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La medicina tiene como propósito principal lograr una mejor calidad de vida en los pacientes. Para que esto sea posible no es suficiente conformarse con estudiar y tratar el aspecto físico de estos, también es igualmente importante tener la posibilidad de curar su alma. Luego de explicar y analizar diferentes conceptos y realidades de lo que son el alma y el espíritu, notamos que es perfectamente posible para el médico mejorar la calidad de vida espiritual de su paciente una vez que acepte que, aunque no es algo científicamente comprobable, el alma y el espíritu existen y son esenciales para la óptima sanidad y cura de todo ser humano

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The effect of dopamine over pulmonary edema induced by PAF was studied. Thirty preparations of rabbit lungs were used: six control preparations (CP), six PAF preparations (PP) in which we injected a dose of 1 microg/kg of rabbit weight and eighteen dopamine preparations (DAP) divided in three groups of six pretreated with a dose of 1-5 (dopaminergic range), 10-20 (Beta range) and 20-30 ug/kg/min (Alpha range) of dopamine, respectively for 30 min, followed by an injection of PAF as in the PP. DAP at Beta and Alpha-adrenergic range decreased pulmonary artery pressure (Pap) as compared to CP, with values of 11.66 (CI 95%: 10.83-12.48), 11.66 (CI 95%: 9.87-13.44) versus 17.12 (CI 95%: 16.12-18.11) cm of water, respectively. DAP in Beta and Alpha-adrenergic range prevented Pap increment as compared to PP, with values of 17.16 (CI 95%: 16.37-17.94), 17.5 (CI 95%: 14.93-20.06) versus 84 cm of water (CI 95%: 71.41-96.58), respectively. Dopamine, at its three ranges inhibited the augmentation of the fluid filtration rate observed in PP with values of 1.01 (CI 95%: 0.77-1.24), 0.03 (CI 95%: 0.01-0.04) and 0.02 g/min (CI 95%: -0.0004-0.03) versus 2.13 g/min (CI 95%: 1.56-2.69), respectively. We concluded that dopamine has a vasodilator effect on Pap and exerts an inhibiting action over PAF effects in pulmonary circulation. Such effects seem to be mainly mediated by Beta-receptors, rather than by dopaminergic receptors.

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It is well known that scorpion venom induces lung lesions and respiratory distress which are usually classified as pulmonary oedema (PO). Tityus discrepans is a scorpion that lives in the north-central area of Venezuela, is the most common source of human envenomation here and produces PO. We studied the action of the venom of Tityus discrepans on whole rabbits and on their isolated lungs perfused with Krebs saline with 1 g/l of bovine serum albumin (Krebs-BSA saline). Two milligram of venom were diluted in 250 ml of solution (approximately the rabbit's total blood volume) and used to perfuse isolated lungs. Lung oedema occurred in rabbits which received 1 mg/kg of scorpion venom i.p., heparin prevented the production of this lung oedema. T. discrepans venom produced PO, in rabbits pretreated with 15 mg/kg of ajoene. Yet, Tityus venom had no effects on isolated lungs perfused with citrated or heparinized blood, and in lungs perfused with Krebs-BSA with normal Ca2+. These result show that Tityus venom does not act directly on lungs. Otherwise, we have observed that abundant microthrombi occurred in all rabbit lungs exposed to venom in vivo, suggesting that these clotting alterations are fundamental to produce PO. The presence of intravascular microthrombi is not characteristic of the usual PO hinting that scorpion venom induced pulmonary alterations are a different clinical entity. We thus propose that the use of the term pulmonary oedema in scorpionism should abandoned in favor of scorpion venom respiratory distress syndrome.

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We report a 63 years old man presenting with a history of persistent cough and blood streaked sputum. Chest X rays and CAT scans showed a tumoral lesion between the superior and inferior right lobes. The tumor was resected and its pathological examination revealed an inflammatory pseudotumor. It is concluded that this type of tumors must be born in mind in patients with nodular lesions of the lung.

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To determine the effects of pH changes on Pulmonary Artery Pressure (PAP), 18 isolated rabbit lung preparations, perfused with autologous blood mixture and constant PaCO2 have been studied. Each preparation was studied under 3 conditions: Baseline: 30 minutes equilibration period. Acidosis: pH was decreased by 0.2 N HCl infusion, the ventilatory rate was changed and different CO2 mixtures were used to maintain the PCO2 within the initial parameters. Compensated Acidosis (CA): pH was returned to normal values by 0.7 N NaHCO3 infusion maintaining PCO2 in its initial values. The decrease in pH (acidosis) from 7.36 +/- 0.05 to 7.18 +/- 0.06 at constant PCO2, generated a significant increase in PAP (13.6 +/- 3.2 cm H2O to 18.8 +/- 5.2 cm H2O, p < 0.01). The pH increase (CA) from 7.18 +/- 0.06 to 7.40 +/- 0.09 caused the PAP to decrease (18.8 +/- 5.2 cm H2O to 15.9 +/- 4.2 cm H2O); the fluid filtration rate remained unchanged during the whole experiment. It is concluded that blood pH changes at constant PCO2 result in significant changes of PAP. Acidemia produces pulmonary vasoconstriction, which may be a contributing factor in the genesis of pulmonary hypertension in clinical conditions with increased hydrogen ion concentration [H+].

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To study the possible effects of Furosemide at the lung level, two groups of isolated rabbit lung preparation were studied. An experimental group underwent a pulmonary hydrostatic oedema when the pressure of the left auricle (PAI) was increased from 0.45 +/- 0.74 t0 11.8 +/- 2.9 cm of H2O, with that increase in PAI we obtained an increase of 0.457 +/- 0.51 g/min in FFR (Fluid Filtration Rate), during this stable and sustained oedema, a 2 mg/Kg dosis of Furosemide was injected every 10 minutes and the possible changes in PAP, PAI, PVA, TFL, PaO2, PaCO2 and pH was observed, but no changes were observed in these parameters during the Furosemide infusion, and the same effect was observed in the control group were the preparations were maintained in basal conditions and without oedema. These results suggests that the Furosemide hat not a direct cardio-pulmonary effects, and the only possible effects could be by increasing diuresis at renal level.

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INTRODUCTION: We study the effect on Intralipid on pulmonary circulation. METHODS: A 10% infusion of Intralipid was administered at a dose of 0.5/kg in 14 isolated rabbit lungs in which constant blood flow infusion was carried out principally in zone 3. The liquid filtration rate (LFR) and the mean pressure of the pulmonary artery were measured. RESULTS: A constant increase of mean pressure of the pulmonary artery was observed following the infusion (from 12.32 +/- 3.66 cm of H2O to 39.92 +/- 07.68 cmH2O (p < 0.01) which was associated to a significant increase in the rate of liquid filtration (from 0.018 +/- 0.01 g/min to 0.198 +/- 0.04 g/min; p < 0.01). CONCLUSIONS: The administration of Intralipid produces a statistically significant increase of mean pressure of the pulmonary artery and the rate of liquid filtration. This is probably caused by vasoconstriction due to metabolic changes produced by Intralipid on pulmonary circulation.

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The contribution of cyclo-oxygenase and 5-lipoxygenase metabolites on hemodynamics and oedema formation was investigated in 21 isolated rabbit lungs after a 10 min Oleic Acid (OA) infusion, by recording the changes on Fluid Filtration Rate (FFR) and Pulmonary Artery Pressure (PAP). Lungs (n = 7) were pre-treated with indomethacin (cyclo-oxygenase inhibitor) 50 min prior to OA or with Diethylcarbamazine (5-lipoxygenase inhibitor) (n = 7) or not pre-treated at all (control group, n = 7). The FFR in the indomethacin group was significantly greater than in the control and Diethylcarbamazine (DEC) groups 12 min after OA (7.6 +/- 2.3 mg.min-1 vs. 2.3 +/- 0.8 mg.min-1 and 0.96 +/- 0.8 mg.min-1 respectively) (P < 0.01). The FFR in the control lungs 20 min after OA was significantly greater than the corresponding DEC value (4.2 +/- 0.5 mg.min-1 vs. 1.6 +/- 1.0 mg.min-1) (P < 0.01). Mean Pulmonary Artery Pressure (MPAP) increased both in control and indomethacin groups (16.0 +/- 2.0 Torr to 24.3 +/- 3.7 Torr after 20 min OA and 14.4 +/- 2.5 Torr to 24.6 +/- 3.6 Torr at 10 min after OA, respectively), but MPAP value in DEC group did not significantly change 30 min after OA (14.7 +/- 1.5 Torr to 16.0 +/- 2.3 Torr) (P > 0.05). So we conclude that the selective inhibition of the 5-lipoxygenase metabolites (leukotriene-5hete) may play a protective role in OA induced oedema, whereas the selective inhibition of the cyclo-oxygenase pathway may have a deleterious effect on the hemodynamics and endothelial permeability in our experimental condition.

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The contribution of cyclo-oxygenase and 5-lipoxygenase metabolites on hemodynamics and oedema formation was investigated in 21 isolated rabbit lungs after a 10 min Oleic Acid (OA) infusion, by recording the changes on Fluid Filtration Rate (FFR) and Pulmonary Artery Pressure (PAP). Lungs (n = 7) were pre-treated with indomethacin (cyclo-oxygenase inhibitor) 50 min prior to OA or with Diethylcarbamazine (5-lipoxygenase inhibitor) (n = 7) or not pre-treated at all (control group, n = 7). The FFR in the indomethacin group was significantly greater than in the control and Diethylcarbamazine (DEC) groups 12 min after OA (7.6 +/- 2.3 mg.min-1 vs. 2.3 +/- 0.8 mg.min-1 and 0.96 +/- 0.8 mg.min-1 respectively) (P < 0.01). The FFR in the control lungs 20 min after OA was significantly greater than the corresponding DEC value (4.2 +/- 0.5 mg.min-1 vs. 1.6 +/- 1.0 mg.min-1) (P < 0.01). Mean Pulmonary Artery Pressure (MPAP) increased both in control and indomethacin groups (16.0 +/- 2.0 Torr to 24.3 +/- 3.7 Torr after 20 min OA and 14.4 +/- 2.5 Torr to 24.6 +/- 3.6 Torr at 10 min after OA, respectively), but MPAP value in DEC group did not significantly change 30 min after OA (14.7 +/- 1.5 Torr to 16.0 +/- 2.3 Torr) (P > 0.05). So we conclude that the selective inhibition of the 5-lipoxygenase metabolites (leukotriene-5hete) may play a protective role in OA induced oedema, whereas the selective inhibition of the cyclo-oxygenase pathway may have a deleterious effect on the hemodynamics and endothelial permeability in our experimental condition.

RESUMO

The contribution of cyclo-oxygenase and 5-lipoxygenase metabolites on hemodynamics and oedema formation was investigated in 21 isolated rabbit lungs after a 10 min Oleic Acid (OA) infusion, by recording the changes on Fluid Filtration Rate (FFR) and Pulmonary Artery Pressure (PAP). Lungs (n = 7) were pre-treated with indomethacin (cyclo-oxygenase inhibitor) 50 min prior to OA or with Diethylcarbamazine (5-lipoxygenase inhibitor) (n = 7) or not pre-treated at all (control group, n = 7). The FFR in the indomethacin group was significantly greater than in the control and Diethylcarbamazine (DEC) groups 12 min after OA (7.6 +/- 2.3 mg.min-1 vs. 2.3 +/- 0.8 mg.min-1 and 0.96 +/- 0.8 mg.min-1 respectively) (P < 0.01). The FFR in the control lungs 20 min after OA was significantly greater than the corresponding DEC value (4.2 +/- 0.5 mg.min-1 vs. 1.6 +/- 1.0 mg.min-1) (P < 0.01). Mean Pulmonary Artery Pressure (MPAP) increased both in control and indomethacin groups (16.0 +/- 2.0 Torr to 24.3 +/- 3.7 Torr after 20 min OA and 14.4 +/- 2.5 Torr to 24.6 +/- 3.6 Torr at 10 min after OA, respectively), but MPAP value in DEC group did not significantly change 30 min after OA (14.7 +/- 1.5 Torr to 16.0 +/- 2.3 Torr) (P > 0.05). So we conclude that the selective inhibition of the 5-lipoxygenase metabolites (leukotriene-5hete) may play a protective role in OA induced oedema, whereas the selective inhibition of the cyclo-oxygenase pathway may have a deleterious effect on the hemodynamics and endothelial permeability in our experimental condition.

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We studied the effect of varying ventilatory frequency (VF) using intermittent positive pressure ventilation (IPPV) on fluid filtration rate (FFR) in 16 isolated rabbit lung preparations perfused at constant blood flow and airway pressure (AWP). Mean pulmonary artery pressure (MPAP), AWP, pulmonary vascular resistance (PVR), pH, PaO2, PaCO2 and colloid osmotic pressure (COP) were measured. Ventilation was performed by a piston pump ventilator. VF was ahanged every 10 min. by the following schedule 25-40-55-70-40-25 breaths per min. A group of 6 rabbits was ventilated under normal hemodynamic conditions and another group of 10 rabbit was ventilated after the prodution of hydrostatic pulmonary edema. Blood gas exhange was satisfactory in both groups of rabbits. There was not statistically significant correlation between VF and FFR in the two experimental situations (p>0.05). In conclusion, VF variation using IPPV (keeping AWP constant) did not alter liquid transfer between the microvasculature and lung interstitial space under normal hemodynamic conditions nor in hydrostatic lung edema in insolated perfused rabbits lung

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