Rural emergency medical technician pre-hospital electrocardiogram transmission.

INTRODUCTION: Emergent care of the acute heart attack patient continues to be at the forefront of quality and cost reduction strategies throughout the healthcare industry. Although the average cardiac door-to-balloon (D2B) times have decreased substantially over the past few years, there are still vast disparities found in D2B times in populations that reside in rural areas. Such disparities are mostly related to prolonged travel time and subsequent delays in cardiac catherization lab team activation. Urban ambulance companies that are routinely staffed with paramedic level providers have been successful in the implementation of pre-hospital 12-lead electrocardiogram (ECG) protocols as a strategy to reduce D2B times. METHOD: The authors sought to evaluate the evidence related to the risk and benefits associated with the replication of an ECG transmission protocol in a small rural emergency medical service. The latter is staffed with emergency medical technician-basics (EMT-B), emergency medical technician-advanced (EMT-A), and emergency medical technician-intermediate (EMT-I) level. RESULTS: The evidence reviewed was limited to studies with relevant data regarding the challenges and complexities of the ECG transmission process, the difficulties associated with ECG transmission in rural settings, and ECG transmission outcomes by provider level. CONCLUSIONS: The evidence supports additional research to further evaluate the feasibility of ECG transmission at the non-paramedic level. Multiple variables must be investigated including equipment cost, utilization, and rural transmission capabilities. Clearly, pre-hospital ECG transmission and early activation of the cardiac catheterization laboratory are critical components to successfully decreasing D2B times.

The European TREatment of severe Atopic eczema in children Taskforce (TREAT) survey.

BACKGROUND: There is a paucity of evidence for the use of systemic agents in children with atopic eczema refractory to conventional therapy, resulting in considerable variation in patient management. OBJECTIVES: The European TREatment of severe Atopic eczema in children Taskforce (TREAT) survey was established to collect data on current prescribing practice, to identify factors influencing the use of specific systemic agents, and to inform the design of a clinically relevant intervention study. METHODS: Consultant physician members of the paediatric dermatology societies and interest groups of eight European countries were invited to participate in a web-based survey. The multiple-response format questionnaire collated data on clinical practice in general, as well as detailed information on the use of systemic agents in refractory paediatric atopic eczema. RESULTS: In total, 343/765 members (44·8%) responded to the invitational emails; 89·2% were dermatologists and 71% initiate systemic immunosuppression for children with severe atopic eczema. The first-line drugs of choice were ciclosporin (43·0%), oral corticosteroids (30·7%) and azathioprine (21·7%). Ciclosporin was also the most commonly used second-line medication (33·6%), with methotrexate ranked as most popular third choice (26·2%). Around half of the respondents (53·7%) replied that they routinely test and treat reservoirs of cutaneous infection prior to starting systemic treatment. Across the eight countries, penicillins were the first-line antibiotic of choice (78·3%). CONCLUSIONS: In the absence of a clear evidence base, the European TREAT survey confirms the wide variation in prescribing practice of systemic immunosuppression in refractory paediatric atopic eczema. The results will be used to inform the design of a randomized controlled trial relevant to patient management across Europe.

Homozygous variegate porphyria presenting with developmental and language delay in childhood.

Variegate porphyria is an autosomal dominant disorder that usually presents with photosensitivity and acute neurological crises in adulthood. It is caused by heterozygous mutations in the protoporphyrinogen oxidase gene (PPOX). A rarer variant, homozygous variegate porphyria (HVP), presents in childhood with recurrent skin blisters and scarring. More variable features of HVP are short stature, brachydactyly, nystagmus, epilepsy, developmental delay and mental retardation. We describe a child who presented with nystagmus, developmental delay and ataxia, combined with a photosensitive eruption. Analysis of porphyrins in plasma, urine and stool supported a clinical diagnosis of HVP. DNA from the patient showed that he is compound heterozygous for two novel missense mutations in the PPOX coding region: c.169G>C (p.Gly57Arg) and c.1259C>G (Pro420Arg). Interestingly, cranial magnetic resonance imaging showed an absence of myelin, a feature not previously reported in HVP, which expands the differential diagnosis of childhood hypomyelinating leucoencephalopathies.

MBTPS2 mutation in a British pedigree with keratosis follicularis spinulosa decalvans.

Keratosis follicularis spinulosa decalvans (KFSD; OMIM 308800) is an X-linked disorder characterized by widespread hyperkeratotic follicular papules (including keratosis pilaris-like lesions), facial erythema, hypotrichosis and scarring alopecia. KFSD results from mutations in the MBTPS2 gene. Mutations in this gene also underlie ichthyosis follicularis, alopecia and photophobia syndrome. We report a British pedigree with KFSD resulting from the mutation p.Asn508Ser. This particular mutation has been reported in three other pedigrees with KFSD (Dutch, American, British) and is the only pathogenic mutation reported in this disorder to date. However, the same mutation has also been reported in a Chinese pedigree with IFAP syndrome, highlighting the clinical heterogeneity and overlapping molecular pathology of these two disorders.

Eczema and cancer risk: a critical appraisal and review of the literature.

AIM: Hwang et al. aimed to evaluate the risk of malignancy among individuals with eczema, allergic rhinitis (AR) and asthma, compared with the general Taiwanese population. HYPOTHESIS: People with atopic conditions, including eczema, have an altered risk of malignancy. SETTING AND DESIGN: This was a prospective nationwide cohort study. The authors used the Taiwanese National Health Insurance Research Database (NHIRD) to compare the incidence of cancers among people with established allergic disease relative to the risk in the general population. STUDY EXPOSURE: Exposure was the presence of one or more atopic conditions (eczema, AR or asthma). Data were extracted on 997,729 randomly selected people registered on the NHIRD at any time point between 1996 and 2008. Eczema was identified via ICD-9-CM codes with the diagnosis being made by a dermatologist, paediatrician or allergist. Follow-up was until 2008, date of first cancer or death. OUTCOMES: The outcome was a new diagnosis of malignancy, identified via catastrophic illness insurance certificates, again using ICD-9-CM diagnostic codes. PRIMARY OUTCOME MEASURE: Standardized incidence ratios (SIRs) for cancers overall and different types of malignancy among patients with eczema, AR or asthma were calculated against the expected number of cancer cases in the general population, adjusted for age and sex. RESULTS: The number of patients identified with eczema, AR and asthma was 34,263, 225,315 and 107,601, respectively. Overall cancer rates in patients with these conditions were not significantly different from those in the general population [SIR eczema = 0·97 (95% confidence interval 0·87-1·09), SIR AR = 1·02 (0·98-1·05) and SIR asthma = 1·01 (0·97-1·04)]. However, when the results for eczema were stratified by age, people aged between 20 and 39 years appeared to have a 56% increase in risk in relation to 'any cancer' [SIR = 1·56 (1·13-2·09)]. Looking at individual cancer types in patients with eczema, only the risk of brain cancer was significantly raised [SIR = 2·52 (1·15-4·79)]. Patients who had had all three allergic conditions had a reduced SIR for 'cancers overall' [SIR = 0·59 (0·37-0·88)]. This inverse association was less strong for those with eczema and asthma [SIR = 0·73 (0·55-0·97)] or asthma and AR [SIR = 0·79 (0·73-0·84)] and statistically only of borderline significance for those with eczema and AR [SIR = 0·85 (0·67-1·07)]. CONCLUSIONS: Hwang et al. conclude that the relationship between allergic diseases and cancer risk is complex and site specific. The risk of malignancy was highest in all atopic conditions in the 20-39-year age group. In patients with eczema, the incidence of brain cancer was higher than expected, which the authors note is at odds with previous studies. However, numbers were too small to allow stratification by histological subtypes. The authors warn against deriving conclusions for rarer cancers and that borderline SIRs must be interpreted with caution.

Pulsed intravenous cyclophosphamide and methylprednisolone therapy in refractory pemphigus.

BACKGROUND: Pemphigus is a rare autoimmune blistering disorder. The mainstay of current treatment is high-dose oral corticosteroid therapy in combination with a steroid-sparing agent. Adjuvant therapy is important for disease control and to reduce the iatrogenic effects of oral prednisolone. Pulsed therapy with intravenous methylprednisolone and cyclophosphamide (PPC) has been shown to be an effective treatment but there are currently few data on its use in patients who have failed to respond to conventional immunosuppression. OBJECTIVES: To report the clinical and immunological responses of 21 patients with pemphigus refractory to prednisolone and azathioprine or mycophenolate mofetil treated in our department with a standard protocol of monthly PPC. METHODS: Patients with pemphigus were identified who had undergone PPC therapy during the period between 1997 and 2006. Initial clinical severity and response to treatment was assessed. In addition, change in intercellular antibody titres and desmoglein 1 and 3 antibodies to PPC therapy was also recorded. RESULTS: Of the 21 patients treated, seven had an excellent response, two a good response, five a moderate response, six a minimal response and one patient had no clinical response. Four patients achieved complete clinical remission and the number of pulses for these patients varied between 11 and 22. We observed significant reductions in indirect immunofluorescence titres for normal human skin substrate (P = 0.0078) and antidesmoglein 1 and 3 autoantibody levels (P = 0.007 and P = 0.0085, respectively) from pre-PPC therapy to 1 year after the last pulse. All patients were able to reduce their prednisolone dose from a pre-pulsing median dose of 40-10 mg at the last pulse with a median dose reduction of 66% (P < 0.001). The most common adverse effect was transient lymphopenia (12 patients); nonlife-threatening sepsis (seven patients) and premature ovarian failure (two patients) also occurred. CONCLUSIONS: PPC can be an effective treatment for refractory pemphigus but its adverse effects should be considered prior to therapy and closely monitored in patients on treatment.

Imiquimod and lentigo maligna: a search for prognostic features in a clinicopathological study with long-term follow-up.

BACKGROUND: Melanoma in situ/lentigo maligna (LM) is a potential precursor of LM melanoma. It occurs most commonly in elderly individuals on sun-exposed skin of the head and neck. Although surgical excision is the treatment of choice, this may not be desirable or feasible for large lesions at functionally or cosmetically important sites. Imiquimod is a topical immunomodulator which can generate a local cytotoxic response with potentially antiviral and antitumour effects. OBJECTIVES: To present our experience of LM treated with imiquimod. METHODS: A retrospective review was performed of all patients with facial LM treated in our unit with topical imiquimod between January 2001 and December 2006. Pretreatment diagnostic biopsies were also reviewed and histologically graded. RESULTS: Forty-eight patients were treated with imiquimod. There were 37 responders and 11 treatment failures (of whom two were 'partial responders'). Of the 37 responders, 31 showed a clinical inflammatory response to imiquimod. One patient in whom treatment failed subsequently developed invasive disease. The mean follow-up duration was 49 months. We could not identify histological features of prognostic significance. However, the ability to develop an inflammatory reaction to imiquimod was a strong predictor of therapeutic benefit. CONCLUSIONS: We consider imiquimod to have a role in the treatment of LM in patients in whom surgery may be contraindicated or for those in whom the cosmetic or functional consequences may be considerable. Until better characterized, its use should probably be confined to centres with experience in the detection and treatment of LM and melanoma.

Impaired hormonal responses to hypoglycemia in spontaneously diabetic and recurrently hypoglycemic rats. Reversibility and stimulus specificity of the deficits.

To evaluate the roles of iatrogenic hypoglycemia and diabetes per se in the pathogenesis of defective hormonal counterregulation against hypoglycemia in insulin-dependent diabetes mellitus (IDDM), nondiabetic, and spontaneously diabetic BB/Wor rats were studied using a euglycemic/hypoglycemic clamp. In nondiabetic rats, recurrent (4 wk) insulin-induced hypoglycemia (mean daily glucose, MDG, 59 mg/dl) dramatically reduced glucagon and epinephrine responses by 84 and 94%, respectively, to a standardized glucose fall from 110 to 50 mg/dl. These deficits persisted for > 4 d after restoring normoglycemia, and were specific for hypoglycemia, with normal glucagon and epinephrine responses to arginine and hypovolemia, respectively. After 4 wk of normoglycemia, hormonal counterregulation increased, with the epinephrine, but not the glucagon response reaching control values. In diabetic BB rats (MDG 245 mg/dl with intermittent hypoglycemia), glucagon and epinephrine counterregulation were reduced by 86 and 90%, respectively. Chronic iatrogenic hypoglycemia (MDG 52 mg/dl) further suppressed counterregulation. Prospective elimination of hypoglycemia (MDG 432 mg/dl) improved, but did not normalize hormonal counterregulation. In diabetic rats, the glucagon defect appeared to be specific for hypoglycemia, whereas deficient epinephrine secretion also occurred during hypovolemia. We concluded that both recurrent hypoglycemia and the diabetic state independently lead to defective hormonal counterregulation. These data suggest that in IDDM iatrogenic hypoglycemia magnifies preexisting counterregulatory defects, thereby increasing the risk of severe hypoglycemia.

Multiple alterations in insulin responses to glucose in islets from 48-h glucose-infused nondiabetic rats.

To examine the biochemical mechanisms by which hyperglycemia produces insulin secretory abnormalities, we studied isolated islets from control rats and rats infused for 48 h with a 50% glucose solution. To preserve the effects of in vivo hyperglycemia during in vitro handling for islet isolation, our standard isolation procedure utilized buffers containing 16.8 mM glucose. Islets from infused rats released similar amounts of insulin in low or high glucose during first incubations at 37 degrees C (92.4 +/- 7.0 ng.10 islets-1.45 min-1 at 2.8 mM, 84.4 +/- 4.1 ng.10 islets-1.45 min-1 at 16.8 mM) in contrast with control (uninfused) islets (18.6 +/- 2.8 ng.10 islets-1.45 min-1 at 2.8 mM and 109.8 +/- 8.0 ng.10 islets-1.45 min-1 at 16.8 mM glucose) (P less than 0.01). Secretion by islets of glucose-infused rats was lower during 60-min second incubations at 28 mM glucose than in first incubations of the same islets in low glucose (P less than 0.01). This phenomenon is comparable to the paradoxical hypersecretion observed during the first 10-15 min of exposure of glucose-infused pancreas to low-glucose perfusions. Paradoxical secretion in low glucose waned rapidly, so that during second incubations at 37 degrees C, little immunoreactive insulin release occurred at 2.8 mM glucose, despite the persistence of two additional lesions. The glucose-insulin dose-response curves in second incubations showed a leftward shift for glucose-infused islets, with two- to threefold higher secretion at 5.6-8.4 mM glucose than control islets. This is termed sensitization to glucose.(ABSTRACT TRUNCATED AT 250 WORDS)

Reversible impairment of glucose-induced insulin secretion in SHR/N-cp rats. Genetic model of type II diabetes.

The SHR/N-cp rat is a new genetically obese model for non-insulin-dependent diabetes mellitus. Expression of the diabetes is enhanced by a high-sucrose (54%) diet. After 4 wk on the diet, the cp/cp rats weigh significantly more than their +/? controls, have postprandial hyperglycemia (greater than 400 mg/dl), and are hyperinsulinemic, with immunoreactive insulin (IRI) levels 10- to 20-fold greater than controls. Total pancreatic IRI tends to be increased 1.6-fold in the cp/cp rats (although not significantly). There is no increase in pancreatic proinsulin content as a percent of total IRI. Studies of in vitro pancreatic function were carried out with the isolated nonrecirculating perfused pancreas method. The cp/cp rats (n = 10) showed impaired or absent IRI responses to 16.5 mM glucose, whereas +/? rats (n = 9) responded with classic biphasic curves. Comparison of insulin secreted in 20 min revealed a greater than 53% decrease in IRI secretion in cp/cp rats (P less than .05). A paradoxical hypersecretion of IRI at glucose concentrations of 0-2.7 mM was noted in cp/cp but not lean rats, i.e., 1.8 +/- 0.2 mU/min IRI in cp/cp rats vs. 0.04 +/- 0.007 mU/min in +/? rats. Perfusion of pancreases for 45 min with buffers containing no glucose resulted in restoration of a normal biphasic IRI response to 16.5 mM glucose in the cp/cp rats, whereas response in the lean rats was markedly reduced. Brisk IRI responses to 10 mM arginine in buffers with no glucose also occurred in cp/cp but not +/? rats. Glucagon secretion was relatively suppressed in the cp/cp rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Province of residence and active syphilis infection among Zambian men and women: new evidence from population-based data.

This study examined the risk factors for active syphilis infection in a subset of nationally-representative population-based survey of Zambian men and women. Syphilis prevalence was 6.5% for women = 2107) and 7.4% for men (N = 1745). In the multivariate model, province was a strong risk factor for active syphilis infection, with Copperbelt, Eastern, Luapula, Lusaka, North-Western and Western Provinces presenting significantly higher risk for women, and Copperbelt, Eastern and Lusaka Provinces presenting significantly higher risk for men compared to the Northern Province. In addition to province, age, education, age at first intercourse, marital status, history of genital sore or discharge, and having ever paid for sex were independent predictors of syphilis infection. Given the ongoing HIV-1 epidemic in Zambia, more aggressive diagnosis and treatment of active syphilis infections, particularly in high-risk provinces, are important strategies to reduce reproductive morbidity and curb HIV-1 transmission.

Antioxytocic and antiprostaglandin-releasing effects of oxytocin antagonists in pregnant rats and pregnant human myometrial strips.

There is now increasing evidence that both oxytocin (OT) and prostaglandin (PG) play a role in term as well as preterm labor. OT stimulates myometrial contractions and uterine PG release. Specific OT antagonists, therefore, may be of value in the treatment of preterm labor. Recently, we have synthesized two highly potent OT antagonists, [1-penicillamine, 4-threonine]OT ([Pen1, Thr4]OT) and [1-penicillamine, 2-phenylalanine, 4-threonine]OT ([Pen1, Phe2, Thr4]OT). We have determined their antioxytocic activity in 21- to 22-day-pregnant rats and on isolated human myometrial strips obtained from term pregnant patients at caesarean section for childbirth. We also studied their effects on PG synthesis and OT-stimulated PG synthesis on uterine slices from pregnant rats. We found that the two OT antagonists were effective inhibitors of the OT responses in pregnant rats and on pregnant human myometrial strips. The two OT antagonists had no agonistic activity on PG release at a dose range that was antioxytocic. When administered together with OT, the PG-releasing action of OT was inhibited. Thus, [Pen1, Thr4]OT and [Pen1, Phe2, Thr4]OT are effective inhibitors of both the uterotonic and PG-releasing actions of OT. The potentials of OT antagonists as tocolytic agents for the treatment of preterm labor should be explored.

Thyrotropin and prolactin responses to thyrotropin-releasing hormone in premenstrual syndrome.

Recent reports of altered TSH responsiveness to its releasing hormone (TRH) in women with premenstrual syndrome (PMS) suggested that subclinical hypothyroidism may be responsible for the mood changes, such as depression, that occur in these women. In this study we measured basal and TRH-stimulated serum TSH and PRL levels in 15 women with PMS and in 19 age-matched normal women. The mean baseline serum TSH concentrations were similar in the 2 groups in both the follicular [normal, 1.3 +/- 0.2 (+/- SE); PMS, 0.9 +/- 0.2 mU/L] and luteal (normal, 1.1 +/- 0.2; PMS, 1.1 +/- 0.2 mU/L) phases of the cycle. The mean baseline serum PRL levels also were similar in the 2 groups in the follicular (normal, 16 +/- 2; PMS, 13 +/- 2 micrograms/L) and luteal (normal, 13 +/- 2; PMS, 14 +/- 2 micrograms/L) phases of the cycle. After TRH administration, peak serum PRL and TSH levels were reached at 15 and 30 min, respectively, and the response curves were virtually identical in the 2 groups in both phases of the cycle. One normal woman had elevated basal and TRH-stimulated TSH concentrations compatible with subclinical hypothyroidism, but had normal noncyclic scores on her prospective rating scales. Our findings suggest that PMS is not associated with thyroid dysfunction or abnormal PRL secretion and that thyroid hormone replacement therapy is not indicated in this condition.

Heart transplantation after cardioverter-defibrillator implantation. A case control study.

A case control study was performed to determine whether previous implantable cardioverter-defibrillator (ICD) insertion adversely affects outcome after heart transplantation. Six male heart transplant recipients who had undergone ICD insertion 12 +/- 5 months before heart transplantation were compared to a cohort of six heart transplant recipients who were matched according to age, preoperative status and hemodynamics, date of transplantation, graft ischemic time, history of a previous cardiac operation, and duration of follow-up. There were no significant differences in operating room time, chest tube drainage, time to extubation, and the duration of intensive care unit or hospital stay between the two groups. Furthermore, there were no significant differences in the number of units of packed cells, fresh frozen plasma, platelets and cryoprecipitate transfused. The number of treated rejection episodes and the number of patients requiring intravenous antibiotics for infection in the first 90 days was identical between groups. It was concluded that heart transplantation after ICD implantation did not appear to carry more risk than heart transplantation after a previous cardiac operation. Our limited experience supports the potential use of the ICD in patients with life-threatening ventricular dysrhythmias who are awaiting transplantation.

Successful use of the "unacceptable" heart donor.

Chronic shortage of donor organs has heightened interest in new strategies for increasing donor availability. Unacceptable hearts for transplant have previously been characterized by donor age greater than 40 years, more than 20% donor/recipient weight mismatch, ischemic time more than 4 hours, and the presence of coronary artery disease. A series of 185 consecutive orthotopic heart transplants were retrospectively examined. A significant number of donor hearts used were unacceptable by one or more of the above criteria. Our current approach is to match donors to recipients using a wide range of criteria. Donors are now accepted from any location in North America. We have accepted donors more than 55 years of age and donors weighing less than 50% of the recipient's body weight. Because of the chronic shortage of donor organs, donor criteria have been effectively liberalized, thereby increasing the donor pool without compromising the overall results of heart transplantation.

Reduced incidence of severe infection after heart transplantation with low-intensity immunosuppression.

Despite advances in immunosuppressive therapy and prolonged graft and patient survival, infection after heart transplantation remains problematic. From January 1987 through June 1989, 104 heart transplantations were performed in 100 patients. Immunosuppression induction was by antilymphocyte globulin for 7 days, with oral cyclosporine introduced on stabilization of kidney function (day 3). Steroid therapy was rapidly tapered, and azathioprine was added only in cases of positive donor crossmatch or steroid-resistant rejection. No reverse isolation was used. Twenty-two deaths occurred, one from sepsis. Actuarial survival at 6 months, at 1 year, and at 2 years was 85% +/- 4%, 81% +/- 3%, and 75% +/- 4%, respectively. Fifty-four patients had 81 infections, of which 21 were bacterial; 83% of these episodes were treated. Sixty infections were opportunistic (85% viral), and only 23% necessitated treatment. Actuarial infection-free rates (all types necessitating treatment) at 1 month, at 6 months, and at 2 years were 83% +/- 4%, 75% +/- 5%, and 75% +/- 5%, respectively. Of the 100 transplant recipients, 66% were treated with azathioprine; 47 patients (69%) had an infection, whereas only seven (19%) of the patients not receiving azathioprine became infected (p less than 0.00001). Rejection was noted in 66% of patients, with a median time to the first episode of 4 weeks. A low-intensity immunosuppressive regimen has resulted in fewer serious infections, with acceptable graft loss from rejection. Increased infection surveillance is required for the first 30 days postoperatively and after treatment of rejection episodes.

A prospective randomized controlled trial of initial immunosuppression with ALG versus OKT3 in recipients of cardiac allografts.

Thirty-nine heart transplant recipients were randomized prospectively to receive OKT3 or antilymphoblast globulin (ALG) for 7 days, having otherwise identical protocols (group 1: OKT3, n = 20 patients; group 2: ALG, n = 19 patients). No preoperative immunosuppression was given. The protocol consisted of methylprednisolone, 500 mg intraoperatively, followed by 1 mg/kg/day, intravenously or orally, tapering to 0.2 mg/kg/day at 1 month; oral cyclosporine starting 3 to 5 days after transplantation; selective use of azathioprine, 1 to 4 mg/kg/day; and either OKT3, 5 mg/day for 7 days, or ALG, 15 mg/kg/day for 7 days. Of the 39 patients in the study, 34 are alive 6 months to 2 years after transplantation. The actuarial survival at 2 years for the OKT3 and ALG groups was 92% (+/- 0.07%) and 83% (+/- 0.09%), respectively (not significant [NS]). The time to first rejection for group 1 was 5.6 weeks and for group 2 was 5.3 weeks (NS). The mean number of rejections for group 1 and group 2 was 2.1 episodes per patient and 1.4 per patient, respectively (NS). Three patients in each group were free of rejection at 6 months. The total number of infections at 6 months was 1.05 per patient in group 1, 0.74 per patient in group 2 (NS), with 35% of patients receiving OKT3 and 52% of patients receiving ALG actuarially free of infection by 6 months after surgery (NS). During the first 24 hours after surgery, no significant differences were noted in mean blood pressure, central venous pressure, or Po2 between the groups.(ABSTRACT TRUNCATED AT 250 WORDS)