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Biomedical subjects

S F Bolling

Publications and source records attributed to S F Bolling.

At least 73 records · Page 4Linked to original sources
PubMed1996

Glucose level and myocardial recovery after warm arrest.

BACKGROUND: During induced cold ischemia for cardiac operations, increasing glucose concentration is not thought to enhance myocardial protection and may detrimentally affect recovery. However, during "warm aerobic" arrest, increased glucose availability as substrate could enhance postischemic metabolic and functional recovery, as during and after ischemia, myocytes shift preference for substrate from fatty acids to glucose. Unfortunately, hyperglycemia may also increase patient susceptibility to neurologic injury. METHODS: This experiment was designed to study the optimal dose of glucose and its effect on function during warm arrest. Isolated, retrograde-perfused rabbit hearts received multidose cardioplegia containing increasing concentrations of glucose, from 0 to 88 mmol/L, and underwent 120 minutes of "warm" 34 degrees C global ischemia. Osmolarities were adjusted equivalently. RESULTS: After 34 degrees C ischemia, hearts treated with 5 to 88 mmol/L glucose showed significantly better functional recovery than those treated with 0 to 1 mmol/L glucose. However, the addition of 22 mmol/L glucose demonstrated optimal recovery with no further incremental enhancement with more glucose. Additional hearts receiving 0 or 22 mmol/L glucose had high-energy phosphates, lactate, CO2, and pH measured. The 22 mmol/L glucose hearts demonstrated active metabolism and significantly better recovery of high-energy phosphate levels than controls. CONCLUSIONS: Increasing glucose level modestly during warm arrest enhanced recovery, but profound hyperglycemia did not incrementally improve this effect, mandating a cautious use of glucose.

Adenine Nucleotides↗
PubMed1996

Regulatory effects of interleukin-10 on lung ischemia-reperfusion injury.

OBJECTIVE: Interleukin-10, a cytokine with antiinflammatory activities, was studied to determine its effects on development of early lung reperfusion injury. METHODS: Adult male rats underwent 90 minutes of left lung ischemia followed by 4 hours of reperfusion. Time-matched sham-operated control rats underwent hilar dissection but not lung ischemia. Lung injury was measured by vascular permeability to bovine serum albumin tagged with iodine 125. To evaluate the effect of exogenous interleukin-10, additional animals received interleukin-10 intravenously before ischemia. To assess the role of endogenous interleukin-10, animals received rabbit antimouse interleukin-10 immunoglobin G (or preimmune rabbit immunoglobin G) before ischemia. RESULTS: Compared with sham control rats, ischemia-reperfusion control rats demonstrated significantly more lung injury. Animals receiving interleukin-10 had significantly less lung injury than did ischemia-reperfusion control rats. Animals receiving antiinterleukin-10 had significantly more lung injury than did animals receiving preimmune immunoglobin G. Alveolar macrophages from animals after 90 minutes of lung ischemia produced more tumor necrosis factor-alpha in culture than did unstimulated macrophages; this production was reduced significantly by the addition of interleukin-10 to the culture medium. CONCLUSION: Endogenous interleukin-10 has a protective effect against early lung reperfusion injury, and interleukin-10 administration can reduce lung reperfusion injury, perhaps in part through its ability to reduce production by alveolar macrophages of tumor necrosis factor-alpha, a known proinflammatory cytokine.

Animals↗
PubMed1996

Perfluorocarbon supplementation and postischemic cardiac function.

BACKGROUND: During induced ischemia for cardiac surgery inefficient anaerobic energy mechanisms predominate. Sustaining aerobic metabolism with perfluorocarbon-supplemented blood cardioplegia theoretically could lead to improved postischemic recovery. Therefore we studied functional recovery after myocardial ischemia, comparing perflubron (C8F17Br) supplemented blood cardioplegia to standard blood cardioplegia. METHODS: Nineteen dogs underwent 15 minutes of 37 degrees C global ischemia on cardiopulmonary bypass, followed by 90 minutes of cardioplegic arrest by use of blood cardioplegia with or without perflubron and then 30 minutes of 37 degrees C reperfusion. During ischemia myocardial oxygen tension, temperature, and pH were measured. Postischemic left ventricular recovery was assessed by means of preload recruitable stroke work, exponential end-diastolic stress-strain regression, and preservation of adenosine triphosphate and energy charge. RESULTS: The addition of perflubron, a new shorter half-life, lecithin-emulsified perfluorocarbon, provided superior myocardial protection when compared with standard blood cardioplegia. This benefit was evidenced by significantly increased recovery of preload recruitable stroke work slope (71% +/- 8% versus 42% +/- 9%), decreased myocardial edema, and enhanced end ischemic myocardial oxygen and pH levels. CONCLUSIONS: The reliable oxygen delivery system and endothelial-preserving properties of the perfluorocarbons may prove to be an invaluable asset in addition to standard blood cardioplegia in the preservation of postischemic ventricular function. These data support the further investigation of perfluorocarbon-enriched blood cardioplegia.

Animals↗
PubMed1996

Mitral valve reconstruction in elderly, ischemic patients.

The role of mitral valve reconstruction is controversial in elderly patients with concurrent ischemic heart disease owing to technical difficulty, prolonged operative times, high mortality, and possible residual mitral regurgitation. However, mitral reconstruction could be most beneficial in this age group due to preservation of left ventricular function, avoidance of anticoagulation, or repeat operation for bioprosthetic degeneration. We studied the outcome of mitral valve reconstruction in 100 consecutive elderly ischemic patients 65 years or older (mean = 73 years; range, 65 to 86 years) operated on between October 1990 and May 1995. Preoperatively all patients were New York Heart Association (NYHA) class III or IV with an ejection fraction of 32 +/- 2%. All patients underwent primary coronary bypass grafting (2.7 +/- 0.2 grafts) and had a flexible mitral annuloplasty ring inserted. Additionally, 54 patients required further complex mitral repairs. All patients had 4+ mitral regurgitation by transesophageal echocardiography prior to operation. After mitral reconstruction, no patient had more than 1+ regurgitation, while most had none and no systolic anterior leaflet motion was noted. There were 4 early (30 day) deaths (4%) and 6 late deaths (6%) at a mean follow-up of 25 months. Patient morbidity has included episodes of mild congestive heart failure (nine), transient ischemic attack (one), endocarditis (one), and respiratory failure (five). There have been one early and two late reoperations for mitral valve replacement. All remaining patients are in NYHA class I or II. While longer-term follow-up is mandatory, coronary bypass grafting and mitral valve reconstruction in the elderly can be accomplished with acceptable surgical mortality and morbidity, yielding reliable improvement in symptoms and quality of life.

Aged↗
PubMed1996

Preventing allograft rejection with CTLA4IG: effect of donor-specific transfusion route or timing.

BACKGROUND: Tolerance to alloantigen in transplant recipients could remove life-long dependence on immunosuppression. Evidence suggests that T-cell responses to alloantigen are dependent not only on T-cell receptor activation but also on costimulation by means of the CD28 receptor. The natural ligands for CD28, expressed on antigen-presenting cells, are B7 family members. CTLA4Ig (a soluble CD28 receptor analog) preferentially binds B7-1 and B7-2 and inhibits CD28 activation. Theoretically, T-cell receptor activation in the presence of alloantigen during CTLA4Ig blockade of CD28-B7 costimulation could render T cells tolerant to that specific alloantigen. In vivo CTLA4Ig significantly increases allograft survival times and can lead to transplantation tolerance. In the rat cardiac allograft model, donor-specific transfusion must be combined with CTLA4Ig to induce tolerance. Previously our laboratory has shown that timing is crucial in the induction of tolerance. METHODS: We examined the effect of differing routes (intravenous, portal vein, or intrathymic), as well as timing (before, at, and after transplantation), of donor-specific transfusion on its ability to synergize with CTLA4Ig using a rat heterotopic major histocompatibility complex-mismatch heart transplant model. RESULTS: We found that tolerance induced by CTLA4Ig and donor-specific transfusion was antigen specific and that timing, but not route of donor-specific antigen administration, had an impact on tolerance induction. Intravenous donor-specific transfusion had a beneficial effect on allograft survival equal to portal vein and intrathymic routes, which have been believed to be more tolerogenic. CONCLUSIONS: Almost universal engraftment can be induced with a combination of intravenous donor-specific transfusion at transplantation plus inhibition of CD28 activation by CTLA4Ig 48 hours after transplantation-a regimen which could have clinical application.

Abatacept↗
PubMed1995

Accuracy of intraoperative transesophageal echocardiography for estimating the severity of functional mitral regurgitation.

Although intraoperative transesophageal echocardiography (TEE) is used to guide mitral valve reconstructive procedures, the effects of hemodynamic alterations accompanying general anesthesia on mitral regurgitation (MR) are unknown. This study was performed to evaluate the effect of general anesthesia on MR jet size using TEE with color Doppler imaging in patients undergoing mitral valve surgery. Matched preoperative TEEs performed with the patient under intravenous conscious sedation, and intraoperative studies performed with the patient under general anesthesia were retrospectively reviewed in 46 patients undergoing mitral valve surgery. Patients were divided into groups based on etiology of MR, including 21 patients with myxomatous degeneration and leaflet flail, 19 patients with structurally normal leaflets and functional regurgitation due to abnormal leaflet coaptation, and 6 patients with rheumatic mitral disease. On both preoperative and intraoperative studies, regurgitation was quantified using maximal jet area and jet diameter at the vena contracta on color flow Doppler. Patients with leaflet flail and patients with functional MR had similar measures of regurgitation severity on preoperative imaging. On intraoperative imaging, regurgitant jet size was unchanged compared with preoperative studies among patients with leaflet flail (jet diameter 1.04 +/- 0.26 vs 1.10 +/- 0.28 cm, area 9.8 +/- 4.5 vs 10.1 +/- 5.2 cm2 on preoperative studies), although jet size decreased significantly in patients with functional MR (jet diameter 0.79 +/- 0.33 vs 1.10 +/- 0.29 cm [p < 0.001], area 5.7 +/- 3.5 vs 10.0 +/- 3.8 cm2 [p < 0.001] on preoperative studies). These findings were not accounted for by variation in heart rate, blood pressures, echocardiographic instrumentation, or Doppler Nyquist limit.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Pattern of injury and the role of neutrophils in reperfusion injury of rat lung.

Using a rat lung model, we sought to characterize the time course for ischemia-reperfusion injury and the role of neutrophils in the development of injury. Adult male Long-Evans rats underwent left thoracotomy with dissection and clamping of the left pulmonary artery, bronchus, and vein for 90 min, resulting in complete left lung ischemia. The lungs were then ventilated and reperfused for up to 4 hr. Time-matched sham animals underwent the identical thoracotomy and hilar dissection, but the lungs were not rendered ischemic. Using vascular permeability of 125I-labeled bovine serum albumin as a measure of reperfusion injury, a bimodal pattern of injury was observed. Compared to sham controls, animals undergoing ischemia-reperfusion demonstrated a significant early phase of lung injury at 30 min of reperfusion (P < 0.0001), followed by partial recovery. A second peak of lung injury was noted after 4 hr of reperfusion (P < 0.001). Myeloperoxidase activity in reperfused lung tissue, a measure of neutrophil sequestration, increased during the reperfusion time course. To determine the role of neutrophils in the development of lung reperfusion injury, additional animals undergoing the identical ischemia-reperfusion protocol received either rabbit anti-rat neutrophil serum or preimmune serum the day prior to operation. Profound neutropenia (< 75/mm3 blood) was confirmed by differential leukocyte counts. Neutropenia had no protective effect against microvascular permeability at 30 min of reperfusion, but there was a significant reduction in lung injury at 4 hr (P < 0.005). We conclude that, during lung ischemia-reperfusion, there is a bimodal pattern of injury, consisting of both neutrophil-independent and neutrophil-mediated events.

Animals↗
PubMed1995

Tumor necrosis factor-alpha and interferon-gamma modulation of nitric oxide and allograft survival.

Tumor necrosis factor-alpha (TNF) and interferon-gamma (IFN) modulate immune responses, as TNF is postulated as a first messenger for priming immune cells and IFN as the second messenger for activation. Nitric oxide (NO) is also an important mediator of immune function, as NO produced by immune cells in response to cytokines such as TNF and IFN may be a cytotoxic end-product effector of immune activation. To examine TNF and IFN modulation of NO production and effects upon allograft survival, we studied the in vitro effect of TNF, IFN, and lipopolysaccharide (LPS, as a nonspecific immune stimulator and TNF promoter) singly or together on NO production in unstimulated rat splenocytes or in response to allogeneic stimulation in MHC mismatch (Brown-Norway, BN, vs Lewis, LEW) mixed lymphocyte reactions. Nitrite as a stable reaction product of NO was determined by a colorimetric method based on the Griess reaction. Interestingly, unstimulated cells had little NO production in response to TNF or IFN; however, following nonspecific (LPS) or allogeneic stimulation there was a significant upregulation of NO production that was synergistically enhanced by the presence of both TNF and IFN. Significantly, anti-TNF antibody inhibited NO production up to 60% in all groups. In vivo studies used a cardiac heterotopic allotransplant model, again BN to LEW. Control recipients received no immunotherapy. Experimental recipients received IFN alone, anti-IFN antibody, anti-TNF antibody, or anti-TNF and anti-IFN antibody. Results from these allograft experiments showed no influence on survival by IFN alone or anti-IFN antibody alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

The mechanism of amino acid loading in improving postischemic myocardial recovery.

During induced ischemia for cardiac surgery, myocardial stunning occurs and aerobic metabolism of glucose, fatty acids, and lactate is altered. Following reperfusion, stunned myocardium uses oxygen and substrate inefficiently, leading to poor functional recovery. However, amino acids may be used as anaplerotic metabolic substrates during and after ischemia, utilizing transamination of amino acids to form high-energy phosphates via the tricarboxylic acid cycle. We investigated if loading hearts with a physiologic spectrum of amino acids prior to ischemia 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 loaded with a 0.05, 0.1, 0.5, 1, 2, or 5% amino acid perfusion prior to cardioplegic ischemia. Following reperfusion, functional recovery revealed that hearts perfused with 0.05 and 0.1% amino acids had improved contractility and compliance vs untreated controls. To determine if the mechanism of amino acid loading in improving postischemic function was enhancement of high-energy phosphate resynthesis, nucleotides and nucleosides were measured. While all preischemic values were equivalent, amino-acid-loaded hearts had significantly greater high energy nucleotides at end ischemia and after reperfusion. These data demonstrate that metabolism, as well as function, is improved with amino acid loading prior to ischemia, which allowed for better internal reparative work during ischemia and external contractile work after ischemia. This strategy may have application in cardiac surgery.

Adenosine Triphosphate↗
PubMed1995

Comparison of early and late complications in patients undergoing coronary artery bypass graft surgery with and without concomitant placement of an implantable cardioverter defibrillator.

Previous studies have reported a significant morbidity and mortality associated with coronary artery bypass graft (CABG) surgery in conjunction with the placement of an implantable cardioverter defibrillator (ICD) with an epicardial lead system. In the absence of a control group, how significantly the component of concomitant placement of the ICD system contributes to these untoward outcomes remains unknown. The purpose of this study was to assess the short- and long-term complications in patients undergoing CABG surgery in conjunction with the placement of an ICD with epicardial leads and to compare these complications with those of patients who had only CABG surgery (control group). The study group (group A) consisted of 56 patients who underwent CABG surgery and placement of an ICD pulse generator with epicardial leads. A control group (group B) consisted of 56 patients who underwent CABG surgery only during the same time period. The two groups were matched for age, sex distribution, left ventricular function, surgical approach, number of bypass grafts per patient, bypass pump time, and length of follow-up period. The early mortality for group A was 7.1% versus 1.8% for group B (p > 0.05). The incidence of early morbidity (congestive heart failure, infection, supraventricular and ventricular arrhythmias) for groups A and B was similar (26.8% vs 25.0%, p > 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1995

Early improvement in congestive heart failure after correction of secondary mitral regurgitation in end-stage cardiomyopathy.

Mitral regurgitation frequently complicates dilated cardiomyopathy, aggravates volume overload of the left ventricle, and contributes to symptoms of congestive heart failure. This study was performed to assess the impact of mitral valve reconstruction in nine consecutive patients with severe mitral regurgitation resulting from end-stage dilated cardiomyopathy. Clinical and echocardiographic follow-up were obtained 17 +/- 5 and 16 +/- 6 weeks after surgery, respectively. There were no operative or early deaths. All patients noted symptomatic improvement postoperatively, and there was a decrease of at least one New York Heart Association functional class (3.9 +/- 0.3 to 1.7 +/- 0.5, p < 0.001). Quantitative echocardiography/Doppler demonstrated a small but significant decrease in left ventricular end-diastolic volume (317 +/- 111 ml to 291 +/- 105 ml, p = 0.04) and increases in ejection fraction (18 +/- 5% to 24 +/- 9%, p = 0.02) and forward cardiac output (3.1 +/- 1.0 to 4.6 +/- 0.8 L/min, p < 0.01) on follow-up. Mitral valve reconstruction for the correction of mitral regurgitation in patients with end-stage dilated cardiomyopathy results in improved symptomatic status on early follow-up accompanied by evidence of improvement in left ventricular performance.

Adult↗
PubMed1995

Functional recovery after ischemia: warm versus cold cardioplegia.

Warm continuous retrograde cardioplegia has been introduced for myocardial protection during cardiac operations, particularly in the setting of acute myocardial ischemia because of its theoretical advantage of producing arrest without ischemia. To investigate the ability of warm continuous retrograde cardioplegia to provide myocardial protection after acute global ischemia, versus the more commonly used cold intermittent antegrade cardioplegia, 12 dogs were subjected to 15 minutes of normothermic global myocardial ischemia on cardiopulmonary bypass followed by 75 minutes of protected cardioplegic arrest using either warm continuous retrograde cardioplegia or cold intermittent antegrade cardioplegia. Standard blood cardioplegia at clinically used volumes and flow rates was used. Warm continuous retrograde cardioplegia animals received 30 mL/kg antegrade to induce arrest followed by 1.5 to 1.8 mL.kg-1.min-1 retrograde at 37 degrees C, whereas cold intermittent antegrade cardioplegia animals received 30 mL/kg antegrade to induce arrest followed by 15 mL/kg antegrade every 15 minutes at 10 degrees C. Load-insensitive left ventricular systolic function, diastolic function, high energy nucleotides, and edema formation were assessed before and after ischemia. Results showed that myocardial preservation using clinically reported flow rates and volumes of warm continuous retrograde cardioplegia was significantly inferior to that provided by clinically used cold intermittent antegrade cardioplegia, as demonstrated by decreased preload recruitable stroke work slope (28 +/- 11 versus 71 +/- 6), increased alpha constant of the end diastolic stress-strain relationship (14.2 +/- 3.0 versus 3.6 +/- 1.0), decreased total nondiffusable nucleotides (40.7 +/- 2.3 versus 57.4 +/- 2.3 microM/g wet weight) and increased water content (82.2% +/- 0.4% versus 80.4% +/- 0.4%).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate↗
PubMed1995

Disparate effects of nitric oxide on lung ischemia-reperfusion injury.

BACKGROUND: Inhaled nitric oxide (.NO) has been found to be a potent pulmonary vasodilator. We assessed whether .NO, through this function or others, could alleviate lung reperfusion injury. METHODS: Rats underwent thoracotomy, with clamps used to create left lung ischemia. After 90 minutes of ischemia, clamps were released, permitting reperfusion for either 30 minutes or 4 hours. Additional animals received inhaled .NO via the ventilator to determine its effects on reperfusion injury. RESULTS: Lung injury, measured by increased vascular permeability using iodine-125-labeled bovine serum albumin leakage, was significantly increased in ischemic-reperfused animals compared with time-matched shams not undergoing ischemia. Inhaled .NO delivered at the start of reperfusion worsened injury at 30 minutes but was protective at 4 hours. The increased injury could be avoided either by delaying .NO for 10 minutes or by treating the animals with superoxide dismutase before reperfusion. .NO reversed postischemic pulmonary hypoperfusion at 4 hours, as measured by labeled microspheres. Lung neutrophil content was significantly reduced at 4 hours in .NO-treated animals. CONCLUSIONS: .NO is toxic early in reperfusion, due to its interaction with superoxide, but is protective at 4 hours of reperfusion, due to reversal of postischemic lung hypoperfusion and reduction of lung neutrophil sequestration.

Administration, Inhalation↗
PubMed1995

Early outcome of mitral valve reconstruction in patients with end-stage cardiomyopathy.

Uncontrollable severe mitral regurgitation is a frequent complication of end-stage cardiomyopathy, significantly contributing to heart failure in these patients, and predicts a poor survival. Although elimination of mitral valve regurgitation could be most beneficial in this group, corrective mitral valve surgery has not been routinely undertaken in these very ill patients because of the presumed prohibitive operative mortality. We studied the early outcome of mitral valve reconstruction in 16 consecutive patients with cardiomyopathy and severe, refractory mitral regurgitation operated on between June 1993 and April 1994. There were 11 men and five women, aged 44 to 78 years (64 +/- 8 years) with left ventricular ejection fractions of 9% to 25% (16% +/- 5%). Preoperatively all patients were in New York Heart Association class IV, had severe mitral regurgitation (graded 0 to 4+ according to color flow Doppler transesophageal echocardiography) and two were listed for transplantation. Operatively, a flexible annuloplasty ring was implanted in all patients. Four patients also had single coronary bypass grafting for incidental coronary disease. In four patients the operation was performed through a right thoracotomy because of prior coronary bypass grafting, and four patients also underwent tricuspid valve reconstruction for severe tricuspid regurgitation. No patient required support with an intraaortic balloon pump. There were no operative or hospital deaths and mean hospital stay was 10 days. There were three late deaths at 2, 6, and 7 months after mitral valve reconstruction, and the 1-year actuarial survival has been 75%. At a mean follow-up of 8 months, all remaining patients are in New York Heart Association class I or II, with a mean postoperative ejection fraction of 25% +/- 10%. There have been no hospitalizations for congestive heart failure, and a decrease in medications required has been noted. For patients with cardiomyopathy and severe mitral regurgitation, mitral valve reconstruction as opposed to replacement can be accomplished with low operative and early mortality. Although longer term follow-up is mandatory, mitral valve reconstruction may allow new strategies for patients with end-stage cardiomyopathy and severe mitral regurgitation, yielding improvement in symptomatic status and survival.

Adult↗
PubMed1995

Retrograde cerebral perfusion during hypothermic circulatory arrest reduces neurologic morbidity.

Hypothermic circulatory arrest has become an accepted technique for a variety of cardiac and complex aortic operations. However, prolonged periods (> 45 min) of hypothermic circulatory arrest in older patients is associated with marginal cerebral protection and an increased incidence of adverse neurologic events. In an effort to minimize such morbidity, we used a technique of retrograde cerebral perfusion with continuous monitoring of cerebral hemoglobin oxygen saturation during hypothermic circulatory arrest in 35 patients who underwent thoracic aortic operations or resection of intracardiac tumor. There were 27 men and 8 women (mean age 60 years, range 21 to 83 years). Sixteen patients had acute dissection, 6 had contained rupture of a thoracic aortic aneurysm, 10 had either a chronic dissection or aneurysm, and 3 had hypernephromas extending into the heart. Six patients underwent root replacement by means of an open technique for their distal anastomosis, 7 underwent root and partial arch replacement, 12 had root and total arch replacement, 7 had total arch replacement, and 3 had resection of tumor in the heart and retrohepatic vena cava. Seven patients had simultaneous coronary artery bypass grafting, 3 had replacement of one of the arch vessels, and 2 patients had a cesarean section. Sixteen cases were emergency, 6 urgent, and 13 elective. Nine (26%) were reoperations. Thirty-four patients underwent the procedure via a median sternotomy and one patient through a posterolateral thoracotomy. The mean retrograde cerebral perfusion time was 63 minutes (range 35 to 128 minutes), with 30 (86%) patients having more than 45 minutes, 12 (34%) having more than 65 minutes, and 4 (11%) having more than 90 minutes. There was 1 operative death caused by a preoperative myocardial infarction from an aortic dissection, and there were 2 late deaths (multiple organ failure and ruptured total aortic aneurysm). One patient had a stroke with a residual right hemiplegia and a pronounced aphasia. There were no other significant neurologic events or reoperations for bleeding. The average length of stay for patients having elective operations was 11 days and for those having emergency operations, 27 days. At a mean follow-up of 6 months all surviving patients (91%) are well. Hypothermic circulatory arrest is a relatively simple technique that provides a bloodless field and good visualization without the need for aortic crossclamps. Moreover, retrograde cerebral perfusion with continuous monitoring of cerebral oxygen saturation extends the "safe" time for hypothermic circulatory arrest, allowing ample opportunity to perform complicated cardiac and aortic operations with reduced risk of adverse neurologic events.

Aortic Dissection↗
PubMed1995

The regional effect of retrograde cardioplegia in areas of evolving ischemia.

Retrograde cardioplegia (RCP) is often used for myocardial protection during coronary bypass grafting, but the regional effect of RCP in areas of evolving ischemia is unknown. We examined the functional and metabolic indices of regional myocardial preservation following acute coronary occlusion with evolving ischemia in a canine model. Following the institution of 37 degrees C cardiopulmonary bypass in 14 dogs, the left anterior descending artery (LAD) was occluded for 15 min. The hearts were then subjected to 90 min of cardioplegic arrest (12 degrees C, 15 mL/kg every 30 min). Seven had antegrade cardioplegia (ACP) alone, while seven had ACP until arrest, then RCP. No topical cooling was used. The LAD occlusion was released after the first bolus of cardioplegia. Regional temperature and pH were measured in the LAD and circumflex (nonischemic) distributions. After 90 min of ischemia and 30 min of reperfusion, all dogs were weaned from bypass. Postischemic function was determined globally by the return of developed pressure (%dP/dt) and regionally by ultrasonic wall crystals. End-ischemic ATP preservation in the LAD distribution was assessed by HPLC (mm ATP/mg protein). Results show that regional functional and metabolic indices were better maintained with RCP in the ischemic LAD distribution. Although only moderate reduction of global function was seen with ACP, the severe reduction noted in LAD regional wall motion with ACP reflects poor regional protection that can be significantly improved in evolving ischemia with RCP.

Animals↗
PubMed1994

alpha-Interferon treatment for idiopathic hypereosinophilic syndrome.

Idiopathic hypereosinophilic syndrome (HES) is a poorly understood disorder characterized by a markedly elevated peripheral blood eosinophil count in the absence of known associated causes of hypereosinophilia. Idiopathic hypereosinophilic syndrome is associated with eosinophil-induced organ damage, including endomyocardial and pulmonary fibrosis, stroke, and gastrointestinal disease. Treatment of idiopathic HES is centered on the reduction of peripheral circulating eosinophils in an effort to diminish tissue infiltration and destruction. Multiple cytotoxic agents have been tried, with variable results. Prednisone and hydroxyurea have remained the therapies of choice in long term treatment of idiopathic HES. We report here the successful 2 year treatment of aggressive idiopathic HES, refractory to hydroxyurea and prednisone, with alpha-interferon.

Adult↗