Effect of saline infusion for the maintenance of blood volume on pulmonary gas exchange during temporary abdominal aortic occlusion.

We analyzed the effects of saline infusion for the maintenance of blood volume on pulmonary gas exchange in ischemia-reperfusion syndrome during temporary abdominal aortic occlusion in dogs. We studied 20 adult mongrel dogs weighing 12 to 23 kg divided into two groups: ischemia-reperfusion group (IRG, N = 10) and IRG submitted to saline infusion for the maintenance of mean pulmonary arterial wedge pressure between 10 and 20 mmHg (IRG-SS, N = 10). All animals were anesthetized and maintained on spontaneous ventilation. After obtaining baseline measurements, occlusion of the supraceliac aorta was performed by the inflation of a Fogarty catheter. After 60 min of ischemia, the balloon was deflated and the animals were observed for another 60 min of reperfusion. The measurements were made at 10 and 45 min of ischemia, and 5, 30, and 60 min of reperfusion. Pulmonary gas exchange was impaired in the IRG-SS group as demonstrated by the increase of the alveolar-arterial oxygen difference (21 +/- 14 in IRG-SS vs 11 +/- 8 in IRG after 60 min of reperfusion, P = 0.004 in IRG-SS in relation to baseline values) and the decrease of oxygen partial pressure in arterial blood (58 +/- 15 in IRG-SS vs 76 +/- 15 in IRG after 60 min of reperfusion, P = 0.001 in IRG-SS in relation to baseline values), which was correlated with the highest degree of pulmonary edema in morphometric analysis (0.16 +/- 0.06 in IRG-SS vs 0.09 +/- 0.04 in IRG, P = 0.03 between groups). There was also a smaller ventilatory compensation of metabolic acidosis after the reperfusion. We conclude that infusion of normal saline worsened the gas exchange induced by pulmonary reperfusion injury in this experimental model.

Effect of saline infusion for the maintenance of blood volume on pulmonary gas exchange during temporary abdominal aortic occlusion

We analyzed the effects of saline infusion for the maintenance of blood volume on pulmonary gas exchange in ischemia-reperfusion syndrome during temporary abdominal aortic occlusion in dogs. We studied 20 adult mongrel dogs weighing 12 to 23 kg divided into two groups: ischemia-reperfusion group (IRG, N = 10) and IRG submitted to saline infusion for the maintenance of mean pulmonary arterial wedge pressure between 10 and 20 mmHg (IRG-SS, N = 10). All animals were anesthetized and maintained on spontaneous ventilation. After obtaining baseline measurements, occlusion of the supraceliac aorta was performed by the inflation of a Fogarty catheter. After 60 min of ischemia, the balloon was deflated and the animals were observed for another 60 min of reperfusion. The measurements were made at 10 and 45 min of ischemia, and 5, 30, and 60 min of reperfusion. Pulmonary gas exchange was impaired in the IRG-SS group as demonstrated by the increase of the alveolar-arterial oxygen difference (21 ± 14 in IRG-SS vs 11 ± 8 in IRG after 60 min of reperfusion, P = 0.004 in IRG-SS in relation to baseline values) and the decrease of oxygen partial pressure in arterial blood (58 ± 15 in IRG-SS vs 76 ± 15 in IRG after 60 min of reperfusion, P = 0.001 in IRG-SS in relation to baseline values), which was correlated with the highest degree of pulmonary edema in morphometric analysis (0.16 ± 0.06 in IRG-SS vs 0.09 ± 0.04 in IRG, P = 0.03 between groups). There was also a smaller ventilatory compensation of metabolic acidosis after the reperfusion. We conclude that infusion of normal saline worsened the gas exchange induced by pulmonary reperfusion injury in this experimental model.

Hemodynamic improvement in hemorrhagic shock by aortic balloon occlusion and hypertonic saline solutions.

The initial treatment of uncontrolled hemorrhage shock from an abdominal source is controversial. The hemodynamic effects of transfemoral diaphragmatic aortic occlusion with a balloon followed by a single bolus of hypertonic saline solutions have been evaluated in 28 dogs. The animals were submitted to pressure-driven hemorrhage for 90 min, according to mean arterial pressure in the abdominal aorta and randomized into four groups, according to the treatment employed at 34 min after hemorrhage. Group 1 dogs (controls) received isotonic NaCl (0.9%, 208 mOsm/l, 4 ml/kg) without aortic occlusion; group 2 underwent aortic occlusion and received isotonic NaCl (0.9%, 308 mOsm/l, 4 ml/kg): group 3 were occluded and received hypertonic NaCl (7.5%, 2400 mOsm/l, 4 ml/kg); group 4 were occluded and received hypertonic sodium acetate (10.5%, 2400 mOsm/l, 4 ml/kg). There were no significant differences between groups at basal measures and also after 30 min of continuous bleeding, when animals presented with severe shock, and significant decreases in mean arterial pressure, cardiac index, systolic index and cardiac filling pressures; the systemic vascular resistance index was increased. Control animals remained in severe shock throughout the experiment and three died. The recovery of mean arterial pressure in aortic-occluded dogs given isotonic NaCl was associated with a marked increase in systemic vascular resistance index, without improvements in cardiac index, systolic index and cardiac filling pressures. In occluded dogs given hypertonic NaCl and NaAc the mean arterial pressure recovery lasted longer, with lower increases in systemic vascular resistance index, while the cardiac index, systolic index and cardiac filling pressures showed a marked albeit transient increase. Injection of hypertonic saline following aortic occlusion produced significantly better hemodynamic profiles and should be seriously considered for the first treatment in severe uncontrolled hemorrhagic shock from an abdominal vascular source.

[Effect of dopamine in dopaminergic doses on pulmonary circulation of dogs in normoxia and hypoxia]. / Efeitos da dopamina em doses dopaminérgicas sobre a circulação pulmonar de cães em normóxia e hipóxia.

PURPOSE: To study if dopamine in dopaminergic doses (1.5 and 4.0 micrograms/kg/min) had some effect on the pulmonary vasoconstriction mechanism, and if in those doses the drug had some action on systemic and pulmonary hemodynamic variables, as well as in the pulmonary gas exchange. METHODS: Seventeen normal mongrel dogs, anesthetized and paralized under mechanical ventilation were submitted to two different gas mixtures: room air (F1O2 = 0.2093 -10 dogs) and hypoxic mixture (F1O2 = 0.125 -7 dogs). Dopamine was infused in both groups during 15 min in the two doses 1.5 and 4.0 micrograms/km/min, separated by a period of 30 min. RESULTS: Pulmonary hemodynamics and gas exchange variables after infusion of dopamine at 1.5 and 4.0 micrograms/km/min in dogs in normoxia and hypoxia. [table: see text] CONCLUSION: Dopamine in the used doses had no action on the pulmonary circulation and on the hypoxic pulmonary vasoconstriction mechanism; pulmonary gas exchange was not affected by dopamine in both doses during normoxia and hypoxia; in the experimental model there was no evidence of dopaminergic receptors in the pulmonary vessels.

Effects of almitrine on the ventilatory control, breathing pattern and maximal exercise tolerance in hypoxemic patients with chronic obstructive pulmonary disease.

Almitrine bismesylate improves arterial blood gases in patients with chronic obstructive pulmonary disease (COPD), but side effects such as increase of ventilatory drive and dyspnea have been reported in some studies. We studied 18 COPD patients (mean age = 59.1 years; mean FEV1 = 0.92 1; mean PaO2 = 58.6 mmHg) in a double-blind randomized study using placebo or almitrine 50 mg twice a day by mouth, for 60 days. In contrast to the placebo group, 40% of the patients in the almitrine group presented a significant increase in PaO2 and a decrease in P(A-a)O2 > or = 5 mmHg during submaximal exercise after 60 days of treatment. Ventilatory drive and the breathing pattern were measured at rest and during submaximal exercise. Both groups showed high levels of ventilatory drive and a tachypneic breathing pattern before drug treatment and no modification was found 30 and 60 days after treatment. Metabolic, cardiovascular and ventilatory variables were studied during an incremental to maximum exercise symptom-limited test (cycloergometry). Maximal VO2 ranged from 46 to 52% and heart rate from 76 to 78% in relation to the predicted values. The percent ratio of ventilation at maximal exercise to maximal voluntary ventilation at rest ranged from 86 to 94%. These results show that the reduction of ventilatory capacity was the main factor decreasing the aerobic performance of our COPD patients. Maximal exercise tolerance (VO2 max) did not change after almitrine treatment. Negative factors like an increase in neuromuscular drive did not occur, and positive factors like an increase in PaO2 and oxygen transport had no critical influence on exercise performance in our ventilatory-limited COPD patients.

Effects of almitrine on the ventilatory control, breathing pattern and maximal exercise tolerance in hypoxemic patients with chronic obstructive pulmonary disease

Almitrine bismesylate improves arterial blood gases in patients with chronic obstructive pulmonary disease (COPD), but side effects such as increase of ventilatory drive and dyspnea have been reported in some studies. We studied 18 COPD patients (mean age=59.1 years; mean FEV1=0.921; mean PaO2=58.6mmHg) in a double-blind randomized study using placebo or almitrine 50 mh twice a day by mouth, for 60 days. In contrast to the placebo group, 40 per cent of the patients in the almitrine group presented a significant increase in PaO2 and a decrease in P(A-a))2>=5mmHg during submaximal exercise after 60 days of treatment. Ventilatory drive and the breathing pattern were measured at rest and during submaximal exercise. Both goups showed high levels of ventilatory drive and atachypneic breathing pattern before drug tratment and no modification was found 30 and 60 days after treatment. Metabolis, cardiovascular and ventilatory variables were studied during an incremental to maximum exercise symptom-limited test (cycloergometry). Maximal VO2 ranged from 46 to 52 per cent and heart rate from 76 to 78 per cent in relation to the predicted values. The percent ratio of ventilation at maximal exercise to maximal voluntary ventilation at rest ranged from 86 to 94 per cent. These results show that the reduction of ventilatory capacity was the main factor decreasing the aerobic performance of our COPD patients. Maximal exercise tolerance (VO2 max) did not change after almitrine treatment. Negative factors like an increase in neuromuscular drive did not occur, and positive factors like an increase in PaO2 and oxygen transport had no critical influence on exercise performance in our ventilatory-limited COPD patients.

[The effect of nifedipine on hemodynamics and gas exchange in dogs with experimental acute respiratory insufficiency]. / Ação da nifedipina na hemodinâmica e nas trocas gasosas em cães com insuficiência respiratória aguda experimental.

PURPOSE: Evaluate the action of nifedipine, a calcium channel blocking agent, on the hemodynamics and gas exchange experimental acute respiratory failure. METHODS: Lung injury was provoked in sixteen mongrel dogs with intratracheal instillation of hydrochloric acid (HC1) (0.1N; pH = 2.0; 2.0 ml/kg body weight). As steady state was achieved after HC1 instillation (maintenance of a stable arterial PO2), saline 1 ml (six dogs) or nifedipine (ten dogs) 30 micrograms/kg for body weight were intravenously injected. The hemodynamic variables and gas exchange parameters were analyzed before HC1, after HC1 and 10 and 30 minutes after nifedipine or saline. RESULTS: The intratracheal instillation of HC1 provoked significant drop of PaO2, of systemic oxygen transport index (ITO2S), and increase of venous admixture (QVA/Q). Nifedipine provoked significant reduction of the mean systemic arterial pressure (Pas), and of the systemic (IRVS) and pulmonary vascular resistance index (IRVP), with significant increase of cardiac (IC) and systolic index (IS), with no changes ot the mean arterial pulmonary (Pap) and capillary pressures (Pcap). After nifedipine there was a significant increase of PaO2, PvO2, and ITO2S, with no significant variations of QVA/Q and alveolar arterial O2 difference (P(A-a)O2). CONCLUSION: Nifedipine promoted systemic vasodilation, and probably by increasing the venous return and/or by a reflex mechanism, the cardiac output increased, augmenting the ITO2S. The IRVP decreased in the nifedipine group, with no significant alterations of Pap and Pcap, probably consequent to the systemic vasodilation provoked by the drug. The arterial PO2 augmented in the nifedipine group, as a consequence of mixed venous PO2 increase, since no changes occurred in QVA/Q, P(A-a)O2, inspired fraction of O2 and alveolar ventilation.

[Idiopathic pulmonary hemosiderosis in the adult: a case report]. / Hemossiderose pulmonar idiopática do adulto: descrição de um caso.

The case of idiopathic pulmonary hemosiderosis in a 20 year old male is presented. Iron deficiency anemia, recurrent hemoptysis and micronodular infiltrate in lower lung areas were the most important signs observed. The transbronchial biopsy showed alveolar and interstitial hemorrhage and hemosiderin in the pulmonary macrophages. Treatment was started with prednisone, but the addition of immunosuppressive drugs (cyclophosphamide) was needed, followed by a clinical remission.

Correlation between arterial oxygen and carbon dioxide levels and response to almitrine bismesylate in normal dogs

The objectives of this study were: 1) to test the action of small doses of almitrine bismesylate (0.004 mg/Kg body weight/min) on the arterial blood gases and on pulmonary and systemic circulation during hypoventilation under controlled mechanical ventilation; and 2) to investigate possible correlations between arterial blood. O2 and CO3 levels and the response to the drug. Twenty one dogs divided into two groups were studied under controlled ventilation in a double-blind fashion: hypoventilation + placebo (HP) (seven dogs); hypoventilation + almitrine (HA) (fourteen dogs). The results showed no significant variations of the gas ex-change and hemodynamic varibles in the HP group. In the HP group, during almitrine bismesylate infusion, despite the lack of variation in the pulmonary ventilation, the PaO2 increased from 46.1 torr to 51.7 torr, the PaCO2 decreased from 61.9 torr to 57.7 torr. There were no significant variations of hemodynamic variables in the HA group. Thus we conclude that the drug improved arterial blood gases (PaO2 increased) with small increase in alveolar ventilation (PaCO2 decreased) despite the lack of changes in pulmonary ventilation, and that the drug has action on the arterial PO2 potentiated by hypoxemia and hypercapnia

[Pulmonary hypertension in adult respiratory distress syndrome: review of the literature]. / Hipertensão pulmonar na síndrome do desconforto respiratório do adulto: revisão da literatura.

This paper is a review of clinical and experimental studies on pulmonary hypertension in acute respiratory distress syndrome (ARDS) and its consequences on the outcome of such syndrome. The most probable causes: hypoxic pulmonary vasoconstriction, vasoconstriction provoked by vasoactive substances, extra and intraluminal occlusions are discussed. The authors also discuss the action of vasoactive drugs on the pulmonary circulation and on the pulmonary gas exchange.

[The role of angiotensin-converting enzyme inhibitor (captopril) on the mechanism of hypoxic pulmonary vasoconstriction. Experimental study in dogs]. / Papel do inibidor da enzima conversora da angiotensina (captopril) no mecanismo da vasoconstricção pulmonar hipóxica. Estudo experimental em cães.

In order to evaluate the action of an angiotensin converting enzyme inhibitor (Captopril) on the pulmonary hypoxic vasoconstriction, twenty one mongrel dogs were studied in two groups: group I with hypoxia, group II with normoxia. The dogs were anesthetized, intubated, and had their femoral vein and artery cannulated for blood-gas sampling and pressure records. They were mechanically ventilated with hypoxic gas mixtures (12.3% O2-87.7% N2)--group I and room air group II, at random. In both groups we measured, before and after administration of captopril 3 mg/kg intravenously, gas exchange and hemodynamic variables, as well as plasmatic levels of renin and angiotensin converting enzymes (ACE). Our results showed that the group I dogs decreased the systemic and pulmonary vascular resistances with small changes in pulmonary arterial pressures and no significant variations of pulmonary systemic resistances ratio. There were no significant variations of the same variables in the group II dogs. The gas exchange has not changed in either group of animals. In the group I dogs Captopril provoked systemic and pulmonary vasodilatation, with no gasometric and ventilation/perfusion ratio changes. In our experimental model we could not conclude that Captopril inhibited the hypoxic pulmonary vasoconstriction and/or that the angiotensin II had some action on the hypoxic pulmonary vasoconstriction mechanism, but there are some evidences favoring that hypothesis.

Gas exchange during differential mechanical ventilation after unilateral lung injury induced by hydrochloric acid: experimental study in dogs

In order to test gas exchange in lungs with unilateral injury, when mechanical ventilation is needed, three groups (G-I, G-II, G-III) of seven dogs each were studied. Injury was induced in the left lung by injecting 0,lN, 1.0 ml per kg of body weight of hydrochloric acid, pH = 2.00. For groups I and II a conventional volumetric artificial ventilator was used. G-I was the control group. In group II a bilateral positive end-expiratory pressure (PEEP) was introduced during the last phase (phase 3) of the experiment, and in group III, a prototype of a volume cycled ventilator, with separated bellows, was used delivering tidal volumes separately to each lung through a Carlens' tube. In G-III, PEEP was introduced only to the injured lung in the last phase of the experiment. Phase l (Fl), basal phase, was similar in the three groups; phase 2 (F2) was the period after instillation of hydrochloric acid and phase 3 was the period after a 5 cmH2O bilateral PEEP was used in G-II, and a selective PEEP to the left lung was used in G-III. In each phase of the experiment, hemodynamic and gas exchange variables were obtained. Our results allowed the following conclusions: the differential lung ventilation technique maintained the alveolar ventilation of the dogs and the differential lung ventilation with unilateral PEEP was better for gas exchange (phase 3) than the conventional ventilation with bilateral PEEP (CPPB).

[Hemodynamic and pulmonary effects of nifedipine]. / Efeito hemodinâmico sistêmico e pulmonar da nifedipina.

The authors reviewed the actions of nifedipine, a blocker of calcium channels, on the systemic and pulmonary circulation. The mechanism of action of the drug on the systemic and pulmonary circulation and on the gas exchange is discussed. The main effects of nifedipine on the coronary circulation and indications for therapeutic use of the drug are discussed on the topics of coronary insufficiency, systemic and pulmonary blood hypertension, acute respiratory failure, and Raynaud's phenomenon.

[Effects of captopril on hemodynamics, gas exchange and exercise capacity in patients with pulmonary hypertension secondary to chronic obstructive pulmonary disease]. / Efeitos do captopril na hemodinâmica, nas trocas gasosas e na capacidade de exercício em portadores de hipertensão pulmonar secundária a doença pulmonar obstrutiva crônica.

Captopril, a potent inhibitor of angiotensin converting enzyme, was tested in patients with COPD (means forced expired volume in the first second--FEV1 = 0.73 l) and pulmonary hypertension (PAP = 41.3 mmHg). In the first phase of the experiment, patients underwent and incremental exercise test to the limit of tolerance. These were double blind, randomized, cross-over studies, where the patients received oral placebo (Pl) or captopril (Cp) 25 mg, on different days. In a second phase, the patients were submitted to hemodynamic and gasometric studies in the supine position, before placebo, the 60 min after and immediately after exercise (cycling-like leg movements). After 30 min of rest the same protocol was repeated with oral administration of 25 mg of captopril. In the metabolic evaluation (cycloergometry) captopril increased significantly exercise tolerance (means VO2-uptake at maximal exercise: CP = 0.81 vs Pl = 0.73 1/min), associated with a slower heart rate and higher O2-pulse at maximal exercise. In the hemodynamic study, when the effects of Cp and Pl were compared, the mean values of pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) were similar at rest, but significantly lower during exercise, after captopril (means PAP Cp = 41.3 vs Pl = 51.2 mmHg; XPVR Cp = 278 vs Pl = 392 dyn. sec. cm5). There were similar systemic hemodynamic effects after Cp, but these were more intense in the pulmonary circulation (lower PVR/SVR ratio post-Cp in relation to post-Pl, during exercise). The cardiac index, systemic O2 transport and arterial and mixed venous blood gases were similar at rest and during exercise, with Pl or Cp.(ABSTRACT TRUNCATED AT 250 WORDS)