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A Bidani

Publications and source records attributed to A Bidani.

At least 37 records · Page 2Linked to original sources
PubMed2000

[Biventricular thrombus complicating peripartum cardiomyopathy. A case report].

The authors report a case of a biventricular thrombus complicating peripartum cardiomyopathy in a 38 years old female. The diagnosis was done by bidimensionnal transthoracic echocardiography which showed 2 thrombi in the apical region of the right ventricle and in the anterior and lateral wall of the left ventricle. With treatment associating salt restriction, diuretics and angiotensin-converting-enzyme- inhibitors, the evolution was good: the thrombi disappeared at the first month for the left ventricular thrombi and after 45 days for the rignt ventricular thrombi. The patient didn't experience any embolic complication.

Adult↗
PubMed1999

Cytokine production by rabbit alveolar macrophages: differences between activated and suppressor cell phenotypes.

The differences between cytokine-producing profiles of activated macrophages (A-M phi) and suppressor macrophages (S-M phi) were examined. A-M phi, which exhibited cytotoxicity against RK-13 cells, were generated from resident rabbit alveolar M phi by treatment with lymphokine solution (culture fluids of rabbit spleen cells stimulated with concanavalin A [Con A]). S-M phi, which were able to inhibit cellular proliferations of rabbit spleen cells stimulated with Con A, were generated from resident alveolar M phi by treatment with 1-methyladenosine (an immunosuppressive molecule in tumourous ascites fluids). When A-M phi were stimulated with lipopolysaccharide (LPS) in vitro, the cells produced significantly more interleukin (IL)-1 (approximately 1.4 times), IL-6 (approximately 2.1 times), IL-12 (approximately 60 times), and tumour necrosis factor-alpha (TNF-alpha) (approximately 37 times) than did resting macrophages (R-M phi) stimulated with LPS as control cells. After the stimulation with LPS, both A-M phi and R-M phi did not produce transforming growth factor-beta (TGF-beta). In contrast, when S-M phi were stimulated with LPS in vitro, the cells produced significantly more TGF-beta (approximately 1.6 times) and significantly less IL-6 (approximately 1.8 times) than did control cells. Also, S-M phi did not produce IL-1, IL-12, and TNF-alpha into their culture fluids after the stimulation with LPS. These results show the differences between cytokine-producing profiles of A-M phi and S-M phi, and characteristics of their cytokine-producing profiles are analogous to T cell subsets. Differences displayed in the cytokine profiles may contribute to the effector (A-M phi) or the suppressor (S-M phi) functions of alveolar M phi.

Animals↗
PubMed1999

Theoretical study of inspiratory flow waveforms during mechanical ventilation on pulmonary blood flow and gas exchange.

A lumped two-compartment mathematical model of respiratory mechanics incorporating gas exchange and pulmonary circulation is utilized to analyze the effects of square, descending and ascending inspiratory flow waveforms during mechanical ventilation. The effects on alveolar volume variation, alveolar pressure, airway pressure, gas exchange rate, and expired gas species concentration are evaluated. Advantages in ventilation employing a certain inspiratory flow profile are offset by corresponding reduction in perfusion rates, leading to marginal effects on net gas exchange rates. The descending profile provides better CO2 exchange, whereas the ascending profile is more advantageous for O2 exchange. Regional disparities in airway/lung properties create maldistribution of ventilation and a concomitant inequality in regional alveolar gas composition and gas exchange rates. When minute ventilation is maintained constant, for identical time constant disparities, inequalities in compliance yield pronounced effects on net gas exchange rates at low frequencies, whereas the adverse effects of inequalities in resistance are more pronounced at higher frequencies. Reduction in expiratory air flow (via increased airway resistance) reduces the magnitude of upstroke slope of capnogram and oxigram time courses without significantly affecting end-tidal expired gas compositions, whereas alterations in mechanical factors that result in increased gas exchanges rates yield increases in CO2 and decreases in O2 end-tidal composition values. The model provides a template for assessing the dynamics of cardiopulmonary interactions during mechanical ventilation by combining concurrent descriptions of ventilation, capillary perfusion, and gas exchange.

Computer Simulation↗
PubMed1999

Dose dependence and time course of smoke inhalation injury in a rabbit model.

The dose dependence and time course of smoke inhalation injury were determined in a rabbit model. Animals were insufflated with 18-90 breaths of cotton smoke or room air (control) at a rate of 18 breaths/min and tidal volume of 12 ml/kg. Smoke-exposed animals exhibited dose-related histologic effects with progressive deterioration of respiratory function during the postexposure period of observation (96 h). The smoke-exposed rabbits had reproducible injuries to both airway mucosa and lung parenchyma, manifested by disruption and sloughing of airway and alveolar epithelia, and exudation of protein-rich fluid and leukocytes into the airway and alveolar spaces. Significant effects were evident by 24 h postexposure. Smoke inhalation also affected the respiratory burst of alveolar macrophages. Generation of superoxide anions by alveolar macrophages at 48 h postexposure was increased significantly after smoke inhalation (54 breaths). The present rabbit model should be useful for studying the interactions between pulmonary epithelial cells and leukocytes after smoke inhalation and for determining the role that abnormal functioning of alveolar macrophages plays in the development of smoke inhalation injury.

Animals↗
PubMed1999

Reduced ventilator pressure and improved P/F ratio during percutaneous arteriovenous carbon dioxide removal for severe respiratory failure.

OBJECTIVE: To evaluate the effect of percutaneous arteriovenous carbon dioxide removal (AVCO2R) on ventilator pressures and P/F ratio in a clinically relevant large-animal model of severe respiratory failure. SUMMARY BACKGROUND DATA: AVCO2R was developed as a simple arteriovenous shunt with a commercially available low-resistance gas exchange device of sufficient surface area for near-total CO2 removal. With an AV shunt 10% to 15% of cardiac output, AVCO2R allows a reduction in ventilator airway pressures without hypercapnia or the complex circuitry and monitoring required for conventional ECMO. METHODS: AVCO2R was applied to a new, clinically relevant large-animal model of severe respiratory failure created by smoke inhalation and cutaneous flame bum injury. Adult sheep (n = 9, 38+/-6 kg) received a 40% total body surface area, third-deinsufflation. After injury, all animals were placed on volume-controlled mechanical ventilation to achieve PaO2 > 60 mmHg and PacO2 < 40 mmHg. Animals were placed on AVCO2R within 40 to 48 hours of injury when the PaO2/FiO2 was <200. Animals underwent cannulation of the carotid artery and jugular vein with percutaneous 10F arterial and 14F venous cannulas. Shunt flow was continuously monitored using an ultrasonic flow probe and calculated as a percentage of cardiac output. RESULTS: AVCO2R flows of 800 to 900 ml/min (11% to 13% cardiac output) achieved 77 to 104 ml/min of CO2 removal (95% to 97% total CO2 production) while maintaining normocapnia. Significant reductions in ventilator settings were tidal volume, 421.3+/-39.8 to 270.0+/-6.3 ml; peak inspiratory pressure, 24.8+/-2.4 to 13.7+/-0.7 cm H2O; minute ventilation, 12.7+/-1.4 to 6.2+/-0.8 L/min; respiratory rate, 25.4+/-1.3 to 18.4+/-1.8 breaths/min; and FiO2, 0.88+/-0.1 to 0.39+/-0.1. The P/F ratio increased from 151.5+/-40.0 at baseline to 320.0+/-17.8 after 72 hours. CONCLUSIONS: Percutaneous AVCO2R allows near-total CO2 removal and significant reductions in ventilator pressures with improvement in the P/F ratio.

Algorithms↗
PubMed1999

Renal injury and salt-sensitive hypertension after exposure to catecholamines.

We investigated whether chronic infusion of phenylephrine could induce structural and functional changes in the kidney of rats with the subsequent development of salt-sensitive hypertension. Rats were infused with phenylephrine (0.15 mmol/kg per day) by minipump, resulting in a moderate increase in systolic blood pressure (BP) (17 to 25 mm Hg) and a marked increase in BP variability as measured by an internal telemetry device. After 8 weeks, the phenylephrine infusion was stopped with the return of BP to normal, and a nephrectomy was performed for histological studies. Glomeruli were largely spared, but focal tubulointerstitial fibrosis was present, with the de novo expression of osteopontin by injured tubules, macrophage and "myofibroblast" accumulation, and focal increases in mRNA for transforming growth factor beta by in situ hybridization. Peritubular capillaries at sites of injury had distorted morphology with shrinkage, rounding, and focal rarefaction, and endothelial cell proliferation was also identified. Rats were randomized to a high (8% NaCl or 1.36 mol/kg) or low (0.1% NaCl or 17 mmol/kg) salt diet. After 4 to 8 weeks, phenylephrine-treated rats on a high salt diet developed marked hypertension, which was in contrast with phenylephrine-treated rats placed on a low salt diet or vehicle-treated rats given a high salt diet. Hypertension after phenylephrine exposure correlated with the initial mean systolic BP (r(2)=0.99) and the degree of BP lability (r(2)=0.99) during the phenylephrine infusion, the amount of osteopontin expressed in the initial biopsy/nephrectomy (r(2)=0.74), and the final glomerular filtration rate (r(2)=0.58). These studies provide a mechanism by which a markedly elevated sympathetic nervous system can induce salt-dependent hypertension even when the hyperactive sympathetic state is no longer engaged.

Adrenergic alpha-Agonists↗
PubMed1999

Percutaneous extracorporeal arteriovenous CO2 removal for severe respiratory failure.

BACKGROUND: In previous animal studies, arteriovenous CO2 removal (AVCO2R) achieved significant reduction in ventilator pressures and improvement in the Pao2 to fraction of inspired oxygen ratio during severe respiratory failure. For our initial clinical experience, 5 patients were approved for treatment of severe respiratory failure and CO2 retention to evaluate the feasibility and safety of percutaneous AVCO2R. METHODS: Patients were anticoagulated with heparin (activated clotting time, 260 to 300 seconds), underwent percutaneous femoral cannulation (10F to 12F arterial and 12F to 15F venous catheters), and then were connected to a low-resistance, 2.5-m2 hollow-fiber oxygenator for 72 hours. RESULTS: Mean AVCO2R flow at 24, 48, and 72 hours was 837.4+/-73.9, 873+/-83.6, and 750+/-104.5 mL/min, respectively, with no vascular complications and no significant change in heart rate or mean arterial pressure. Removal of CO2 plateaued at an AVCO2R flow of 1086 mL/min with 208 mL/min CO2 removed. Average CO2 transfer at 24 and 48 hours was 142+/-17 and 129+/-16 mL/min. Use of AVCO2R allowed a significant decrease in minute ventilation from 7.2+/-2.3 L/min at baseline to 3.4+/-0.8 L/min at 24 hours. CONCLUSIONS: All patients survived the experimental period without adverse sequelae. Percutaneous AVCO2R can achieve approximately 70% CO2 removal in adults with severe respiratory failure and CO2 retention without hemodynamic compromise or instability.

Adult↗
PubMed1999

Early complications. Respiratory failure.

Pulmonary complications following thoracic surgery are common and associated with significant morbidity and mortality. Respiratory failure after pneumonectomy occurs in approximately 5% to 15% of cases and significantly increases patient mortality. Strategies for ventilator support are based on the nature of the underlying complication and the pathophysiology of respiratory failure. This article describes the cause and pathophysiology of respiratory failure and pulmonary embolus postpneumonectomy. Diagnosis, management, and innovative therapies are also reviewed.

Humans↗
PubMed1998

Glutathione S-transferases of rabbit lung macrophages.

The catalytic activities of glutathione S-transferases (GSTs), particularly the alpha-class isozymes, can provide protection against oxidative stress through GSH-mediated metabolism of reactive products of lipid peroxidation. Lipid peroxidation products from oxidative metabolism in alveolar macrophages play an important role in mediating and regulating inflammatory response and injury in the lung. The rabbit has been used as an important animal model for studies of the role of alveolar macrophages in pulmonary pathology. Although rabbit lung macrophages display GST activity, the isozyme-specific expression of GSTs and the catalytic properties of these isozymes has not previously been defined. In present studies, we have purified the GST isozymes of rabbit alveolar macrophages obtained by bronchoalveolar lavage and performed immunologic and kinetic characterization of the purified isozymes. Results of our studies indicate the presence of three alpha-class isozymes (pI 10.2, 9.3, and 6.0) and one micro-class isozyme (pI 7.2). N-terminal sequence analysis of the micro-class isozyme indicated that it was distinct from the two previously described micro-class isozymes of rabbit. Kinetic studies indicated that two cationic alpha-class GSTs (pI 10.2 and 9.3) contribute the large majority of selenium independent GSH-peroxidase activity toward dilinoleoyl phosphatidylcholine hydroperoxide (kcat/Km values of 83.4 and 31.9 s-1 . M-1 . 10(3), respectively). A third alpha-class GST (pI 6.0) was shown to have highest catalytic activity toward conjugation of the 4-hydroxynonenal (4HNE) with GSH (kcat/Km = 1900 s-1 . M-1 . 10(3)). Structural and immunologic characterization of this GST isozyme indicated that it belongs to a subclass of the alpha-classGSTs selectively expressed in mesodermal origin cells that are exposed to high levels of oxidative stress and are characterized by high specific activity toward both lipid hydroperoxides and 4-HNE.

Aldehydes↗
PubMed1998

Effects of concanavalin A on Na(+)-dependent and Na(+)-independent mechanisms for H+ extrusion in alveolar macrophages.

Alveolar macrophages (m phi) possess two parallel mechanisms for plasmalemmal H+ extrusion: a V-type H+ pump (V-ATPase) and a Na+/H+ exchanger (NHE). To investigate the coordinated functioning of the H+ extruders for m phi intracellular pH (pHi) regulation, we investigated the effects of the plant lectin concanavalin A (ConA) on resident alveolar m phi from rabbits. ConA (1 microM, 30-min pretreatment) activated the m phi for phagocytosis of opsonized Escherichia coli. ConA activation did not affect the baseline pHi of m phi or the initial rate of pHi recovery (dpHi/dt) from an intracellular acid load (acid-loaded pHi nadir approximately 6.9). However, the contributions of Na(+)-independent H+ transport (i.e. V-ATPase activity) and Na(+)-dependent H+ transport (i.e. NHE activity) to dpHi/dt were altered significantly. The lectin stimulated Na+/H+ exchange and inhibited V-ATPase activity. In control m phi, V-ATPase-mediated H+ extrusion was responsible for > 80% of dpHi/dt. Conversely, in ConA-treated m phi, Na+/H+ exchange was responsible for approximately 65% of dpHi/dt, and V-ATPase activity was responsible for only 35% of dpHi/dt. These results underscore the complex mechanisms and signaling pathways that coordinate the activities of cellular acid-base transporters in m phi pHi regulation.

Animals↗
PubMed1998

Evidence for pH sensitivity of tumor necrosis factor-alpha release by alveolar macrophages.

Alveolar macrophages (m phi) participate in inflammatory and immune responses in acidic microenvironments such as the interstitial fluids of tumors and abscesses. Two plasmalemmal H+ extruders interact to control the acid-base status of alveolar m phi, namely a V-type H+ pump (V-ATPase) and a Na+/H+ exchanger. The present study examined the effects of extracellular pH (pHo) and H+ transport inhibitors on tumor necrosis factor-alpha (TNF-alpha) release induced by endotoxin (lipopolysaccharide) in rabbit alveolar m phi. The amount and activity of TNF-alpha in m phi-conditioned media were determined by enzyme-linked immunosorbent assay and L929 fibroblast bioassay, respectively. TNF-alpha release was suppressed progressively at lower pHo values (< or = 7.0). Also, bafilomycin A1 (a specific inhibitor of V-ATPases) significantly reduced the amount and activity of TNF-alpha in m phi-conditioned media (pHo 7.4). However, bafilomycin caused a significant increase in the nonspecific cytotoxicity (i.e. bioactivity insensitive to TNF-alpha antibody) of m phi-conditioned media. The effects of bafilomycin specifically on TNF-alpha release followed a time course similar to that of acidic pHo, suggesting that both treatments acted on similar events in the lipopolysaccharide signal transduction pathway. Amiloride (an inhibitor of Na+ transporters including the Na+/H+ exchanger) also suppressed TNF-alpha release but displayed a time course of action different from the acidic pHo or bafilomycin.

Amiloride↗
PubMed1998

Cotton smoke inhalation primes alveolar macrophages for tumor necrosis factor-alpha production and suppresses macrophage antimicrobial activities.

The present study determined the effects of cotton smoke inhalation on the functioning of alveolar macrophages (mphi). Smoke inhalation led to dose-dependent impairment of respiratory gas exchange by 48 h postexposure and pulmonary edema by 96 h. Maximal effects were observed in animals ventilated with 54 breaths of cotton smoke (3-min exposure, 18 breaths/min). Macrophages were obtained at 48 h postexposure by bronchoalveolar lavage of rabbits subjected to 54 breaths of smoke or room air (control). Phagocytosis of opsonized bacteria and adherence to solid substratum were reduced in smoke-exposed mphi. Smoke inhalation primed mphi for release of tumor necrosis factor-alpha (TNF-alpha) induced by lipopolysaccharide (LPS). Smoke-exposed mphi were also primed for TNF-alpha release induced by phorbol myristate acetate, which suggests that the priming event occurred downstream of protein kinase C activation in the signal transduction pathway. Further, smoke exposure attenuated the inhibitory effects of phosphodiesterase inhibitors on LPS-induced TNF-alpha release. Thus, the priming event may be mediated through cAMP and/or protein kinase A. The data indicate that cotton smoke inhalation suppresses the antimicrobial activities of alveolar mphi and can lead to excessive mphi production of TNF-alpha. These mphi effects would be expected to contribute to the pathophysiological abnormalities associated with smoke inhalation injury.

Acute Disease↗
PubMed1998

Kinetics of CO2 excretion and intravascular pH disequilibria during carbonic anhydrase inhibition.

Inhibition of carbonic anhydrase (CA) activity (activity in red blood cells and activity available on capillary endothelium) results in decrements in CO2 excretion (VCO2) and plasma-erythrocyte CO2-HCO(-3)-H+ disequilibrium as blood travels around the circulation. To investigate the kinetics of changes in blood PCO2 and pH during progressive CA inhibition, we used our previously detailed mathematical model of capillary gas exchange to analyze experimental data of VCO2 and blood-gas/pH parameters obtained from anesthetized, paralyzed, and mechanically ventilated dogs after treatment with acetazolamide (Actz, 0-100 mg/kg i.v.). Arterial and mixed venous blood samples were collected via indwelling femoral and pulmonary arterial catheters, respectively. Cardiac output was measured by thermodilution. End-tidal PCO2, as a measure of alveolar PCO2, was obtained from continuous records of airway PCO2 above the carina. Experimental results were analyzed with the aid of a mathematical model of lung and tissue-gas exchange. Progressive CA inhibition was associated with stepwise increments in the equilibrated mixed venous-alveolar PCO2 gradient (9, 19, and 26 Torr at 5, 20, and 100 mg/kg Actz, respectively). The maximum decrements in VCO2 were 10, 24, and 26% with 5, 20, and 100 mg/kg Actz, respectively, without full recovery of VCO2 at 1 h postinfusion. Equilibrated arterial PCO2 overestimated alveolar PCO2, and tissue PCO2 was underestimated by the measured equilibrated mixed venous blood PCO2. Mathematical model computations predicted hysteresis loops of the instantaneous CO2-HCO(-3)-H+ relationship and in vivo blood PCO2-pH relationship due to the finite reaction times for CO2-HCO(-3)-H+ reactions. The shape of the hysteresis loops was affected by the extent of Actz inhibition of CA in red blood cells and plasma.

Acetazolamide↗
PubMed1998

Airway mechanics, gas exchange, and blood flow in a nonlinear model of the normal human lung.

A model integrating airway/lung mechanics, pulmonary blood flow, and gas exchange for a normal human subject executing the forced vital capacity (FVC) maneuver is presented. It requires as input the intrapleural pressure measured during the maneuver. Selected model-generated output variables are compared against measured data (flow at the mouth, change in lung volume, and expired O2 and CO2 concentrations at the mouth). A nonlinear parameter-estimation algorithm is employed to vary selected sensitive model parameters to obtain reasonable least squares fits to the data. This study indicates that 1) all three components of the respiratory model are necessary to characterize the FVC maneuver; 2) changes in pulmonary blood flow rate are associated with changes in alveolar and intrapleural pressures and affect gas exchange and the time course of expired gas concentrations; and 3) a collapsible midairway segment must be included to match airflow during a forced expiration. Model simulations suggest that the resistances to airflow offered by the collapsible segment and the small airways are significant throughout forced expiration; their combined effect is needed to adequately match the inspiratory and expiratory flow-volume loops. Despite the limitations of this lumped single-compartment model, a remarkable agreement with airflow and expired gas concentration measurements is obtained for normal subjects. Furthermore, the model provides insight into the important dynamic interactions between ventilation and perfusion during the FVC maneuver.

Adult↗
PubMed1997

Effects of lidocaine on cytosolic pH regulation and stimulus-induced effector functions in alveolar macrophages.

Local anesthetics influence a variety of stimulus-induced effector functions in leukocytes. The present study determined the effects of lidocaine on intracellular pH (pHi) regulation, superoxide production, and tumor necrosis factor-alpha (TNF-alpha) release in alveolar macrophages (m phi). Resident m phi were obtained by bronchoalveolar lavage of rabbits. The cells were subjected to an intracellular acid load, and subsequent pHi recovery was followed in the presence or absence of bafilomycin A1, a specific inhibitor of V-type H(+)-translocating ATPase (V-ATPase) or amiloride, an inhibitor of Na+/H+ exchange. Lidocaine slowed pHi recovery in a dose-dependent manner. Pretreatment (1 h) with 2.5 mM lidocaine abolished Na+/H+ exchange and reduced the V-ATPase-mediated component of pHi recovery. Lidocaine also significantly depressed the superoxide production induced by phorbol ester. TNF-alpha release induced by endotoxin was not affected significantly by the local anesthetic. Macrophage viability (trypan blue exclusion) and cellular ATP concentration were unaffected. These results indicate that lidocaine inhibits pHi regulatory mechanisms in alveolar m phi. This disruption of pHi regulation could contribute to inhibitory actions of lidocaine on m phi effector functions.

Acid-Base Equilibrium↗
PubMed1997

Total arteriovenous CO2 removal: simplifying extracorporeal support for respiratory failure.

BACKGROUND: To reduce the complexity, complications, and cost of conventional extracorporeal membrane oxygenation, we have developed a technique of simplified arteriovenous extracorporeal CO2 removal (AVCO2R) with a low-resistance membrane gas exchanger for total CO2 removal to provide lung rest in the setting of severe respiratory failure. METHODS: We initially used AVCO2R in healthy animals to quantify the gas exchange capabilities of the system and establish ventilator management protocols for the subsequent studies of AVCO2R in a large animal model of respiratory failure secondary to a severe smoke inhalation injury. RESULTS: In healthy sheep the maximum spontaneous arteriovenous flow ranged from 1,350 to 1,500 mL/min, whereas CO2 removal plateaued at a blood flow of approximately 1,000 mL/min in which 112 +/- 3 mL/min CO2 was removed, allowing an 84% reduction in the minute ventilation of from 6.9 +/- 0.8 L/min to 1.1 +/- 0.4 L/min (p < 0.01) without triggering hypercapnia. A subsequent reduction in extracorporeal flow at a reduced minute volume led to the development of hypercapnia only if it decreased to less than 500 mL/min. We also applied AVCO2R in mechanically ventilated sheep with a severe smoke inhalation injury and removed 95% (111 +/- 4 mL/min) of the total CO2 production. This allowed the minute ventilation to be reduced by 95% and the peak inspiratory pressures by 52% (both p < 0.05) over 6 hours and produced no adverse hemodynamic effects. The partial pressure of arterial oxygen was maintained above 100 mm Hg at a maximally reduced minute volume. The mean AVCO2R flow was 1,213 +/- 29 mL/min, averaging 27% +/- 1% of the cardiac output. CONCLUSIONS: We conclude that AVCO2R in a simple arteriovenous shunt is a less complicated technique than extracorporeal membrane oxygenation and is capable of total CO2 removal that allows a significant reduction in the minute ventilation and peak airway pressure during severe respiratory failure.

Animals↗