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R G Johnson

Publications and source records attributed to R G Johnson.

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

Effects of subtype-selective and balanced angiotensin II receptor antagonists in a porcine coronary artery model of vascular restenosis.

BACKGROUND: Numerous studies have demonstrated the ability of angiotensin II (Ang II) receptor antagonists and angiotensin-converting enzyme (ACE) inhibitors to inhibit intimal hyperplasia after balloon dilation of noncoronary arteries in small-animal models, suggesting an important role for Ang II in the response to injury. Although ACE inhibitors have not been similarly effective in nonhuman coronary models or in human restenosis trials, questions remain regarding the efficacy ACE inhibitors against tissue ACE and the contributions of ACE-independent pathways of Ang II generation. Unlike ACE inhibitors, Ang II receptor antagonists have the potential to inhibit responses to Ang II independent of its biosynthetic origin. METHODS AND RESULTS: In separate studies, three Ang II receptor antagonists, including AT1 selective (L-158,809), balanced AT1/AT2 (L-163,082), and AT2 selective (L-164,282) agents, were evaluated for their ability to inhibit vascular intimal thickening in a porcine coronary artery model of vascular injury. Preliminary studies in a rat carotid artery model revealed that constant infusion of L-158,809 (0.3 or 1.0 mg X kg-1 X d-1) reduced the neointimal cross-sectional area by up to 37% measured 14 days after balloon dilatation. In the porcine studies, animals were treated with vehicle or test compound beginning 2 days before and extending 28 days after experimental angioplasty. Left anterior descending, left circumflex, and/or right coronary arteries were injured by inflation of commercially available angioplasty balloons with placement of coiled metallic stents. Infusion of L-158,809 (1 mg X kg-1 X d-1), L-163,082 (1 mg X kg-1 X d-1), or L-164,282 (1.5 mg X kg-1 X d-1) in the study animals yielded plasma drug levels sufficient either to chronically block or, for L-164,282, to spare pressor responses to exogenous Ang II. Neither L-158,809, L-163,082, nor L-164,282 had statistically significant effects (P=.12, P=.75, and P=.48, respectively, compared with vehicle-treated controls) on neointimal thickness (normalized for degree of injury) measured by morphometric analysis at day 28 after angioplasty. CONCLUSIONS: These findings indicate that chronic blockade of Ang II receptors by either site-selective or balanced AT1/AT2 antagonists is insufficient to inhibit intimal hyperplasia after experimental coronary vascular injury in the pig. The results further suggest that, unlike in the rat carotid artery, Ang II is not a major mediator of intimal thickening in the pig coronary artery.

Angiotensin II↗
PubMed1996

Biochemical and biophysical comparison of native and chemically synthesized phospholamban and a monomeric phospholamban analog.

Phospholamban (PLB) was rapidly isolated from canine cardiac sarcoplasmic reticulum using immunoaffinity chromatography and prepared by solid phase peptide synthesis. The two proteins are indistinguishable when analyzed by SDS-polyacrylamide gel electrophoresis and exhibit pentameric oligomeric states. They are similarly detected on Western blots, are phosphorylation substrates, have identical amino acid compositions that directly reflect their predicted values, yield the same internal amino acid sequences upon CNBr digestion, and have molecular mass values agreeing with the expected value (approximately 6123 Da). Native and synthetic PLB reduced the calcium sensitivity of Ca2+ATPase, which is reversed by anti-PLB antibody. A Cys-to-Ser PLB analog, where the cysteines (36, 41, and 46) were substituted by serines, is monomeric on SDS-polyacrylamide gel electrophoresis, can be phosphorylated, and is recognized by polyclonal antisera. PLB migrates with a sedimentation coefficient of 4.8 S in sedimentation velocity ultracentrifugation experiments, whereas Cys-to-Ser PLB does not sediment, consistent with a monomeric state. Circular dichroism spectral analysis of PLB indicates about 70% alpha-helical structure, whereas Cys-to-Ser PLB manifests only about 30%. Because the physiochemical properties of native and synthetic PLB appear identical, the more readily available synthetic protein should be suitable for more extensive structural studies.

Adenosine Triphosphatases↗
PubMed1996

Interaction of cardiotonic thiadiazinone derivatives with cardiac troponin C.

The cardiotonic effects of thiadiazinone derivative EMD 57033 are mediated by direct actions on myofilaments (Lues, I., Beier, N., Jonas, R., Klockow, M., and Haeusler, G. J. (1993) Cardiovasc. Pharmacol. 21, 883-892). Cardiac troponin C has been postulated to be a potential target of the drug (White, J., Lee, J. A., Shah, N., and Orchard, C. H. (1993) Circ. Res. 73, 61-70). This study tested whether EMD 57033 interacts directly with recombinant human cardiac TnC (hcTnC). EMD 57033 caused concentration-dependent quenching of tyrosine (Tyr) fluorescence of hcTnC in the presence of Ca2+ (100 microM) and little change of the fluorescence in the presence of Mg2+ (2 mM). Kd for the drug-hcTnC interaction in the presence of Ca2+, determined by Tyr fluorescence titrations, was approximately 40 microM. The binding of EMD 57033 was stereo-selective: the optical isomer of EMD 57033 bound hcTnC much more weakly. The Ca2+ dependence and stereo-selectivity of EMD 57033 binding were substantiated by a dialysis-based direct binding assay. EMD 57033 was found to interfere with Ca(2+)-dependent binding of hydrophobic probe 1,1'-bi-(4-anili-no)naphthalene-5,5'-disulfonate (bis-ANS) to hcTnC. The relationships between [Ca2+] and Tyr fluorescence of hcTnC and between [Ca2+] and bis-ANS fluorescence in the presence of hcTnC were substantially altered by EMD 57033 in the range of [Ca2+] where Ca2+/Mg2+ sites of hcTnC were titrated by Ca2+. EMD 57033 was found to bind as tightly to 2 Ca2+.hcTnC as to 3 Ca(2+).hcTnC. These observations were interpreted as indicating that a EMD 57033-binding site is induced by Ca2+ binding, but not Mg2+ binding, to the Ca2+/Mg2+ sites of hcTnC. The drug-binding site most likely resides in the carboxyl domain of hcTnC.

Base Sequence↗
PubMed1996

Percutaneous occlusion of an iatrogenic aortosaphenous vein--coronary vein fistula via retrograde coronary sinus approach.

Inadvertent aortosaphenous vein graft-coronary vein anastomosis during coronary bypass surgery is an uncommon complication. We describe a case of aortosaphenous vein side-to-side anastomosis to an obtuse marginal vein resulting in a large arteriovenous fistula and elective closure, using embolization coils delivered percutaneously via the coronary sinus. The clinical findings, interventional procedure, and follow-up are also presented, with a discussion of alternative techniques used previously to treat iatrogenic aortosaphenous vein graft venous fistulae.

Aged↗
PubMed1996

Effects of neonatal dopamine depletion on sensory inhibition in the rat.

Central dopamine systems appear to play an important role in sensory information processing. In particular, the filtering (or gating) of repetitive auditory stimuli is modulated by pharmacological manipulations that affect dopaminergic neurotransmission. The present study further addressed the role of dopamine in auditory gating. Three-day-old male Sprague-Dawley rats, pretreated with desipramine, received intracisternal injections of 6-hydroxydopamine (6-OHDA; 75 micrograms in 10 microliters) or the vehicle. At 4 months of age the rats were implanted for evoked potential recording and auditory gating was assessed using a paired click paradigm. Neonatally administered 6-OHDA did not alter gating in the adult rats. However, unlike for the control group, systemic amphetamine (1.83 mg/kg, IP) failed to disrupt gating in the treated rats. Apomorphine (1.0 mg/kg, SC) disrupted gating in both groups. Neonatal 6-OHDA treatment caused significant reductions in dopamine levels in the striatum, nucleus accumbens, and substantia nigra/ventral tegmental regions. There was an inverse relationship between substantia nigra/ ventral tegmental area dopamine levels and auditory gating. Overall, the results suggest that amphetamine-induced auditory gating loss requires presynaptic dopamine release, but that the deficiency occurs through postsynaptic dopamine receptor activation.

Animals↗
PubMed1996

Changes in autonomic response of the cerebral circulation after normothermic extracorporeal circulation.

Patients who undergo cardiopulmonary bypass frequently have neuropsychologic dysfunction. This study was undertaken to determine whether altered cerebral perfusion and vascular responses may in part lead to these neuropsychologic changes. Pigs were placed on normothermic cardiopulmonary bypass for 2 hours. Basal cerebral blood flow and in vivo responses to administration by internal carotid artery of neuronally released vasoactive substances were evaluated before and 5 to 15 minutes after termination of cardiopulmonary bypass. Another group of pigs were placed on cardiopulmonary bypass for 2 hours and then perfused off bypass for 1 additional hour. In vitro responses of cerebral arterial microvessels (100 to 175 microns) from both groups were examined in a pressurized (40 mm Hg) no-flow state with videomicroscopy. Vessels from uninstrumented pigs served as control preparations for in vitro studies. Cerebrovascular resistance and cerebral perfusion were maintained constant during cardiopulmonary bypass and after separation from bypass. The internal carotid artery infusion of acetylcholine (cholinergic agonist) caused increased internal carotid artery blood flow before cardiopulmonary bypass but decreased blood flow after cardiopulmonary bypass. After 2 hours of cardiopulmonary bypass, the increase in internal carotid artery blood flow induced by isoproterenol (a beta-adrenoceptor agonist) was reduced, whereas the response to sodium nitroprusside (a guanylate cyclase activator) was unchanged. In vitro acetylcholine-induced microvascular vasodilation was converted to a contractile response and isoproterenol elicited less relaxation after 2 hours of cardiopulmonary bypass. One hour of cerebral perfusion after cardiopulmonary bypass caused a further reduction in isoproterenol-induced relaxation but had no further effect on the cholinergically mediated response. In vitro relaxation responses to sodium nitroprusside and forskolin (an adenylate cyclase activator) were similar in all experimental groups, suggesting that second-messenger mechanisms remain intact after normothermic cardiopulmonary bypass. In conclusion, basal cerebrovascular resistance and internal carotid artery blood flow are maintained if the systemic circulation and pressure are supported with fluid administration after cardiopulmonary bypass. Agonist-induced vasodilation of cerebral microvessels to cholinergic and beta-adrenoceptor stimulation are selectively impaired after normothermic cardiopulmonary bypass, whereas second-messenger mechanisms remain intact.

Acetylcholine↗
PubMed1996

Neutrophil adhesion blockade with NPC 15669 decreases pulmonary injury after total cardiopulmonary bypass.

BACKGROUND: Total cardiopulmonary bypass, in an ovine model, is associated with increased pulmonary thromboxane A2 production, cellular sequestration of white cells and platelets, transient pulmonary hypertention, and increased lung lymph flow and lymph protein clearance when compared with respective findings with partial cardiopulmonary bypass. This study evaluates the effect of neutrophil adhesion blockade on lung injury after cardiopulmonary bypass. METHODS: Two groups of anesthetized sheep were placed on total cardiopulmonary bypass without assisted ventilation. One group of seven sheep was treated before and during total cardiopulmonary bypass with the neutrophil adhesion blocker NPC 15669. A second group of seven sheep did not receive NPC 15669 treatment before total cardiopulmonary bypass. A third group of seven sheep was treated with NPC 15669 before initiation of partial cardiopulmonary bypass with continued assisted ventilation. Aortic occlusion and hypothermia were not used. After 90 minutes all sheep were separated from cardiopulmonary bypass, with resumption of assisted ventilation and pulmonary arterial flow. After 30 minutes the left atrial pressure was elevated mechanically. Hemodynamics, thromboxane A2 levels, platelet levels, and white blood cell and plasma protein concentrations were measured before cardiopulmonary bypass and afterwards at four 15-minute intervals. Samples were taken from the right and left atria simultaneously. Lung lymph protein levels and flow were measured before and after cardiopulmonary bypass at two 30-minute intervals. RESULTS: In the total cardiopulmonary bypass group not treated with NPC 15669 signs of lung injury developed after cardiopulmonary bypass. Animals treated with NPC 15669 did not manifest a similar degree of lung injury after either partial or total cardiopulmonary bypass. Increased pulmonary vascular resistance did not develop in treated sheep nor did sequestration of platelets or white blood cells occur. Despite the drug, increased pulmonary capillary permeability after total cardiopulmonary bypass persisted, but was reduced. CONCLUSIONS: Compared with unmodified total cardiopulmonary bypass, blockade of neutrophil adhesion with NPC 15669 reduces, but does not entirely eliminate, lung derangement after total cardiopulmonary bypass.

Animals↗
PubMed1996

Serotonergic binding in the rat dorsal raphe nucleus: critical role of MAO inhibition.

The biochemical properties of the 5-HT1A receptor in dorsal raphe nucleus (DRN) were investigated using a micropunch procedure. Initially, the Ki value for 5-hydroxytryptamine (5-HT) binding to a site labeled by the 5-HT1A-selective ligand [3H]8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) was 20-fold higher than the KD for [3H]5-HT. In addition, a number of putative 5-HT1A selective ligands displayed poor affinity for the [3H]8-OH-DPAT site. The possibility that these discrepant results were due to metabolism of the receptor ligands was investigated by increasing the concentration of the monoamine oxidase (MAO) inhibitor, pargyline. Increasing the concentration of pargyline reduced, but did not abolish, the discrepancy between the Ki and KD values for 5-HT. However, inclusion of clorgyline, which is a more potent MAO inhibitor, resulted in an-excellent agreement between the Ki and KD values for 5-HT. In addition, when clorgyline was used, 5-HT1A-selective compounds displayed high affinity for the DRN binding site consistent with [3H]8-OH-DPAT labeling a 5-HT1A receptor in this tissue. The present study describes a fast and easy method for measuring biochemical properties in small discrete brain areas. These studies also indicate that pargyline should be replaced in serotonergic binding assays with a more potent inhibitor of monoamine oxidase such as clorgyline.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1996

Properties and regulation of gap junctional hemichannels in the plasma membranes of cultured cells.

During the assembly of gap junctions, a hemichannel in the plasma membrane of one cell is thought to align and dock with another in an apposed membrane to form a cell-to-cell channel. We report here on the existence and properties of nonjunctional, plasma membrane connexin43 (Cx43) hemichannels. The opening of the hemichannels was demonstrated by the cellular uptake of 5(6)-carboxyfluorescein from the culture medium when extracellular calcium levels were reduced. Dye uptake exhibited properties similar to those of gap junction channels. For example, using different dyes, the levels of uptake were correlated with molecular size: 5(6)-carboxyfluorescein (approximately 32%), 7-hydroxycoumarin-3-carboxylic acid (approximately 24%), fura-2 (approximately 11%), and fluorescein-dextran (approximately 0.4%). Octanol and heptanol also reduced dye uptake by approximately 50%. Detailed analysis of one clone of Novikoff cells transfected with a Cx43 antisense expression vector revealed a reduction in dye uptake levels according to uptake assays and a corresponding decrease in intercellular dye transfer rates in microinjection experiments. In addition, a more limited decrease in membrane resistance upon reduction of extracellular calcium was detected in electrophysiological studies of antisense transfectants, in contrast to control cells. Studies of dye uptake in HeLa cells also demonstrated a large increase following transfection with Cx43. Together these observations indicate that Cx43 is responsible for the hemichannel function in these cultured cells. Similar dye uptake results were obtained with normal rat kidney (NRK) cells, which express Cx43. Dye uptake can be dramatically inhibited by 12-O-tetradeconylphorbol-13-acetate-activated protein kinase C in these cell systems and by a temperature-sensitive tyrosine protein kinase, pp60v-src in LA25-NRK cells. We conclude that Cx43 hemichannels are found in the plasma membrane, where they are regulated by multiple signaling pathways, and likely represent an important stage in gap junction assembly.

Alcohols↗
PubMed1996

GH replacement fails to improve ventricular function in hypophysectomized rats with myocardial infarction.

To determine whether growth hormone (GH) replacement improves cardiac function, GH-deficient hypophysectomized rats with moderate myocardial infarction (MI) were studied after 3 wk of treatment with either recombinant rat GH (3.2 mg.kg-1.day-1 sc) or vehicle. The serum insulin-like growth factor I level in rats after GH treatment was approximately 10-fold greater than in vehicle-treated rats. GH replacement prevented a decrease in body weight at 1 wk (+5 +/- 6 vs. -26 +/- 4 g in vehicle group, P < 0.01) and increased body weight at 3 wk (+40 +/- 5 vs. -30 +/- 4 g in vehicle group, P < 0.01) after MI. Infarct size, expressed as a percentage of left ventricular (LV) perimeter, was similar for GH-treated (21 +/- 3%) and vehicle-treated (23 +/- 3%) rats. Basal LV systolic pressure, LV end-diastolic pressure, LV dP/dt, mean arterial pressure and heart rate, and the changes in these parameters in response to isoproterenol and norepinephrine were similar for these two groups. Although GH replacement tended to prevent depression in myocardial contractility during the recovery period after maximal stimulation either by the largest dose of isoproterenol (0.8 microgram/kg iv) or by acute volume loading, differences between the two groups were not statistically significant. In addition, to determine the effects of excess GH treatment in a severe state of cardiac dysfunction, nonhypophysectomized rats with larger infarcts (i.e., > 45% of the LV) were studied after 4 wk of treatment. There were no differences either in hemodynamic indexes or in infarct size between the GH- and vehicle-treated groups, whereas body weight had increased (P < 0.01) in the GH-treated group. Thus, although GH treatment effectively prevents the loss of body weight after MI, neither GH replacement nor excess GH treatment plays an important role in preserving cardiac function in rats with moderate or large MI.

Animals↗
PubMed1996

Death with dignity: there's plenty more that we can do.

The medical profession has seen an accelerated interest in end of life decision making and terminal care. The growing need for attention in these areas requires more of the art of medicine--the human and compassionate side of medicine as opposed to the high technology side.

Decision Making↗
PubMed1996

Comparison of lucifer yellow leakage and cell-to-cell transfer following intracellular injection in normal and antisense Novikoff cells under treatment with low extracellular Ca2+.

Single and paired control Novikoff and connexin 43 antisense-transfected Novikoff cells (antisense cells) were used to investigate the differences of intercellular dye transfer and leakage between these two types of cells. Lucifer Yellow was injected into cells by iontophoresis. There was no dye leakage in single cells of both types in Swims solution. The dye transfer from injected cell to recipient cell in the normal solution was different in the two types of cell pairs. The transfer was significantly suppressed in antisense cells; 46/84 cases were blocked vs. 1/84 in Novikoff cell pairs. Under EGTA treatment, the dye leakage in single antisense cells was suppressed showing an increase in the very slow rate of leakage (16/40 vs. 6/40), and the mean rate of leakage was also significantly low. This suggests that dye transfer and leakage are suppressed in antisense cells and demonstrates that connexin 43 plays an important part both in dye transfer in paired cells and dye leakage in single cells.

Calcium↗
PubMed1995

Accuracy of transesophageal echocardiography for identifying left atrial thrombi. A prospective, intraoperative study.

OBJECTIVE: To determine the ability of transesophageal echocardiography to accurately identify or exclude left atrial thrombi. DESIGN: Prospective cohort study. SETTING: University hospital. PATIENTS: 231 consecutive patients having transesophageal echocardiography before elective repair or replacement of the mitral valve or excision of a left atrial tumor. Fifty-six percent of patients had a history of atrial fibrillation, and 17% had a history of thromboembolism. MEASUREMENT: Identification of left atrial thrombi during transesophageal echocardiographic examination and comparison with direct near-simultaneous visualization during cardiac surgery. RESULTS: Transesophageal echocardiography identified 14 left atrial thrombi in 14 patients (6%). Thrombus size range from 3 to 80 mm. Surgery confirmed 12 of 14 thrombi (86%), including 9 thrombi confined to the left appendage. No additional thrombi were found on direct inspection of the atria (sensitivity, 100% [95% CI, 74% to 100%]; specificity, 99% [CI, 97% to 99.9%]; positive predictive value, 86% [12/14]; negative predictive value, 100% [217/217]; for a population that had a 5.2% prevalence of thrombi). All 12 surgically confirmed thrombi were identified by two independent observers. Neither thrombus seen by only a single observer on transesophageal echocardiography was confirmed during direct inspection of the atria at surgery. CONCLUSION: Transesophageal echocardiography is highly accurate for identifying left atrial thrombi and can be used clinically to exclude left atrial thrombi.

Adult↗
PubMed1995

Solution structure of the cytoplasmic domain of phopholamban: phosphorylation leads to a local perturbation in secondary structure.

Peptides representing the N-terminal domain (Ia) of the cardiac sarcoplasmic reticulum protein phospholamban (residues 1-25 [PLB(1-25)] and a phosphorylated form [pPLB(1-25)]) were synthesized and their conformations examined using circular dichroism and nuclear magnetic resonance spectroscopy. In aqueous solution, both PLB(1-25) and pPLB(1-25) adopt a primarily disordered conformation. In 30% trifluoroethanol/10 mM phosphate, PLB(1-25) exhibits a CD spectrum consistent with 60% helical structure. This value decreases to 27% for the phosphorylated peptide. CD spectra in 2% SDS indicate 40% alpha-helix for PLB(1-25) and 20% for pPLB(1-25). Full chemical shift assignments were obtained by conventional homonuclear NMR methodologies for both PLB(1-25) and pPLB(1-25) in 30% trifluoroethanol/water and 300 mM SDS. The solution structure of PLB(1-25) in 30% TFE/water was determined from distance geometry calculations using 54 NOE distance constraints and 17 torsion angle constraints. In the family of 20 calculated conformers, the root mean square deviation from the mean structure is 0.79 A for backbone heavy atoms of residues 1-17. The structure comprises a regular alpha-helix extending from M1 to S16 with the remaining C-terminal residues disordered. The calculated structure is supported by analysis of C alpha H secondary shifts which are significantly negative for residues 1-16. Chemical shift degeneracy is substantially more extensive in the phospho form and precludes a direct comparison of calculated structures. However, the magnitudes of upfield secondary shifts are decreased by 20% in residues 1-11 and are not significantly helical for residues 12-16 according to the criteria of Wishart et al. [(1992) Biochemistry 31, 1647-1651]. 3JHN alpha coupling constants measured for I12, R13, A15, and S16 also suggest that residues 12-16 undergo a local unwinding of the helix upon phosphorylation. Similar results are obtained for PLB(1-25) and pPLB(1-25) in 300 mM perdeuterated sodium dodecyl sulfate except that differences in backbone dynamics for the helical and nonhelical regions of the peptide are evident in the DQF-COSY line shapes for fingerprint cross-peaks. This disruption of structure at the C-terminus of the helix suggests a model for phosphorylation-induced dissociation of the PLB/Ca(2+)-ATPase complex.

Amino Acid Sequence↗
PubMed1995

Cloning and chromosomal localization of the human A2b adenosine receptor gene (ADORA2B) and its pseudogene.

To determine the chromosomal localization of the human A2b adenosine receptor, the corresponding genomic clone was isolated and used as a probe for fluorescence in situ hybridization to metaphase chromosomes. Partial sequence analysis of the A2b gene (AD-ORA2B) revealed an intron that interrupted the coding region corresponding to the second intracellular loop similar to that reported for A1 and A2a adenosine receptor genes. A pseudogene for the A2b receptor was also identified; it exhibited 79% identity to the A2b adenosine receptor cDNA coding sequence and contained multiple deletions, point mutations, and frame shifts and two in-frame stops. These changes would result in the inability to encode a functional receptor. The genomic clones were utilized to localize the A2b receptor to chromosome 17p12 and the A2b pseudogene to chromosome 1q32.

Chromosome Mapping↗
PubMed1995

Pulmonary injury after total or partial cardiopulmonary bypass with thromboxane synthesis inhibition.

Previous studies have shown an increase in left atrial plasma thromboxane (TBX) level and associated increase in lung injury parameters after total cardiopulmonary bypass (t-CPB) but not after partial cardiopulmonary bypass (p-CPB). We used dazmegrel to study the effect of TBX synthesis inhibition on lung injury after t-CPB compared with p-CPB. Sheep were placed on t-CPB without ventilation and with pulmonary artery occlusion (n = 7) or p-CPB with ventilation and an unrestricted pulmonary artery (n = 7). All sheep were treated with dazmegrel. After 90 minutes we separated the sheep from CPB. Plasma TBX, platelets, white blood cells, protein concentration, lung lymph protein, flow, and pulmonary vascular resistance were measured before and after CPB. Lung biopsies were also obtained. Minimal derangement of these pulmonary parameters was seen after either p-CPB or t-CPB. Inhibition of TBX synthesis virtually eliminated the lung injury previously reported after t-CPB, when compared with p-CPB. Clearly TBX has an important role in mediating lung injury after t-CPB.

Animals↗