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J Boczkowski

Publications and source records attributed to J Boczkowski.

At least 37 records · Page 2Linked to original sources
PubMed1998

Early release of proinflammatory cytokines after lung transplantation.

BACKGROUND: Systemic hypotension may complicate the early postoperative period after lung transplantation. A release of proinflammatory cytokines secondary to lung ischemia/reperfusion injury could be involved in the pathogenesis of this early hemodynamic failure (EHF). STUDY OBJECTIVE: To assess prospectively whether the occurrence of EHF is associated with a release of cytokines in the systemic circulation. DESIGN: Blood samples were taken daily during the first postoperative week in 26 patients who underwent a double or a single-lung transplantation. These patients were divided into three groups: 7 patients who experienced EHF and subsequently died (EHF group); 15 patients without EHF (control group); and 4 patients without EHF but with an identified sepsis (sepsis group). The serum levels of interleukin (IL)-1beta, tumor necrosis factor-alpha (TNF-alpha), IL-6, and IL-8 were compared among the three groups. RESULTS: In the EHF group, the levels of each cytokine peaked at day 1 postoperatively. Cytokine levels at day 1 were significantly higher in the EHF group than in the control group (p<0.0006) or in the sepsis group (p<0.003 except for TNF-alpha). CONCLUSION: We conclude that EHF is associated with a massive release of proinflammatory cytokines that could play a determinant role in the pathogenesis of this complication.

Adolescent↗
PubMed1997

Predominant role of A1 adenosine receptors in mediating adenosine induced vasodilatation of rat diaphragmatic arterioles: involvement of nitric oxide and the ATP-dependent K+ channels.

1. We investigated, by intravital microscopy in rats, the role of the subtypes of adenosine receptors A1 (A1/AR) and A2 (A2AR) in mediating adenosine-induced vasodilatation of second and third order arterioles of the diaphragm. 2. Adenosine, and the A1AR selective agonists R(-)-N6-(2-phenylisopropyl)-adenosine (R-PIA) and N6-cyclo-pentyl-adenosine (CPA) induced a similar concentration-dependent dilatation of diaphragmatic arterioles. The non selective A2AR subtype agonist N6-[2-(3,5-dimethoxyphenyl)-2-(2-methylphenyl) ethyl]adenosine (DPMA) also dilated diaphragmatic arterioles but induced a significantly smaller dilatation than adenosine. By contrast the selective A(2a)AR subtype agonist 2-[p-(2-carboxyethyl)phenyl amino]-5'-N-ethyl carboxamido adenosine (CGS 21680) did not modify diaphragmatic arteriolar diameter. 3. The non selective adenosine receptor antagonist 1,3-dipropyl-8-p-sulphophenylxanthine (SPX, 100 microM) and the selective A1AR antagonist 8-cyclopentyl-1,3-dipropylxanthine (CPX, 50 nM) significantly attenuated adenosine-induced dilatation of diaphragmatic arterioles. By contrast, adenosine significantly dilated diaphragmatic arterioles in the presence of A2AR antagonist 3,7-dimethyl-1-propargylxanthine (DMPX, 10 microM). 4. The dilatation induced by adenosine was unchanged by the mast cell stabilizing agent sodium cromoglycate (cromolyn, 10 microM). 5. The nitric oxide (NO) synthase inhibitor N omega-nitro-L-arginine (L-NOARG, 300 microM) attenuated the dilatation induced by adenosine, and by the A1AR and A2AR agonists. 6. The ATP-dependent K+ channel blocker glibenclamide (3 microM) significantly attenuated diaphragmatic arteriolar dilatation induced by adenosine and by the A1AR agonists R-PIA and CPA. By contrast, glibenclamide did not significantly modify arteriolar dilatation induced by the A2AR agonist DPMA. 7. These findings suggest that adenosine-induced dilatation of diaphragmatic arterioles in the rat is predominantly mediated by the A1AR, via the release of NO and activation of the ATP-dependent K+ channels.

Adenosine↗
PubMed1997

Expiratory flow limitation in COPD patients after single lung transplantation.

Expiratory flow limitation and dyspnea during resting breathing are common in patients with severe chronic obstructive pulmonary disease (COPD). Although single lung transplantation (SLT) is used to treat end-stage COPD, its effects on flow limitation and dyspnea are not well established. We assessed expiratory flow-limitation and dyspnea in 13 COPD patients after SLT at rest in the sitting and supine positions by applying negative pressure at the mouth during tidal expiration (negative expiratory pressure [NEP] technique). If NEP increases flow throughout the control tidal volume (VT), flow limitation is absent (not flow limited [NEL]). If NEP does not increase flow during part of the control VT, flow limitation is present. After SLT, lung function improved in all but one patient. Twelve patients were NFL during resting breathing in both positions studied. The patient whose lung function did not improve after SLT was flow-limited (FL) both when seated and supine. This patient also exhibited moderately severe chronic dyspnea (Medical Research Council [MRC] score = 3). In the nine other patients in whom dyspnea was assessed, it was slight (MRC score = 1). In conclusion, after SLT for end-stage COPD, expiratory flow limitation at rest is uncommon in both the seated and supine positions. This is consistent with the finding that after SLT the degree of chronic dyspnea is generally slight.

Dyspnea↗
PubMed1997

Expiratory flow limitation in stable asthmatic patients during resting breathing.

Application of negative pressure at the mouth during tidal expiration (NEP) provides a simple, rapid, noninvasive method for detecting expiratory flow limitation during spontaneous breathing. Patients in whom NEP elicits an increase in flow throughout expiration are not flow-limited (FL). In contrast, patients in whom application of NEP does not elicit an increase in flow during most or part of tidal expiration are considered FL. We have used the NEP technique to assess the prevalence of expiratory flow limitation during resting breathing in sable asthmatic patients in both the seated and supine positions. In patients in the sitting position, we have also assessed flow limitation with the conventional method, based on comparison of tidal and maximal expiratory flow-volume (MEFV) curves. We studied 13 patients (FEV1 range: 48 to 94% predicted) with both the NEP and conventional techniques. According to the NEP technique, none of the patients was FL in the seated and only two were FL in the supine position. By contrast, on the basis of the conventional method, six of the patients would have been classified as FL in the sitting position. We conclude that: (1) most stable asthmatic patients do not exhibit tidal expiratory flow limitation during resting breathing; and (2) the conventional method for assessing flow limitation may lead to erroneous conclusions.

Adolescent↗
PubMed1996

Induction of diaphragmatic nitric oxide synthase after endotoxin administration in rats: role on diaphragmatic contractile dysfunction.

Nitric oxide (NO), a free radical that is negatively inotropic in the heart and skeletal muscle, is produced in large amounts during sepsis by an NO synthase inducible (iNOS) by LPS and/or cytokines. The aim of this study was to examine iNOS induction in the rat diaphragm after Escherichia Coli LPS inoculation (1.6 mg/kg i.p.), and its involvement in diaphragmatic contractile dysfunction. Inducible NOS protein and activity could be detected in the diaphragm as early as 6 h after LPS inoculation. 6 and 12 h after LPS, iNOS was expressed in inflammatory cells infiltrating the perivascular spaces of the diaphragm, whereas 12 and 24 h after LPS it was expressed in skeletal muscle fibers. Inducible NOS was also expressed in the left ventricular myocardium, whereas no expression was observed in the abdominal, intercostal, and peripheral skeletal muscles. Diaphragmatic force was significantly decreased 12 and 24 h after LPS. This decrease was prevented by inhibition of iNOS induction by dexamethasone or by inhibition of iNOS activity by N(G)-methyl-L-arginine. We conclude that iNOS was induced in the diaphragm after E. Coli LPS inoculation in rats, being involved in the decreased muscular force.

Abdominal Muscles↗
PubMed1996

Role of prostaglandins and nitric oxide on halothane-induced arteriolar dilatation in rat diaphragm.

The effects of anaesthetics on the microcirculation of the diaphragm are incompletely understood. Therefore, we assessed by in vivo intravital microscopy in rats the action of halothane on diaphragmatic arteriolar diameter and the role of nitric oxide and prostaglandins on halothane-induced diaphragmatic arteriolar diameter. We studied 54 rats anaesthetized with thiopentone. Dose-response curves to topically applied Krebs' solution saturated with halothane at increasing concentrations of 0%, 1%, 3% and 5% were carried out in the presence of an inhibitor of nitric oxide synthesis (N omega-nitro-L-arginine (LNA), 300 mumol litre-1) or inhibitors of prostaglandin synthesis (mefenamic acid 20 mumol litre-1 or indomethacin 20 mol litre-1) or in the absence of any inhibitor. We found dose-dependent arteriolar dilatation which was abolished by mefenamic acid and indomethacin. In contrast, the effect of halothane was not modified by LNA. These data demonstrated that halothane-induced arteriolar dilatation in the diaphragm of the rat was mediated by prostaglandins but not by nitric oxide.

Anesthetics, Inhalation↗
PubMed1995

Effects of inhibition of nitric oxide synthesis on TNF alpha serum levels in E. coli endotoxemic rats.

We investigated the effects of nitric oxide (NO) synthesis inhibition on mortality rate and TNF alpha serum levels in rats inoculated with E. Coli endotoxin (30 mg/kg i.v.) Pre-treatment of endotoxemic rats with NG-monomethyl-L-arginine (L-NMMA), an inhibitor of NO synthesis by both the constitutive and the inducible isoforms of the NO synthase, did not change the mortality rate but significantly reduced TNF alpha serum levels. By contrast, administration of aminoguanidine, a more specific inhibitor of the inducible NO synthase, did not modify serum TNF alpha. These results suggest that, in E. Coli endotoxemic rats, NO synthetized by the constitutive isoform of the NO synthase positively modulates TNF alpha synthesis.

Amino Acid Oxidoreductases↗
PubMed1994

Role of nitric oxide and prostaglandins in the regulation of diaphragmatic arteriolar tone in the rat.

We evaluated by intravital microscopy in rats the relative importance of nitric oxide (NO) and prostaglandins in 1) the maintenance of basal diaphragmatic arteriolar tone and 2) the response of diaphragmatic arterioles to the endothelium-dependent vasodilator acetylcholine (ACh). One hundred two mechanically ventilated rats were studied. Separate applications of N omega-nitro-L-arginine (L-NNA) and mefenamic acid (MA), which are specific inhibitors of NO and prostaglandin synthesis, respectively, elicited a significant reduction in basal diaphragmatic arteriolar diameter. A dramatic potentiation of the effect of each inhibitor was observed when both agents were applied simultaneously. ACh application induced a significant and dose-dependent increase in arteriolar diameter that was not significantly modified by the separate application of L-NNA or MA. Conversely, the simultaneous administration of L-NNA and MA almost completely prevented ACh-induced arteriolar dilatation. Dilatation in response to sodium nitroprusside was not significantly modified in the presence of both inhibitors. These results suggest that NO and prostaglandins act in concert to regulate basal diaphragmatic arteriolar tone and to mediate diaphragmatic arteriolar response to ACh.

Acetylcholine↗
PubMed1994

Effects of mechanical ventilation on diaphragmatic contractile properties in rats.

We measured in rats the effects of 48 h of mechanical ventilation on the weight, contractile properties, and enzymatic profile of the diaphragm, the soleus and the extensor digitorium longus (EDL) muscles. Eighteen animals were randomly divided into a mechanically ventilated (MV, n = 9) group or a control (C, n = 9) group. During the 48 h of mechanical ventilation, animals in the MV group were anesthetized with sodium thiopental and enterally fed with a gastric catheter. Group C animals were neither anesthetized nor mechanically ventilated during the 48-h experimental period, and they had access to food and water ad libitum. Muscular contractile properties were measured in vitro by analysis of force-frequency curves and twitch characteristics. The weights of the three muscles were significantly reduced in the MV group compared with those in the C group. This was accompanied in the diaphragm by a reduction in the normalized force generated for all the frequencies of stimulation, except 20 Hz, whereas twitch characteristics were not modified. The forces generated by the soleus and EDL were not significantly reduced in the MV group compared with those in the C group. Diaphragm, soleus, and EDL citrate synthase and lactate dehydrogenase activities were not significantly different in the two groups. We conclude that mechanical ventilation for 48 h in rats produces a selective force reduction in the diaphragm.

Animals↗
PubMed1992

Does a subparalysing dose of vecuronium enhance diaphragm fatigue?

We have examined, in six healthy volunteers, the effect of a subparalysing dose of vecuronium on the development of diaphragm fatigue. Vecuronium was given as a 0.5-mg bolus i.v. followed by 0.5 mg infused over 30 min; as a control, saline was given in random order. Diaphragm strength was assessed by measuring transdiaphragm pressure and by electromyography. Diaphragm fatigue was induced by breathing against an inspiratory resistance. The plasma concentration of vecuronium varied between 15 and 30 ng ml-1 15 min after administration of vecuronium was started. Peripheral neuromuscular block was not detected in any subject. Diaphragm fatigue developed within the same period in both groups: mean 334 (SD 166) s after saline and 345 (190) s after vecuronium. The electromyographic pattern of diaphragm fatigue and the time constant of relaxation of transdiaphragm pressure after fatigue were similar in both groups. We conclude that, at low plasma concentrations of vecuronium, similar to those present in the postoperative period, there was no predisposition to diaphragm fatigue.

Adult↗
PubMed1992

Effects of endotoxic shock on diaphragmatic function in mechanically ventilated rats.

Diaphragmatic function was investigated in mechanically ventilated rats during endotoxic shock (group E, n = 18) and after saline solution injection (group C, n = 8). Endotoxic shock was produced by a 1-min injection of Escherichia coli endotoxin (10 mg/kg iv) suspended in saline. Diaphragmatic strength was assessed before (T0) and 15 (T15) and 60 (T60) min after injection by measuring transdiaphragmatic pressure (Pdi) generated during bilateral phrenic stimulation at 0.5, 10, 20, 30, 50, and 100 Hz. Diaphragmatic neuromuscular transmission was assessed by measuring the integrated electrical activity of the diaphragm. Diaphragmatic endurance was assessed 75 min after injection from the rate of Pdi decline after a 30-s continuous 10-Hz phrenic stimulation. In 16 additional animals, diaphragmatic glycogen content was determined 60 min after inoculation with endotoxin (n = 8) or 0.9% sodium chloride solution (n = 8). Diaphragmatic resting membrane potential (Em) was measured in 16 additional animals 60 min after endotoxin (n = 8) or saline injection (n = 8). Mean blood pressure decreased from 74 +/- 3 to 53 +/- 6 mmHg at T60 in group E, whereas it was maintained in group C. At T60 Pdi was decreased in group E for frequencies of 50 and 100 Hz and was associated with a decreased diaphragmatic electromyographic activity of 25.3 +/- 2.5 and 26.5 +/- 5.2% for 50- and 100-Hz stimulations, respectively, in comparison with T0 values.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

In vivo effects of Escherichia coli endotoxemia on diaphragmatic microcirculation in rats.

We investigated the effects of Escherichia coli endotoxin administration on diaphragmatic microcirculation in rats by in vivo videomicroscopy. Rats were allocated into three groups: 1) intravenous inoculation of 10 mg/kg of E. col endotoxin (group E, n = 25), 2) intravenous inoculation of sterile 0.9% NaCl (group C, n = 20), and 3) induction of a controlled hemorrhage by reducing the vascular volume via an arterial catheter (group H, n = 15). Mean blood pressure (BP) and arteriolar diameters were measured at 15-min intervals and capillary perfusion pattern at 30-min intervals for 1 h. BP decreased similarly in groups E and H, whereas it was maintained in group C. Arterioles were classified as second (A2, n = 46), third (A3, n = 22), and fourth (A4, n = 21) order, according to their relative localization in the network. Basal diameters were the same in the three groups: 38.16, 17.33, and 6.80 microns in group C; 38.17, 17.41, and 7.04 microns in group E; and 37.82, 19.19, and 6.99 microns in group H for A2, A3, and A4, respectively. During the observation period, a significant and similar vasoconstriction of A2 arterioles was observed in groups E and H but not in group C. By contrast, in the three groups, no significant changes in diameter were found for the A3 and A4 arterioles. Capillary perfusion was markedly impaired in group E: at 60 min the percentage of non-perfused capillaries was 40.92 +/- 6.65% in group E compared with 21.17 +/- 5.45% in group C (P less than 0.05) and 18.18 +/- 8.11% in group H (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Diaphragmatic microcirculation during halothane and isoflurane exposure in pentobarbital-anesthetized rats.

We investigated the effects of halothane and isoflurane on diaphragmatic microcirculation in pentobarbital-anesthetized rats by in vivo video microscopy. After a baseline period, rats were randomly allocated into three groups according to administration of 0.5, 0.75, and 1 minimal alveolar concentration (MAC) of either halothane (group Hal, n = 16), isoflurane (group Iso, n = 14), or no halogenated agent (group C, n = 20) in three succeeding steps of 15 min. Mean arterial blood pressure (MAP), arteriolar diameters, and functional capillary density were analyzed in the last 3 min of each step. MAP remained unchanged in group C but decreased in a dose-dependent manner in both halogenated receiving groups. MAP was significantly lower in rats breathing Hal compared with those breathing Iso. Arterioles were classified in second (A2, n = 39), third (A3, n = 24), and fourth (A4, n = 30) order according to their relative location in the network. No changes in A2 and A3 diameters were noted in either group. A4 diameters remained unchanged in groups C and Iso, whereas a significant reduction was found in group Hal at 0.75 and 1 MAC exposure (P < 0.05 compared with baseline and with groups C and Iso, respectively). During Iso exposure, functional capillary density was not significantly different when compared with baseline and group C, whereas in group Hal it decreased significantly at 0.5, 0.75, and 1 MAC, amounting to 61.1 +/- 9, 30.7 +/- 10.3, and 22.8 +/- 6.3%, respectively, of baseline (P < 0.01 vs. baseline and P < 0.05 vs. groups Iso and C for 0.75 and 1 MAC).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗
PubMed1992

Effects of N-acetylcysteine on diaphragmatic function and malondialdehyde content in Escherichia coli endotoxemic rats.

We evaluated the effects of sublethal Escherichia coli endotoxemia with or without concomitant administration of N-acetylcysteine, an antioxidant agent, on diaphragmatic strength, endurance, and malondialdehyde (MDA) content in rats. One hundred ninety rats were inoculated subcutaneously on 2 successive days with 0.6 and 1.2 mg/100 g body weight of E. coli lipopolysaccharide respectively (E animals, n = 100) or saline (C group, n = 90). E and C animals were divided into two groups based on administration of endotoxin or saline alone (E group, n = 55; C group, n = 47, respectively) or endotoxin or saline plus N-acetylcysteine (1 g/kg body weight/day intraperitoneally) (E-NAC group, n = 45; C-NAC group, n = 43, respectively). Diaphragmatic strength was assessed in vivo 48 h after the first endotoxin or saline administration by measuring the transdiaphragmatic pressure (Pdl) generated during electrical stimulation of the phrenic nerves at 0.5, 10, 20, 30, 50, and 100 Hz. Endurance index was calculated as the percent ratio of Pdl generated after 30 s of phrenic stimulation at 10 Hz divided by the initial force. Diaphragmatic MDA (fluorometric technique) was measured 0, 6, 18, 30, 42, and 48 h after the first dose of endotoxin or saline. Pdl for 50 and 100 Hz was significantly reduced in Group E as compared with group C. This phenomenon was associated with a reduced endurance performance as assessed by a lower diaphragmatic endurance index in E as compared with C animals (90.9 +/- 4.2 versus 114.3 +/- 4.1 respectively; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcysteine↗
PubMed1990

A preparation for in vivo study of the diaphragmatic microcirculation in the rat.

A new preparation is described for the study of the microcirculation of the rat diaphragm by in vivo microscopy. After midline laparotomy, the abdominal site of the diaphragm muscle was exposed. The rat was mechanically ventilated and placed in the Trendelenburg position, thus allowing a microscope placed on a three-dimensional articulated system to be set up perpendicular to the diaphragm. The diaphragm was then transilluminated by inserting fiberoptic microprobes into the thorax cavity by thoracotomy in the fifth intercostal space. This preparation allowed us to describe the morphological characteristics of the arteriolar network in vivo. As regards the venular network, two parts were distinguished: one part collects the blood of the external half of the diaphragm, runs roughly parallel to the arterioles, and converges toward the internal mammary and intercostal veins; the other part collects the blood of the central half of the diaphragm and converges on the central venous arcade along its central tendon. Anastomotic channels between these two parts were observed, as well as spontaneous inversion of the direction of the blood flow, indicating the presence of unsteady pressure gradients in some branches of the venular network. Capillary density was also studied by measuring intercapillary distance, whose mean value was 21.43 +/- 0.67 microns. No differences in intercapillary distance were found between the external and central parts of the diaphragm. In conclusion, we describe a preparation which allowed us to study the diaphragmatic microcirculation for at least 2 hr under good hemodynamic conditions. The study of this specific microcirculation is important because the diaphragm's metabolism and functions are specific and because it is essential to life that its perfusion should be adapted to its specific metabolic requirements.

Animals↗
PubMed1990

Preventive effects of indomethacin on diaphragmatic contractile alterations in endotoxemic rats.

We evaluated the effects of a sublethal Escherichia coli endotoxemia with and without concomitant administration of indomethacin on diaphragmatic strength in an in vivo rat model. Ninety-six rats were inoculated subcutaneously on two successive days with 0.3 and 0.6 mg/100 g body weight of E. coli lipopolysaccharide, respectively (E animals, n = 64), or saline (C group, n = 32). E animals were divided into two groups based on subcutaneous administration of endotoxin alone (E group, n = 32) or endotoxin plus indomethacin (2.5 mg/kg body weight/day) (EI group, n = 32). Diaphragmatic strength was evaluated in 14 animals from each group 2 days after the first endotoxin or saline administration. Diaphragmatic strength was assessed by measuring the transdiaphragmatic pressure (Pdi) during electrical stimulation of the phrenic nerves at different frequencies (0.5, 10, 20, 30, 50, and 100 Hz). Lung histologic examination and measurements of lung weights were performed 1 and 2 days after the first endotoxin or saline administration in nine animals of each group each day. A slight increase in the number of neutrophils without alveolar septal thickening and alveolar edema was observed in the lungs of endotoxin-inoculated animals. No differences in the lung weight to body weight ratio nor in the dry to wet weight ratio of the lungs were noted between C, E, and EI groups. Diaphragmatic weight was not different in the three groups, whereas the weights of the extensor digitorum longus, tibialis anterior, and soleus muscles were significantly reduced in E compared with C and EI animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Dopamine effects on diaphragmatic strength during acute respiratory failure in chronic obstructive pulmonary disease.

STUDY OBJECTIVE: To assess the effects of dopamine, which has an inotropic effect on the myocardium and increases renal and splanchnic blood flow, on diaphragmatic contraction. DESIGN AND PATIENTS: We studied the changes in transdiaphragmatic pressure during electrical bilateral supramaximal stimulation of the phrenic nerves in eight patients with chronic obstructive pulmonary disease during acute respiratory failure. In three patients, changes in diaphragmatic blood flow were also evaluated. METHODS: All patients were intubated and artificially ventilated. Stimulated transdiaphragmatic pressure, cardiac output, evaluated with a Swan Ganz catheter, and diaphragmatic blood flow, evaluated by timed volume collections of left phrenic venous effluent (a catheter was introduced into the right femoral vein and advanced into the left inferior phrenic vein) were measured before dopamine infusion, every 10 minutes after the onset of dopamine infusion (10 micrograms/kg body weight.min during 30 minutes) and 15 minutes after the end of dopamine infusion. Arterial blood gases and pH were measured before and at the end of dopamine infusion. MEASUREMENTS AND MAIN RESULTS: Arterial blood gases and pH were maintained within normal range by mechanical ventilation throughout the study. With dopamine infusion, heart rate increased by 17% (P less than 0.001) and cardiac output by 40% (P less than 0.001) on the average. The increase in cardiac output was accompanied by a marked increase in diaphragmatic blood flow (30% on the average) in the three patients in whom it was measured (P less than 0.001). Diaphragmatic strength also increased significantly during dopamine administration. Transdiaphragmatic pressure for an identical phrenic stimulation increased by 30% (P less than 0.001) on the average. The changes in cardiac output, diaphragmatic blood flow, and transdiaphragmatic pressure persisted throughout the infusion period; all values returned to control values 15 minutes after the end of dopamine administration. CONCLUSIONS: Dopamine has a potent effect on diaphragmatic strength generation and diaphragmatic blood flow in patients with chronic obstructive pulmonary disease during acute respiratory failure. It is possible to improve diaphragmatic contraction in these patients by administering pharmacologic agents that augment diaphragmatic blood flow.

Action Potentials↗