Biomedical subjects

R Greco

Publications and source records attributed to R Greco.

At least 37 records · Page 2Linked to original sources

PubMed2000

Increased bone turnover in epileptic patients treated with carbamazepine.

Bone turnover has been investigated in 12 epileptic patients before and after treatment with carbamazepine and in 15 sex- and age-matched control subjects. We found higher values of markers of bone formation (serum bone alkaline phosphatase, osteocalcin, and propeptides of types I and III procollagen) and of bone resorption (serum telopeptide of type I collagen and urine N-telopeptides of type I collagen) in patients than in controls. Our study demonstrates that carbamazepine induces an increase of bone turnover.

Adolescent↗

PubMed2000

Pulmonary venous flow and mitral inflow velocity pattern in uncomplicated obesity: evidence for late diastolic dysfunction.

BACKGROUND: Active left ventricular relaxation, assessed by Doppler isovolumic relaxation time, is impaired in obesity. There is little information on left ventricular passive properties during filling. METHODS: To evaluate left ventricular late diastolic stiffness in obesity, Doppler echocardiographic interrogation of mitral inflow tract and pulmonary vein flow velocities were obtained from 47 normotensive, young obese subjects (11 males, 36 females) and 43 normotensive, young normal-weight volunteers (13 males, 30 females) of comparable age. RESULTS: After controlling the effect of blood pressure and left ventricular mass, isovolumic relaxation time was prolonged in obese subjects (p < 0.0001 vs normal-weight controls). No difference was found in transmitral peak early and late flow velocities. Obese subjects exhibited prolonged pulmonary vein reverse flow velocity during atrial contraction (p < 0.004), and a higher difference or ratio between duration of pulmonary reverse flow and duration of transmitral forward late flow (6 +/- 31 vs -20 +/- 39 ms or 1.06 +/- 0.3 vs 0.84 +/- 0.3, p < 0.002 and p < 0.001, respectively). These differences were also confirmed after controlling blood pressure and left ventricular mass. Non-invasively estimated left ventricular end-diastolic pressure was higher in obese subjects than in controls (p < 0.002). At multivariate analysis a higher body mass index was the sole predictor of prolonged difference between duration of pulmonary reverse flow and duration of transmitral forward late flow (beta = 0.38, p < 0.001). CONCLUSIONS: Obesity is associated with prolonged left ventricular active relaxation and abnormalities of filling pressure not detectable by the sole mitral inflow velocity pattern. These latter abnormalities are consistent with the presence of early increased left ventricular passive stiffness.

Adult↗

PubMed2000

Cardiac abnormalities in type 1 diabetes.

BACKGROUND: Left ventricular (LV) structural and hemodynamic consequences of type 1 diabetes mellitus are not fully understood. METHODS: To evaluate LV geometry, systolic and diastolic function in type 1 diabetes, Doppler echocardiograms were performed in 40 normotensive, type 1 diabetic patients without coronary heart disease or valvular lesions (22 men, 18 women, mean age 43 +/- 6 years, body mass index 24.7 +/- 2.8 kg/m2) and in 40 age and sex-matched non-diabetic normotensive controls (22 men, 18 women, mean age 43 +/- 5 years, body mass index 23.2 +/- 2.8 kg/m2), in a case-control design. RESULTS: Patients had higher systolic blood pressure than controls (p < 0.03) and comparable diastolic blood pressure and heart rate. LV dimension and mass were higher in patients than in controls (both p < 0.0001) whereas relative wall thickness did not differ. For comparable levels of end-systolic stress, patients exhibited a higher ejection fraction than controls (p < 0.01) and normal midwall shortening. Cardiac output was also higher (p < 0.001), whereas total peripheral resistance was lower in patients than in controls (p < 0.0001). Isovolumic relaxation time and E deceleration were prolonged in patients and peak A velocity was greater than in controls (all p < 0.01), whereas the difference in duration between A and pulmonary vein peak reverse flow at atrial contraction was comparable. In subgroup analyses, all reported features were independent of a) presence of target organ damage; b) duration of disease; c) levels of glycosylated hemoglobin. CONCLUSIONS: In normotensive patients with type 1 diabetes: 1) there was a moderate increase in LV mass; 2) LV chamber function was supernormal and wall mechanics was normal; 3) LV active relaxation was impaired but chamber stiffness was normal.

Adult↗

PubMed1999

Apoptosis of Caco-2 intestinal cells invaded by Listeria monocytogenes: protective effect of lactoferrin.

The apoptosis of infected hepatocytes is a critical step in nonspecific defense against Listeria monocytogenes infection. We have observed that infection by L. monocytogenes in enterocyte-like cells (Caco-2) results in apoptosis. However, a large fraction of infected intestinal epithelial cells escape from cellular condensation and fragmentation, typical of programmed cell death, and become necrotic. The balance between apoptosis and necrosis seems to be influenced by the number of internalized bacteria. The presence of 1 mg/ml of bovine lactoferrin, an iron-binding protein, added to monolayers before the bacterial infection, decreases the number of internalized bacteria and therefore the overall number of dead cells, and, more importantly, all dead cells are killed by apoptosis and not necrosis.

Animals↗

PubMed1999

Carnitine deficiency and hyperammonemia in children receiving valproic acid with and without other anticonvulsant drugs.

Plasma ammonia and total and free carnitine were measured in 84 children requiring anticonvulsant drugs: 32 patients (group A) on valproic acid alone, 28 children (group B) on polytherapy including valproic acid, and 24 patients (group C) on polytherapy without valproic acid. The other anticonvulsant drugs used in groups B and C were carbamazepine and phenobarbital. Plasma ammonia concentrations were elevated in both group A and B compared with controls. Group B patients showed significantly higher hyperammonemia than group A (59.9 +/- 16.3 micrograms/dl vs. 36.7 +/- 12.4 micrograms/dl; P < 0.05). Group C patients had plasma ammonia levels similar to those of controls (31.1 +/- 14.7 micrograms/dl vs. 29.7 +/- 12.1 micrograms/dl; NS). In both group A and group B patients, plasma ammonia levels were correlated with the valproic acid dosage (r = 0.32, P < 0.01) and with serum concentrations of valproic acid (r = 0.41, P < 0.001). Moreover, a significant correlation between plasma ammonia and duration of valproic acid therapy was found in the patients as a whole (r = 0.31, P < 0.01). Plasma total and free carnitine concentrations were significantly reduced in groups A and B (total carnitine 36.9 +/- 6.9 mumol/l vs. 32.9 +/- 9.7 mumol/l; free carnitine 28.9 +/- 5.1 mumol/l vs. 25.7 +/- 4.3 mumol/l, respectively) compared with group C patients who did not receive valproic acid and in whom values were similar to controls (total carnitine 46.1 +/- 9.0 mumol/l vs. 47.7 +/- 10.1 mumol/l; free carnitine 40.1 +/- 7.1 mumol/l vs. 42.9 +/- 8.0 mumol/l, respectively). Twenty-eight patients (18 of group A and 10 of group B) were re-evaluated and showed a complete normalization of plasma ammonia, and total and free carnitine levels which were similar to controls. Our data suggest that hyperammonemia is an important problem in patients receiving valproic acid, particularly in association with other anticonvulsant drugs. This increase of plasma ammonia and the concomitant reduction of carnitine seem to be transient and completely reversible.

Adolescent↗

PubMed1999

Lung transplantation from ventilated non-heart-beating donors: experimental study in a neonatal swine model.

BACKGROUND/PURPOSE: A shortage of transplantable lungs is a constant and frustrating reality. The use of organs retrieved from ventilated non-heart-beating donors (VNHBD) may alleviate this problem. The purpose of this work was to assess lung function of donor grafts subjected to different time lengths of in situ warm ischemia (WIT). METHODS: Twenty piglets weighing between 6 and 8 kg were allocated randomly to the following study groups: Sham (n = 5), heart-beating donors, non warm ischemia; I-30 (n = 5), I-60 (n = 5) and I-90 (n = 5), VNHBD-WIT of 30, 60, and 90 minutes, respectively. Recipients were rendered dependent on the single left transplanted lung by clamping right pulmonary artery and bronchus 1 hour after transplantation. Assessment of pulmonary function was monitored hourly by hemodynamic, oxygenation, and pulmonary mechanic measurements during a period of 6 hours after reperfusion. Lung grafts were weighed pre- and posttransplantation. RESULTS: Final mean lung weight was significantly greater in VNHBD (92.5+/-3.1 v Sham values 75.6 g+/-2.4; P < .01). Cold ischemic time averaged 80.1+/-2.7 minutes. After right lung exclusion, hemodynamic changes consisted of a sustained increase in pulmonary vascular resistance and a reduction in cardiac output. Lung mechanics also deteriorated with a gradual rise in airway resistance and a fall in compliance. CONCLUSIONS: These data suggest that posttransplantation lung graft function from VNHBD with up to 90 minutes of WIT, is preserved and equivalent to those achieved by grafts harvested after heart-beating donation.

Analysis of Variance↗

PubMed1999

Platelet count and function in children receiving sodium valproate.

To evaluate whether valproic acid (VPA) can cause thrombocytopenia and impaired platelet function, the authors prospectively studied 20 children (12 female and eight male; age range 4.9-9.2 years) before and after 6 months of VPA monotherapy. Fifteen healthy sex- and age-matched children served as control subjects. VPA was prescribed at normal dosages (19.7 +/- 9.9 mg/kg), and plasma levels were within the therapeutic range (60.1 +/- 16.5 microg/mL). At the first evaluation, no significant difference between patients and control subjects was observed for platelet count and function. At the second evaluation the platelet counts were significantly lower in the patients (194,200 +/- 37,800/microL; range 157,700-222,400) than in the control subjects (291,100 +/- 41,300/microL; range 261,000-332,500; P < 0.01). Significant differences occurred between patients and control subjects in the release of adenosine triphosphate (ATP) after collagen and adenosine diphosphate (ADP) stimuli and in aggregation after stimulation with collagen, ADP, and arachidonic acid. Significant correlations between platelet count, aggregation, and ATP release and VPA dosage and plasma concentration were also observed. VPA can cause a decreased platelet count and aggregation and ATP release impairment. These side effects can appear after a few months of therapy and with plasma valproate levels within the normal range. They do not seem to be associated with clinical symptoms, and drug discontinuation is not necessary.

Adenosine Triphosphate↗

PubMed1999

Porins and lipopolysaccharide (LPS) from Salmonella typhimurium induce leucocyte transmigration through human endothelial cells in vitro.

Bacteria or bacterial products may constitute important inducers of surface molecule expression on endothelial cells and leucocytes. This study was undertaken to determine the effects of the Salmonella typhimurium porins, LPS-S and LPS-R on the transendothelial migration of leucocytes through human umbilical vein endothelial cells (HUVEC). Treatment of the HUVEC with either porins or LPS-S or LPS-R increased the transmigration of different leucocyte populations, in particular that of neutrophils. The maximal increase occurred using LPS-S treatment, whereas porin stimulation fell between LPS-S and LPS-R. The transmigration increase was dose-dependent and reached its maximum at about 100-1000 ng/ml of stimulus. Optimal endothelial activation occurred after 2-4 h and 4-6 h using LPS and porin, respectively. Stimulation of leucocytes with either porins or LPS slightly increased their transmigration through non-activated endothelial cells. Transmigration increased remarkably during the simultaneous stimulation of endothelial cells by IL-1ss together with either porins or LPS. To assess participation of E-selectin, intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and leucocyte adhesion complex (CD11/18) in porin- or LPS-mediated leucocyte migration, blocking MoAbs were used. Each blocking MoAb partially and selectively decreased leucocyte transmigration. The obtained results contribute to clarify some aspects of the inflammatory process at sites of infection.

Antibodies, Monoclonal↗

PubMed1999

Centro-temporal spikes in non-epileptic children: a long-term follow up.

OBJECTIVE: This study was undertaken in order to determine the natural evolution of centro-temporal spikes (CTS) in a healthy paediatric population. METHODOLOGY: Forty children and adolescents (mean age +/- SD: 9.9 +/- 4.1 years) with non-epileptic disturbances (tics, headache, pavor nocturnus, vertigo, etc), who showed CTS during routine EEG recordings were studied. No patient suffered from seizures. A clinical and electroencephalographic follow-up of at least 5.5 years was carried out in all subjects. RESULTS: At the follow-up examination, 33 of the 40 cases (82.5%) had no CTS or other epileptic discharges in awake and sleep EEGs, while six subjects continued to show CTS discharges in sleep EEG. Among those subjects who showed persistence of CTS in sleep EEG, rolandic epilepsy developed in two cases, while all other subjects continued to be seizure free. CONCLUSIONS: This study demonstrates that CTS can be present in non-epileptic children and adolescents; in the majority of subjects this EEG abnormality disappears spontaneously and only a small percentage of subjects who have persistence of this pattern develops rolandic epilepsy.

Action Potentials↗

PubMed1999

31-43 amino acid sequence of the alpha-gliadin induces anti-endomysial antibody production during in vitro challenge.

BACKGROUND: Wheat gliadin is the culprit antigen of coeliac disease (CD). Two short sequences of NH2-terminal portion of gliadin seem to be responsible for CD. Antiendomysial antibodies (EMA), highly sensitive and specific for CD, are detectable in the culture media from treated CD patients, after in vitro challenge with peptic-tryptic (PT) digest of gliadin. In this study we detected EMA production after in vitro challenge with 31-43 peptide. We used 56-68 peptide, lacking toxic sequences, as a negative control. METHODS: Duodenal samples from 11 treated CD patients and 9 control patients were cultured with 31-43 and 56-68 peptides and PT gliadin. Indirect immunofluorescence analysis was used for EMA detection. RESULTS: EMA were detected in culture media of 10 of 11 specimens challenged with PT-gliadin and in the media of all specimens challenged with 31-43 peptide. No EMA were detectable in any treated patients cultured with 56-68 peptide or with medium alone. No EMA were observed in cultures of control specimens. DISCUSSION: The ability of the 31-43 sequence of the alpha-gliadin to induce EMA production suggests its involvement in the pathogenesis of CD. Furthermore, it may be a more useful antigenic substance than PT gliadin for both in vitro and in vivo studies of CD.

Adult↗

PubMed1999

Function search in a large transcription factor gene family in Arabidopsis: assessing the potential of reverse genetics to identify insertional mutations in R2R3 MYB genes.

More than 92 genes encoding MYB transcription factors of the R2R3 class have been described in Arabidopsis. The functions of a few members of this large gene family have been described, indicating important roles for R2R3 MYB transcription factors in the regulation of secondary metabolism, cell shape, and disease resistance, and in responses to growth regulators and stresses. For the majority of the genes in this family, however, little functional information is available. As the first step to characterizing these genes functionally, the sequences of >90 family members, and the map positions and expression profiles of >60 members, have been determined previously. An important second step in the functional analysis of the MYB family, through a process of reverse genetics that entails the isolation of insertion mutants, is described here. For this purpose, a variety of gene disruption resources has been used, including T-DNA-insertion populations and three distinct populations that harbor transposon insertions. We report the isolation of 47 insertions into 36 distinct MYB genes by screening a total of 73 genes. These defined insertion lines will provide the foundation for subsequent detailed functional analyses for the assignment of specific functions to individual members of the R2R3 MYB gene family.

Arabidopsis↗

PubMed1999

Epilepsy with myoclonic absences with early onset: a follow-up study.

We studied six children (four girls and two boys) suffering from cryptogenic myoclonic absence seizures with early onset. The age at onset of the seizures ranged between 6 and 27.8 months (mean age +/- SD: 18.5+/-12.4 months). The neurologic evaluation was normal in all patients at the first hospital admission. After the diagnosis, we followed up all children for at least 5 years. At the end of follow-up, two of these patients (a girl and a boy) showed severe mental retardation, a high number (from one to three per day) of seizures, and persistent pathologic electroencephalograms. The other patients showed normal electroencephalograms: all of them were seizure free and without mental retardation. The two patients with mental retardation have been treated with polytherapy. In all other children we used valproate alone successfully. Our data suggest that myoclonic absence seizures with early onset can have a good long-term prognosis. Valproate is a useful anticonvulsant drug in these patients. Mental retardation is present only in patients with poor seizure control.

Anticonvulsants↗

PubMed1999

[Hemodynamics and oxygenation in experimental lung lobe transplantation].

INTRODUCTION: Lung transplantation is the only valid treatment for the severe neonatal pulmonary hypoplasia. The objective of this work is to develop and to establish a model of lobar lung transplantation. MATERIAL AND METHODS: Twenty pigs were used. Neonates 2-3 weeks; adults 10-12 weeks. Donors weighed 15 to 20 kg and recipients 5 to 7. In Group A animals were used to assess surgical anatomy and to develop surgical technique and instrumentation's model. The remainder animals (Group B) underwent left lobar lung transplantation. Hemodynamic and oxygenation data were collected before and after six hours of right lung exclusion. RESULTS: All animals tolerated right lung exclusion. There was a significant increase in mean pulmonary artery pressure and a sustained reduction in cardiac output. Oxygenation values were not affected during unilateral lung perfusion. CONCLUSIONS: The neonatal pig has a good tolerance to reduced-size lung transplantation. Lobar lung transplantation could increase substantially the donor's lung pool.

Animals↗

PubMed1999

Phospholipase A2 enzymes regulate alpha IIb beta3-mediated, but not Fc gammaRII receptor-mediated, pp125FAK phosphorylation in platelets.

The alphaII(b)beta3 integrin and FcgammaRII receptors mediate, respectively, platelet adhesion and spreading on fibrinogen and immunoglobulin (IgG) coated surfaces. Platelet adhesion to fibrinogen resulted in a partial conversion of the faster to the slower migrating (phosphorylated) form of Ca(+2)-sensitive cytosolic phospholipase A2(cPLA2) but failed to trigger arachidonic acid (AA) release. Full mobility shift of cPLA2 and a massive release of AA release were stimulated by platelet adhesion to IgG or addition of thrombin to the fibrinogen adherent platelets. IgG and thrombin induced AA production were blocked by methyl arachidonyl fluorophosphonate (MAFP), an irreversible inhibitor of cPLA2 and the Ca(+2)-independent phospholipase A2 (iPLA2). In contrast, bromoenol lactone (BEL), a specific inhibitor of iPLA2 had no effect on the release of AA. MAFP and BEL prevented pp125FAK phosphorylation and platelet spreading on fibrinogen having no effect on pp125FAK phosphorylation or platelet spreading on immobilized IgG. We conclude that alpha(IIb)beta3-mediated pp125FAK phosphorylation and platelet spreading on fibrinogen are regulated by PLA2 enzymes.

Arachidonic Acid↗

PubMed1999

[Extracorporeal respiratory assistance (ECRA): initial experiences in Spain].

UNLABELLED: The attendance respiratory extracorporeal (AREC) is an oxygenation form for membrane extracorporeal with flow tidal and veno-venous cannula described by Chevalier et al. in 1990. We present our clinical experience so much with AREC in system veno-venous flow tidal as veno-arterial. From october of 1997 until the present time we have treated three patients by means AREC, in two patients with veno-venous system and in one veno-arterial. In all the cases bomb Collin-Cardio has been used with bladder for flow tidal and membrane of oxygenation of 0.8 m2, being inserted a system of alternative clamp of the branches of the circuit. The system AREC has been used in two patients with congenial diaphragmatic hernia, right in a case and left in the other one. The gestational age was of 38 and 36 weeks with a weight of 3,200 and 2,900 grams. Both patients were remitted from other centers by failure of the conventional treatment. In both cases the indication of AREC was the sharp deterioration of the general state with failure of the conservative treatment, being the previous oxygenation index of 109 and 112. The third patient precised veno-arterial AREC for ventricular failure during the correction of the congenital heart disease, this patient was 5 month old and the weight was 5,000 grams. The duration of AREC in the cases of congenital diaphragmatic hernia was of 14 and 10 days. In a patient the diaphragmatic hernia was corrected at the 55 hours of being in AREC. In the second case the hernia had been surgical corrected in another center. The exit of AREC in both cases carries out after a discreet improvement of the lung function. Both patients died at the 24 and 48 hours of the decannulation for cerebral hemorrhage and respiratory failure. The third patient stayed stable in veno-arterial AREC during 4 days, with hemodynamic support of 130 ml/kg/min, retiring the support to present absence of cerebral activity. CONCLUSIONS: With the derived limitations of the extreme severity of the treated cases and the current phase of beginning of the AREC team, we think that it is a useful and available technique in our country, for the handling of patient with cardiorespiratory failure while waiting for improvement of their base pathology.

Age Factors↗

PubMed1998

Overexpression of a hydrogen peroxide-resistant periplasmic Cu,Zn superoxide dismutase protects Escherichia coli from macrophage killing.

We have studied the effect of H2O2 on the activity of the Escherichia coli Cu,ZnSOD showing that, unlike the bovine enzyme, this bacterial Cu,ZnSOD is highly resistant to inactivation by hydrogen peroxide. In view of the key role played by oxygen radicals in bacterial killing by phagocytes, we have tested the ability of E. coli strains expressing different amounts of Cu,ZnSOD in the periplasmic space to survive the phagocytic attack of activated macrophages. Overexpression of the enzyme effectively protected the bacterial cell from macrophage killing. The results obtained support the hypothesis that in pathogenic bacteria periplasmic Cu,ZnSOD may reduce the oxyradical damages induced by the respiratory burst and therefore be important in virulence.

Animals↗

PubMed1998

Different bronchial responsiveness to Ach between normal and OA-sensitized guinea pigs after acoustic stress: a role for adenosine.

Noise-exposure makes non-sensitized guinea pigs hyporesponsive to Acetylcholine (Ach), while in Ovalbumin (OA)-sensitized guinea pigs the responsiveness to the cholinergic mediator is not modified by acoustic stress (Nieri et al., 1996). The occurrence of bronchial hyporesponsiveness after acoustic stress in non-sensitized guinea pigs was verified also with histamine, obtaining a result similar to that observed with Ach. Moreover, the role of adenosine as modulator of the bronchial responsiveness to Ach after noise-exposure was assessed both in normal and in sensitized guinea pigs. In non-sensitized noise-exposed guinea pigs, the hyporesponsiveness to Ach was abolished by pretreatment of the animals with the peripheral A1/A2 antagonist 8-p-(sulfophenyl)theophylline (8-pSPT, 3 mg/kg i.v.) or with the A2-selective blocker 3,7-dimethyl-1-propargylxanthine (DMPX, 80 microg/kg i.v.) but not with the A1-selective antagonist Xanthine Amine Congener (XAC, 0.1 mg/kg i.v.). In sensitized guinea pigs, pretreatment with theophylline (25 mg/kg i.v.) makes noise-exposed animals again hyporesponsive to Ach, while no effect was obtained with the selective A1 and A2 antagonists employed. Also enprofylline (10 mg/kg i.v.), a phosphodiesterase inhibitor more potent than theophylline, does not modify the responsiveness to Ach in sensitized noise-exposed guinea pigs. The overall data presented suggest the involvement of the peripheral purinergic system in the regulation of airway reactivity after the stressful condition and indicate an altered functionality of this system as a consequence of sensitization. Furthermore, noise-exposure makes it possible to reveal in guinea pigs an opposite influence by theophylline on airway responsiveness to Ach, in sensitized, with respect to normal, animals.

Acetylcholine↗

PubMed1998

Warm ischemic time tolerance after ventilated non-heart-beating lung donation in piglets.

OBJECTIVE: The availability of lungs for transplantation could be ameliorated with the use of organs retrieved from ventilated non-heart-beating donors (VNHBD). The aim of this work is to determine the limit to tolerable in situ warm ischemia time (WIT) for lung grafts after circulation is stopped. METHODS: Twenty piglets underwent left lung allotransplantation. Animals were randomly allocated based on the donor's status before lung harvesting into the following study groups: Sham (n = 5), Heart-beating donors-non-warm ischemia; I-30 (n = 5), I-60 (n = 5) and I-90 (n = 5), VNHBD-WIT of 30, 60 and 90 min, respectively. Right pulmonary artery and bronchus were permanently occluded one hour after transplantation. Assessment of pulmonary function was monitored hourly by hemodynamic, oxygenation and pulmonary mechanic measurements during a period of 6 h after reperfusion. Lung grafts were weighed pre- and post-transplantation. RESULTS: Cold ischemic time was similar for all groups, and averaged 80.1+/-2.7 min. Final mean lung weight was significantly greater in VNHBD (92.5+/-3.1 g vs. Sham values 75.6+/-2.4 g, P < 0.01). After right lung exclusion, hemodynamic changes consisted of a sustained increase in pulmonary vascular resistance and a reduction in cardiac output. Lung mechanics also modified, with a rise in airway resistance and a fall in compliance. CONCLUSIONS: Post-transplantation lung graft function from VNHBD with up to 90 min of WIT, is equivalent to those achieved by grafts harvested after heart-beating donation. This method may be a promising strategy of increasing the pulmonary donor pool.

Animals↗