Viruses in maize and Johnsongrass in southern Ohio.

The two major U.S. maize viruses, Maize dwarf mosaic virus (MDMV) and Maize chlorotic dwarf virus (MCDV), emerged in southern Ohio and surrounding regions in the 1960s and caused significant losses. Planting resistant varieties and changing cultural practices has dramatically reduced virus impact in subsequent decades. Current information on the distribution, diversity, and impact of known and potential U.S. maize disease-causing viruses is lacking. To assess the current reservoir of viruses present at the sites of past disease emergence, we used a combination of serological testing and next-generation RNA sequencing approaches. Here, we report enzyme-linked immunosorbent assay and RNA-Seq data from samples collected over 2 years to assess the presence of viruses in cultivated maize and an important weedy reservoir, Johnsongrass (Sorghum halepense). Results revealed a persistent reservoir of MDMV and two strains of MCDV in Ohio Johnsongrass. We identified sequences of several other grass-infecting viruses and confirmed the presence of Wheat mosaic virus in Ohio maize. Together, these results provide important data for managing virus disease in field corn and sweet corn maize crops, and identifying potential future virus threats.

Laparoscopic repair of traumatic intrapericardial diaphragmatic hernia.

Diaphragm rupture is associated with approximately 5% of blunt abdominal trauma. However, rupture of the central tendon of the diaphragm leading to an intrapericardial diaphragmatic hernia is very rare, with less than 100 cases reported in the world literature. All previously reported cases have been repaired via laparotomy or thoracotomy. In this paper, we present the first laparoscopic repair of a traumatic intrapericardial diaphragmatic hernia.

A comparison of the risks of venous thromboembolic disease in association with different combined oral contraceptives.

AIMS: In October 1995 in response to the results of three studies, the Committee on the Safety of Medicines advised doctors and pharmacists that oral contraceptives containing desogestrel (DSG) and gestodene (GST) were associated with around a two-fold increase in the risk of thromboembolism compared with those containing other progestogens. The objective of this study was to estimate the risk of idiopathic venous thromboembolic disease (VTE) in users of combined oral contraceptives (COCs), to compare the risk between formulations and to examine the effect of using age banding as opposed to matching by exact year of birth. METHODS: A nested case control study was conducted using the General Practice Research Database. Women with a VTE event recorded between 1992 and 1997, who were treated with an anticoagulant, from consideration of their prescription records were likely to have been using a COC prescription on the day of the event and also had no exclusion factors, were deemed cases. For comparison with the previous studies, two nested case control studies were undertaken. Study 1 used controls matched by practice and year of birth. Study 2 used controls matched by practice and within 5 years age bands. RESULTS: We found an incidence of idiopathic VTE amongst users of combined oral contraceptives of 3.8 per 10 000 exposed women years. Incidence rates increased markedly after 35 years of age. The nested case-control study using controls matched by year of birth showed no significant difference in risk between the major COC formulations. With levonorgestrel (LNG) 150 microgram and ethinyloestradiol (EE) 30 microgram as the reference, the adjusted ORs for GST 75 microgram and EE 30 microgram was 1.3 (95% CI 0.8, 2.1), for DSG 150 microgram and EE 30 microgram it was 1.0 (95% CI 0.7, 1.7) and for DSG 150 microgram and EE 20 microgram it was 0.8 (95% CI 0.4, 1.6). Using less rigorous matching criteria, matching controls to cases within 5 years age bands, the ORs increased. When a mixed group of COCs, characterized by having LNG as the progestogen component was used as the reference category, there was an elevation in the ORs for the newer products. We found a significant association between idiopathic VTE and current smoking (OR 2.0 (1.4, 2.7)), BMI over 35 (OR 3.8 (1.8, 8.0)) and asthma (OR 1.9 (1.3, 2.9)). The OR for women who had proxy evidence of general ill health (indicated by the number of prescriptions issued) was 2.2 (1.7, 3.7). CONCLUSIONS: The results of this study indicate that a number of the characteristics of the women taking COCs affect the risk of VTE. There is no evidence to support the hypothesis that there is any difference in risk between COC formulations containing under 50 microg ethinyloestradiol.

Validation of the diagnosis of venous thromboembolism in general practice database studies.

AIMS: The study was conducted to determine whether the method for selecting cases of venous thromboembolism (VTE) from general practice databases significantly affected the findings of an epidemiological study. METHODS: Cases of VTE were identified from the UK General Practice Research Database (GPRD) by searching for codes for deep vein thrombosis (DVT) and pulmonary embolism (PE). These had to be supported by evidence of anticoagulation and be exposed to a combined oral contraceptive (COC) at the time of the event. Additional information about the event was sought from general practitioners who were requested to complete a questionnaire and to supply anonymised copies of hospital letters and discharge summaries. RESULTS: Of the 285 cases identified from the GPRD, additional information was available for 177 VTE events. This information showed that 84% of those events were supported by hospital investigations or a death certificate. Using only verified cases, rather than all GPRD identified events, did not alter the results of the epidemiological study. CONCLUSIONS: The GPRD provides information of sufficiently high quality to allow valid epidemiological research of VTE events. Excluding cases without a database record of hospital admission would lead to valid events being overlooked, and an under-estimate of the disease incidence.

Oral contraceptives and venous thromboembolic disease. Analyses of the UK General Practice Research Database and the UK Mediplus database.

The results of three independent studies of venous thromboembolic disease (VTE) and oral contraceptives are reviewed together with two further cohort/case-control studies which we conducted using the MediPlus and General Practice Research Database (GPRD) databases. These latter studies jointly involved 395 cases and uniquely examined the association between VTE and individual combined oral contraceptive (COC) formulations. The two studies yielded very similar results. Crude incidence rates for idiopathic VTE of 4.6 and 3.8 were found per 10,000 exposed woman-years (EWY), in the MediPlus and GPRD studies respectively. Incidence rates increased markedly with age, and in both databases the rates amongst users of levonorgestrel products were lower than those amongst users of desogestrel and gestodene products. A case fatality rate of 3% and a mortality rate of 10 per million EWY were estimated. Odds ratios (OR) were calculated for confounding variables and different COC formulations. Both database studies indicated an excess of current smokers and women with high body mass indices amongst cases. There were significantly more cases with asthma in the GPRD study and cases who had been using their COC for less than a year. No statistically significant differences between COC formulations were found in the analyses where controls were matched to cases by practice and year of birth in both the MediPlus and GPRD studies. In the GPRD study we also ran a study where controls were matched by practice and within 5 year age bands. In this study the OR were consistently higher for the newer or 'third generation' products than when controls were matched by year of birth. However only the acne formulation/OC containing cyproterone acetate and 35 microg ethinyloestradiol yielded a significant OR of 2.3. It may be concluded that improvements in prescribing are paramount as the results strongly indicate that overweight women and those who smoke are at a greater risk of VTE. Further study is required to elucidate the possibility that asthma or its treatment may predispose to VTE, alone or in combination with other risk factors. However, neither the MediPlus nor GPRD studies indicate that any one COC formulation poses a greater risk of VTE than another.

Relationship between the regional and national incidence of transient ischaemic attack and stroke and performance of carotid endarterectomy.

OBJECTIVES: To examine the relationship between the incidence of transient ischaemic attack (TIA) and stroke on a national and regional level and the rate of carotid endarterectomy (CEA). SUBJECTS: Patients entered onto a national primary care computerised database with a new diagnostic code of stroke or TIA between 1992 and 1995. METHODS: Analysis of data from the primary care database and routine data sources. Main outcome measures were incidence of TIA and stroke and rates of CEA. RESULTS: The mean incidence per 100,000 of the population was 292 (TIA) and 356 (stroke) in England, 391 and 497 in Scotland and 349 and 448 in Northern Ireland. There was a variation in the incidence of TIA and stroke between both the regions and the regions and countries which was significant. There was a national increase in the rate of CEA between 1990 and 1995 which showed a marked variation across the regions. The inter-regional variation in rate of CEA correlated with the inter-regional difference in incidence of disease. CONCLUSIONS: The incidence of TIA and stroke may be higher than previously recognised, and varies significantly between the regions. This is generally associated with the variation in performance of CEA.

The risks of venous thromboembolic disease among German women using oral contraceptives: a database study.

This study investigated the risk of venous thromboembolic disease (VTE) between second and third generation combined oral contraceptives, using the German MediPlus database of patient records. Women studied included 42 patients between the ages of 18 and 49 years, with a diagnosis of VTE treated with an anticoagulant, who were exposed to an oral contraceptive (OC). Four controls per patient (168), matched by year of birth and exposure to an OC on the even day, were identified. More women were users of second generation than third generation OC, and none were using progestogen-only pills. There was no significant difference between patients and control subjects with respect to the type of OC used on the event day (unadjusted odds ratio for third versus second generation users was 0.77; 95% confidence interval [CI] 0.38-1.57). There was no significant age difference between second and third generation users among patients or control subjects. Between January 1 and the event date, there was no significant difference between the patients and control subjects in terms of the number of oral contraceptive prescriptions, number of consultations for psychotherapeutic complaints, or mixed physical and psychotherapeutic consultations; however, patients did demonstrate significantly more consultations for purely physical complaints compared with control subjects (p < 0.0001). There were no significant consultation differences between patients with pulmonary emboli (n = 6) and other VTE patients (n = 36). No significant differences with respect to VTE risk between users of second and third generation oral contraceptives were found in this study. Consultations (physical) for patients were higher than for control subjects before the VTE event. If consultation rate relates to the general health status of a person, this might indicate that VTE risk is higher among women of poorer health, but that this is not related to the type of progestogen in the oral contraceptive that they use.

PIP: The German MediPlus database of patient records from 451 practices was used to investigate the risk of venous thromboembolism (VTE) in users of second- and third-generation combined oral contraceptives (OCs). Cases included 42 women 18-49 years of age with a diagnosis in 1992-95 of a VTE treated with an anticoagulant and with a history of OC use. Also enrolled were 168 controls (4 per case), matched to cases by year of birth and exposure to an OC on the event day. 64.3% of cases and 53.0% of controls had used a second-generation OC; use of a third-generation OC was reported by 35.7% of cases and 38.1% of controls. No significant differences in terms of VTE risk factors were identified between users of second- and third-generation OCs. The odds ratio for VTE among users of third-generation compared to second-generation OCs was 0.77 (95% confidence interval, 0.38-1.57). There were no significant differences between cases and controls in terms of the type of OC used, age, the total number of OC prescriptions issued, number of consultations for psychotherapeutic complaints, and number of consultations for mixed psychotherapeutic and physical complaints. Although cases had more consultations for physical complaints before the VTE (presumed to be a proxy for poor general health), this was not related to the type of progestogen in the OC.

Adenosine inhibition of neutrophil damage during reperfusion does not involve K(ATP)-channel activation.

This study tests the hypothesis that cardioprotection exerted by adenosine A2-receptor activation and neutrophil-related events involves stimulation of ATP-sensitive potassium (K(ATP)) channels on neutrophils during reperfusion. The adenosine A2 agonist CGS-21680 (CGS) inhibited superoxide radical generation from isolated rabbit polymorphonuclear neutrophils (PMNs) in a dose-dependent manner from 17.7 +/- 2.1 to 7.4 +/- 1.3 nmol/5 x 10(6) PMNs (P < 0.05). Pinacidil, a K(ATP)-channel opener, partially inhibited superoxide radical production, which was completely reversed by glibenclamide (Glib). Incremental doses of Glib in combination with CGS (1 microM) did not alter CGS-induced inhibition of superoxide radical generation. CGS significantly reduced PMN adherence to the endothelial surface of aortic segments in a dose-dependent manner from 189 +/- 8 to 50 +/- 6 PMNs/mm2 (P < 0.05), which was also not altered by incremental doses of Glib. Infusion of CGS (0.025 mg/kg) before reperfusion reduced infarct size from 29 +/- 2% in the Vehicle group to 15 +/- 1% in rabbits undergoing 30 min of ischemia and 120 min of reperfusion (P < 0.05). Glib (0.3 mg/kg) did not change the infarct size (28 +/- 2%) vs. the Vehicle group and did not attenuate infarct size reduction by CGS (16 +/- 1%). Glib did not change blood glucose levels. Cardiac myeloperoxidase activity was decreased in the ischemic tissue of the CGS group (0.15 +/- 0.03 U/100 mg tissue) compared with the Vehicle group (0.37 +/- 0.05 U/100 mg tissue; P < 0.05). We conclude that adenosine A2 activation before reperfusion partially reduces infarct size by inhibiting neutrophil activity and that this effect does not involve K(ATP)-channel stimulation.

Basal nitric oxide expresses endogenous cardioprotection during reperfusion by inhibition of neutrophil-mediated damage after surgical revascularization.

Ischemia-reperfusion damages endothelium and impairs basal production of nitric oxide. Basally released nitric oxide is cardioprotective by its inhibition of neutrophil activities. Loss of endogenous nitric oxide with endothelial injury may occur during two phases: cardioplegic ischemia and reperfusion (aortic declamping). This study tested the hypothesis that inhibition of endogenously released nitric oxide in hearts subjected to regional ischemia, cardioplegic arrest, and reperfusion (1) restricts endogenous cardioprotection and permits neutrophil-mediated damage and (2) expresses damage during the reperfusion phase. L-Nitro-arginine was used to block basal nitric oxide production. In 22 anesthetized dogs, the left anterior descending artery was ligated for 90 minutes followed by 1 hour of arrest with cold multidose (every 20 minutes) blood cardioplegia. Dogs were divided into three groups: the first group received standard unsupplemented blood cardioplegia (group 1, n = 8), in the second group L-nitro-arginine was administered as an additive to blood cardioplegic solution (1 mmol) and as an infusion during reperfusion (34 mg/kg) (group 2, n = 7), and in the third group L-nitro-arginine was administered only at reperfusion (group 3, n = 7). The ligature was released during the second infusion of cardioplegic solution. Infarct size (triphenyltetrazolium chloride) was increased in group 3 (L-nitro-arginine only at reperfusion) compared with that in group 1 (standard blood cardioplegia) (49% +/- 6% vs 34% +/- 2%, respectively), but was not further extended in group 2 (L-nitro-arginine as an additive to blood cardioplegic solution and at reperfusion) (56% +/- 3%, p > 0.05 vs group 3), which suggests primarily a reperfusion process. Polymorphonuclear neutrophil-specific myeloperoxidase activity in the area at risk was elevated comparably in groups 2 and 3 (group 2: 2.9 +/- 0.5 units/gm tissue, p = 0.06 vs group 1; group 3: 3.9 +/- 1.0 units/gm tissue, p < 0.05 vs group 1) compared with that in the standard blood cardioplegia group (1.7 +/- 0.3 units/gm tissue), suggesting polymorphonuclear neutrophil accumulation occurs primarily during reperfusion. Polymorphonuclear neutrophil adherence in ischemic-reperfused left anterior descending artery segments was comparably greater in group 2 (L-nitro-arginine as an additive to blood cardioplegic solution and at reperfusion: 195 +/- 21 polymorphonuclear neutrophils/mm2 of artery, p < 0.05 vs group 1) and group 3 (L-nitro-arginine only at reperfusion: 224 +/- 20 polymorphonuclear neutrophils/mm2 of artery, p < 0.05 vs group 1) relative to that in group 1 (108 +/- 19 polymorphonuclear neutrophils/mm2 of artery). There was no significant adherence to nonischemic circumflex arteries. We conclude that blockade of endogenous nitric oxide augments postischemic injury mediated by polymorphonuclear neutrophils, and this damage is expressed primarily during the reperfusion phase.

Leukocyte modulation inhibits endotoxin-induced disruption of intracellular calcium homeostasis.

OBJECTIVE: Sepsis is associated with disruption of intracellular calcium homeostasis. The specific mechanisms responsible for these changes remain unclear. This study attempts to modify endotoxin-induced alterations in erythrocyte intracellular calcium dynamics through modulation of the activated leukocyte and its products. METHODS: Paired anticoagulated whole-blood specimens were obtained from healthy adult volunteers (n = 30). Specimens were incubated with 2 micrograms/mL endotoxin [lipopolysaccharide (LPS)] or saline control in the presence and absence of the white blood cell. Studies were repeated in specimens pretreated with allopurinol, superoxide dismutase, and pentoxifylline (PTX). After incubation, erythrocytes were separated, washed, and loaded with the fluorescent calcium chelator, FURA-2. Free cytosolic calcium concentration was determined on 10(6) cells using fluorescent spectroscopy. Values were computer-calculated every 1.8 seconds for 1 minute, and mean results were used for analysis. Differences were evaluated by analysis of variance. RESULTS: The LPS resulted in a significant increase in intracellular calcium concentration (LPS 70.95 nM vs. control 44.04 nM). This increase was dependent on the presence of the white blood cell and could not be induced in its absence (control 30.15 --> LPS 32.78). Pretreatment inhibited these endotoxin-induced alterations: allopurinol, 50.49 nM; superoxide dismutase, 49.12 nM; and PTX, 40.23 nM (p < 0.01). CONCLUSIONS: Endotoxin induces a significant increase in intracellular calcium concentration. This alteration seems to be mediated by activated neutrophils and can be ameliorated by both leukocyte modulation (PTX) and free radical scavengers.

Effect of sepsis on erythrocyte intracellular calcium homeostasis.

OBJECTIVES: To examine erythrocyte intracellular calcium dynamics in clinical sepsis and experimental endotoxemia. DESIGN: Prospective, multiexperimental study utilizing in vitro manipulation and evaluation of human erythrocytes. SETTING: University research laboratory. PATIENTS: Healthy, elective surgical patients, "septic" surgical patients, and normal volunteers. INTERVENTIONS: For all experimental studies, whole blood specimens were incubated with 2 micrograms/mL of Escherichia coli endotoxin (experimental) or an equivalent volume of phosphate buffered saline (control). Incubations were performed in specimens pretreated with 0.4 mM of verapamil and/or 50 mM of dantrolene. Incubations were performed in the presence and absence of extracellular calcium. Incubations were also performed utilizing pre- and posttreatment with 1 mM of adenosine 5'-triphosphate (ATP) and/or 30 mM of adenosine. MEASUREMENTS AND MAIN RESULTS: Free cytosolic calcium concentration was determined by fluorescent spectroscopy, utilizing the calcium chelator, FURA-2AM. Sepsis was associated with a significant increase in erythrocyte intracellular calcium concentration as compared with nonseptic controls (96.26 vs. 45.38 nM; p < .001). Similar changes could be induced by endotoxin incubation of whole blood (84.52 vs. 40.45 nM; p < .001). This endotoxin-induced increase was independent of extracellular calcium concentration and was only partially ameliorated by calcium-channel blockade. Inhibition of intracellular calcium release was ineffective in altering the endotoxin-induced increase in the erythrocyte intracellular calcium value. In contrast, pretreatment with either adenosine or ATP minimized these increases. Posttreatment with ATP, but not adenosine, allowed partial reversal of this endotoxin-induced increase in intracellular calcium. CONCLUSIONS: Sepsis induces alterations of erythrocyte intracellular calcium homeostasis. A significant increase in free cytosolic concentrations of intracellular calcium is characteristic of this altered homeostasis. These changes are reproducible by the incubation of whole blood with endotoxin. This increase in cytosolic calcium concentration appears to be independent of extracellular calcium concentration, transmembrane calcium channels, and/or intracellular calcium stores. It can, however, be modulated through provision of high-energy phosphates and/or their precursors to the cell itself.

Sepsis-induced alterations in the erythrocyte membrane.

Sepsis is known to alter red blood cell (RBC) deformability, and this change in flexibility may play a role in the pathophysiology of the hemodynamic alterations characteristic of the septic syndrome. The etiology of this red cell change is unclear. This study evaluates erythrocyte size and cell membrane fluidity during clinical (septic surgical patients) and experimental (endotoxin incubation) sepsis. Membrane lipid viscosity was assessed by fluorescent spectroscopy. Mean corpuscular volume and hemoglobin concentration was determined by automated counter. There was a significant increase in erythrocyte membrane lipid viscosity (P < 0.001) in both the clinical and experimental septic models. No difference was detected, however, in RBC mean corpuscular volume or hemoglobin concentration. These findings suggest that sepsis-induced alterations in erythrocyte deformability are due primarily to an increase in the membrane lipid viscosity and are unrelated to alterations in the cell surface area to volume ratio.

The effect of endotoxin on neonatal erythrocyte intracellular calcium concentration.

Erythrocyte membrane deformability is dependent on the maintenance of "normal" intracellular calcium (Ca) levels. Red cell flexibility is known to be altered in the septic neonate. In turn, this adversely affects viscosity and compromises flow in the microcirculation. It has been suggested that this may play a role in the mesenteric hypoperfusion associated with necrotizing enterocolitis. This study was designed to determine the effect of endotoxin on erythrocyte Ca homeostasis in the neonate. Paired specimens were obtained from the umbilical cord of 10 healthy neonates. The samples were incubated with either buffered saline (control) or 2 micrograms/mL of Escherichia coli endotoxin (LPS). Erythrocytes were then isolated, washed, and loaded with the fluorescent Ca chelator, FURA-2. The free cytosolic Ca concentration was determined by spectroscopic analysis of the ratio of fluorescent intensities at 340 nm and 380 nm. Results were obtained every 1.8 seconds for 1 minute, and the mean value was used for analysis. In 10 additional neonates, the white blood cells were removed before incubation in saline and LPS, and the erythrocytes were evaluated as described above. Differences were analyzed statistically by the paired t test. In the presence of white blood cells, endotoxin resulted in a significant increase in free cytosolic Ca concentration (LPS, 42.602 +/- 5.166 nmol; control, 31.661 +/- 4.002 nmol; P < .02). However, no significant difference were detected when cells were incubated in the absence of white blood cells (LPS, 32.374 +/- 2.479 nmol; control, 34.021 +/- 2.549 nmol). Endotoxin induces a significant increase in neonatal free cytosolic Ca concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of endotoxin on the neonatal erythrocyte.

Intestinal ischemia is considered a major factor in the development of necrotizing enterocolitis (NEC). Despite this, the majority of affected infants lack documentation of clinical events associated with obvious gut hypoperfusion. Recent evidence in adults suggests that endotoxin may impair flow in the microcirculation through alterations in erythrocyte deformability. As the gut serves as a semipermeable reservoir of endotoxin in the stressed neonate, such localized activity may result in intestinal ischemia at the microcirculatory level through alterations in the red cell membrane. This study evaluates the role of endotoxin on neonatal erythrocyte membrane viscosity. Paired anticoagulated whole blood specimens were obtained from the umbilical cord of 10 neonates at delivery. Samples were incubated with either 2 micrograms/mL of E coli endotoxin (LPS) or an equal volume of saline (control). Following incubation, erythrocytes were isolated, washed, and incorporated with the fluorescent membrane probe TMA-DPH. Membrane viscosity was assessed by spectroscopic analysis of the fluorescent emissions induced by excitation of the probe at 365 nm. Results were calculated as anisotropy and analyzed for differences by ANOVA. Endotoxin resulted in a significant increase in red cell membrane viscosity as compared to control (LPS 291.2 +/- 5.1 v Control 271.7 +/- 3.3, P < .01). As the effects of endotoxin are known to be primarily the result of white blood cell (WBC) activation, this study was repeated in an additional 10 neonates in whom WBCs were removed prior to endotoxin/saline incubation.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of the leukocyte in endotoxin-induced alterations of the red cell membrane. Second place winner of the Conrad Jobst Award in the Gold Medal paper competition.

Sepsis and endotoxemia are known to be associated with alterations in the red cell membrane that result in diminished flexibility. This decreased flexibility may be responsible, in part, for the microcirculatory abnormalities accompanying sepsis. The etiology of these sepsis-associated changes remains unclear. This study evaluates the role of the white blood cell in these abnormalities. Specimens were obtained from 44 volunteers and divided into two treatment groups. Group I specimens were incubated with Escherichia coli endotoxin (2 micrograms/ml) followed by removal of the white blood cells. The white blood cells were removed from group II specimens before endotoxin incubation. Paired, saline-incubated samples served as controls. After incubation, washed erythrocytes were evaluated for deformability and membrane viscosity. Deformability was assessed by filtration through 4.7-microns membranes. Red cell deformability was expressed as filtration rate (volume of cells per second per square centimeter). Membrane viscosity was assessed by fluorescent spectroscopy of cells into which the membrane probe 1(4-(trimethylamino)-phenyl)-6-phenyl-1,3,5-hexatriene had been incorporated. Results were expressed as anisotropy. Endotoxin resulted in a significant increase in erythrocyte membrane viscosity (experimental, 0.296 +/- 0.002 vs. control, 0.284 +/- 0.002, P < 0.001). This was reflected by a significant decrease in cellular deformability (experimental, 142.55 +/- 6.55 vs. control, 157.86 +/- 8.63, P < 0.01). However, these alterations are not a direct effect of endotoxin, but require the presence and participation of the white blood cell and/or its mediators (experimental, 0.301 +/- 0.002 vs. control, 0.300 +/- 0.001, P = NS).

Concomitant cardiac and pulmonary operation: the role of cardiopulmonary bypass.

To assess the safety and efficacy of concomitant pulmonary resection and cardiac operation requiring cardiopulmonary bypass, the records of 19 patients were reviewed. Eighteen patients (94.7%) presented with cardiac symptoms and were found to have pulmonary pathology of indeterminate etiology. Pulmonary resections were performed through a median sternotomy in all but 1 patient, who underwent posterolateral thoracotomy and right middle lobectomy after repositioning because dense adhesions prevented adequate dissection through the initial incision. A total of 24 resections were performed. Sixteen (66.7%) were performed on cardiopulmonary bypass. Six wedge resections (25.0%) were performed before bypass. Two lobectomies (8.3%) were performed after infusion of protamine sulfate. Nine patients (47.4%) had benign pathology, 7 (36.8%) had primary carcinoma, and 3 (15.8%) had metastatic disease. Bleeding complications occurred in 15.8% of patients (3/19). There was 1 perioperative death (5.3%), which was due to adult respiratory distress syndrome after intraoperative hemorrhage followed lobectomy for bullous disease. Another patient required lateral extension of the sternotomy during an episode of exsanguinating intraparenchymal pulmonary hemorrhage, which resulted in lobectomy, as well as costochondral and sternal osteomyelitis. A third patient required exploration for bleeding at the staple line. Postoperative complications occurred in 7 patients (36.8%) and were predominantly respiratory (5/7, 71.4%) (p = 0.006). The median postoperative hospitalization was 15 days. Although comparison of patients who underwent pulmonary resection during bypass with those who had resection either before heparinization or after protamine infusion showed no significant difference with respect to age, incidence of malignancy, operation performed, complications, postoperative hospitalization, or survival, this was probably due to the small number of patients in the study.(ABSTRACT TRUNCATED AT 250 WORDS)