in the adenosine-augmented groups, whereas adenosine triphosphate decreased equally in all four groups, which indicates that augmenting myocardial adenosine had no effect on depletion of adenosine triphosphate during ischemia. After reperfusion, adenosine triphosphate levels were depressed in the control group but increased in the other groups above baseline values, which suggests that improvement in functional recovery was due to accelerated repletion of adenine nucleotide stores in the adenosine-augmented groups.

Adenosine↗
PubMed1989

Enhanced myocardial protection with adenosine.

This study was undertaken to investigate whether adenosine administered during cardioplegic arrest could enhance myocardial protection and improve recovery of function after ischemia. Isolated perfused rabbit hearts were subjected to 120 minutes of hypothermic (32 degrees C) multidose cardioplegia-induced ischemia. Control hearts (n = 23) received modified St. Thomas's cardioplegia, and the remaining hearts received cardioplegia with either 100 microM (n = 11), 200 microM (n = 11), or 400 microM (n = 11) adenosine. After ischemia and 45 minutes of reperfusion, left ventricular contractility was superior in all groups of adenosine-treated hearts compared with control hearts. Furthermore, there was a significant incremental increase in functional recovery with increasing dose of adenosine. Postischemic diastolic stiffness was significantly better in all adenosine groups compared with controls. No differences were noted in coronary flow or myocardial water content between adenosinetreated and control hearts. These data demonstrate that adenosine administered in these concentrations provides myocardial protection and improved recovery of both systolic and diastolic function after global ischemia, presumably metabolically by reducing depletion of adenosine triphosphate or enhancing repletion of adenosine triphosphate and enabling improved postischemic recovery.

Adenosine↗
PubMed1989

Amrinone versus conventional therapy in pulmonary hypertensive patients awaiting cardiac transplantation.

Pulmonary hypertension is associated with an increased perioperative mortality for orthotopic heart transplantation. A transpulmonary gradient greater than 15 mm Hg or a pulmonary vascular resistance greater than 5 Woods units increases mortality secondary to right heart failure. This study compares amrinone with conventional therapy in 38 transplant candidates with pulmonary hypertension. All patients had elevated transpulmonary gradient, pulmonary vascular resistance, or both. Group 1 (n = 21) received prolonged continuous intravenous amrinone therapy, whereas group 2 (n = 16) received high-dose oral diuretics, digitalis, and captopril. Both groups 1 and 2 had decreased pulmonary hypertension, transpulmonary gradient, and pulmonary vascular resistance. However, amrinone was more effective, with a 86% response rate versus 63% response for conventional therapy. Survival awaiting transplantation was significantly higher in group 1 (20 of 22, 91%) than in group 2 (10 of 16, 63%). Although both groups 1 and 2 had significantly decreased pulmonary vascular resistance, only group 2 had significantly decreased systemic vascular resistance. Comparison of pulmonary vascular resistance after therapy showed that the response in group 1 (amrinone) was significantly lower than the response in group 2 (conventional therapy), suggesting that amrinone may function as a direct vasodilator of the pulmonary vasculature. There were no operative deaths or episodes of perioperative right heart failure in either group. Amrinone appears to be more effective and safe than conventional therapy in the treatment of prospective heart transplant candidates with pulmonary hypertension.

Adult↗
PubMed1989

Comparison of polyclonal antibody sera for early prophylaxis following cardiac transplantation.

In order to test different polyclonal antibody regimes as early prophylaxis against cardiac rejection, 42 patients (ages 30 to 60 years) transplanted at the University of Michigan from December 1986 to August 1988 were randomized to receive antithymocyte globulin (ATGAM, Upjohn, n = 19) or antilymphoblast globulin (MALG, University of Minnesota, n = 23). Cyclosporine (CYA), steroids, and azathioprine (AZA) administration was similar in all randomized patients during early prophylaxis. CYA was begun preoperatively and maintained at a serum level of 250-300 ng/ml. After an initial steroid taper, patients were maintained on 0.3 mg/kg/day. AZA was begun after polyclonal prophylaxis at 1-2 mg/kg. All patients received either ATGAM or MALG for 7 days or until the serum CYA reached 250 ng/ml. Although sex, pretransplant hemodynamics, follow-up length, total drug dose, mortality (one per group), postoperative white blood cell and lymphocyte counts did not differ between groups, MALG significantly delayed the first rejection episode as compared to ATGAM (35 +/- 4 vs 22 +/- 3 days, P less than 0.05). Additionally, there was decreased rejection during follow-up for the MALG group with 1.5 +/- 0.2 rejections per patient as compared to 2.3 +/- 0.3 with ATGAM. Furthermore, the significant infection rate with MALG was only half that of the ATGAM group (6/23 vs 11/19) (P less than 0.05). The beneficial effect of MALG may be due to immune-specific differences in its polyclonal spectrum.

Adult↗
PubMed1989

The role of amrinone in potential heart transplant patients with pulmonary hypertension.

Orthotopic heart transplantation is contraindicated in patients with pulmonary hypertension and an elevated pulmonary vascular resistance. In an attempt to make otherwise unacceptable patients possible candidates for heart transplantation, amrinone was administered intravenously to 27 individuals with a transpulmonary gradient and pulmonary vascular resistance in the abnormal range. Twenty-four of 27 patients (89%) responded positively. Twenty-one of 27 (78%) went on to transplantation and 20 of 21 (95%) survived the procedure. A second study compared amrinone therapy with conventional therapy in 38 potential transplant candidates with pulmonary hypertension. Amrinone was more effective in reducing pulmonary hypertension than conventional therapy with high-dose diuretics, digitalis, and captopril (86% v 63%). Survival rate of those awaiting transplantation was also significantly higher in the amrinone group (91% v 63%). Although the protocol for comparing the two regimens does not allow for extrapolation of the results (amrinone was administered in-hospital under close monitoring, whereas conventional therapy was self-administered at home), the findings confirm the clinical impression that amrinone seems more effective and safer than conventional therapy in the treatment of potential heart transplant patients with pulmonary hypertension.

Amrinone↗
PubMed1989

Distribution of cardioplegic solution infused antegradely and retrogradely in normal canine hearts.

The adequacy of retrograde delivery of cardioplegic solution to the right ventricle and interventricular septum is controversial. To address this issue quantitatively, we infused blood cardioplegic solution labeled with radioactive microspheres (15 microns diameter) into the coronary sinus (n = 8 dogs) at a pressure of 51 +/- 1 mm Hg (mean +/- standard error of the mean) to be compared with the same quantity of labeled cardioplegic solution (20 ml/kg) delivered through the aorta (n = 6 dogs) at 97 +/- 7 mm Hg. Both methods of delivery produced cardiac arrest, but retrograde infusion required a significantly longer time to complete the infusion (6.2 +/- 0.8 minutes versus 1.5 +/- 0.1 minutes, p less than 0.01). Greater than 99% of the microspheres passing through the vasculature of the left ventricle were trapped in the left ventricular myocardium with antegrade infusion, and the distribution of the cardioplegic solution was uniform. Antegrade delivery (cardioplegic flow x infusion time) averaged approximately 3.0 to 4.0 ml/gm, except at the apex, where delivery averaged approximately 2.0 ml/gm. With retrograde infusion, 93% of the microspheres perfusing the left ventricle were trapped and delivery of the cardioplegic solution was not uniform. In the anterolateral free wall, delivery of cardioplegic solution averaged between 1.5 and 2.9 ml/gm (p less than 0.001 compared with antegrade) and only 0.6 to 0.8 ml/gm in the posteroseptal region of the basal left ventricle (p less than 0.001 compared with the antegrade group and anterolateral samples of the retrograde group). In the middle portion of the right ventricle, antegrade trapping of microspheres was 99% and delivery of cardioplegic solution averaged approximately 2.0 ml/gm. With retrograde delivery, only 16.5% (range 11.8% to 26.0%) of the microspheres passing through the right ventricular vasculature were trapped in the right ventricular myocardium, which indicates that substantial shunting had occurred. Corrected for the high shunt fraction, retrograde delivery of cardioplegic solution to the middle portion of the right ventricle averaged only 0.5 ml/gm (p less than 0.01). Retrograde delivery to the atrial septum and right atrium was also low. Because retrograde delivery of cardioplegic solution was markedly nonuniform, we conclude that inadequate cardioplegic delivery to the middle portion of the right ventricle and posteroseptal portion of the left ventricle could result with cardioplegic infusion through the coronary sinus.

Animals↗
PubMed1989

Hypothermia or continuous ventilation decreases ischemia-reperfusion injury in an ex vivo rat lung model.

The susceptibility of lung tissue to ischemia-reperfusion injury has made distant procurement of heart-lung allografts difficult. The effects of hypothermia, ventilation without perfusion, and various reperfusion solutions (PSS/Ficoll or whole blood) on the development of ischemia-reperfusion lung injury were investigated. Use of an ex vivo rat lung model in which the above variables were individually varied permitted a direct approach for these studies. Normothermic ischemia for 1 hour caused significant damage, documented by increased iodine 125 bovine serum albumin (125I-BSA) in alveolar lavage fluid and lung parenchyma compared with nonischemic controls. Hypothermic (4 degrees C) ischemia for 4 hours in lungs reperfused with salt solution and for as many as 12 hours in lungs reperfused with whole blood caused no significant increase in 125I-BSA in alveolar lavage fluid and lung parenchyma compared with nonischemic controls. Lungs ventilated without perfusion showed no increase in 125I-BSA leakage compared with controls. The ex vivo rat lung model is excellent for studying ischemia-reperfusion injury. It is reproducible, allows for variance of reperfusion solutions, and permits change in temperature and ventilation easily.

Animals↗
PubMed1988

Surgical management of children and young adults with the Wolff-Parkinson-White syndrome.

The Wolff-Parkinson-White syndrome, as originally described, includes palpitations, tachycardia, and an abnormal electrocardiogram (short PR interval and wide QRS complex). The clinical manifestations are dependent upon a reentrant tachycardia supported by an accessory connection bridging the atrioventricular junction and frequently appear during the first two decades of life. Palpitations are the usual symptoms; less frequently, severe symptoms, such as syncope and sudden death, may result from very rapid atrioventricular conduction across the accessory connection during atrial fibrillation. We report the surgical management of 30 young patients with this syndrome, including 6 with life-threatening tachycardia. Surgical interruption of the accessory connection(s) was curative in 90% (27/30) of the patients; life-threatening symptoms were eliminated in the other three. Based on the limited knowledge of the natural history of the Wolff-Parkinson-White syndrome, the individual patient symptoms, and the electrophysiologic properties of each patient's accessory pathway(s), an algorithm is presented outlining the treatment options. This experience strongly suggests that surgical treatment of the Wolff-Parkinson-White syndrome is safe, effective, and possibly the preferred treatment for this disorder in selected young symptomatic patients.

Adult↗
PubMed1988

Xanthine oxidase inhibition attenuates ischemic-reperfusion lung injury.

Ischemic-reperfusion lung injury is a factor potentially limiting the usefulness of distant organ procurement for heart-lung transplantation. Toxic oxygen metabolites are considered a major etiologic factor in reperfusion injury. Although oxygen-free radicals may be generated by many mechanisms, we investigated the role of xanthine oxidase in this injury process by using lodoxamide, a xanthine oxidase inhibitor, to inhibit ischemic-reperfusion injury in an isolated rat lung model. Isolated rat lungs were perfused with physiologic salt solution (PSS) osmotically stabilized with Ficoll until circulating blood elements were nondetectable in the pulmonary venous effluent. Lungs were rendered ischemic by interrupting ventilation and perfusion for 2 hr at 37 degrees C. After the ischemic interval, the lungs were reperfused with whole blood and lung injury was determined by measuring the accumulation of 125I-bovine serum albumin in lung parenchyma and alveolar lavage fluid as well as by gravimetric measurements. Lung effluent was collected immediately pre- and postischemia for analysis of uric acid by high-pressure liquid chromatography. Lodoxamide (1 mM) caused significant attenuation of postischemic lung injury. Uric acid levels in the lung effluent confirmed inhibition of xanthine oxidase. Protection from injury was not complete, however, implying that additional mechanisms may contribute to ischemic-reperfusion injury in the lung.

Animals↗