SUMMARYIn anaesthetized, mechanically ventilated, indomethacin-treated pigs, we infused E. coli endotoxin (LPS, 20 ag kg-' h-', I.V.). After 150 min of endotoxaemia, 10 mg kg-1 glibenclamide (an ATPsensitive K+ channel antagonist) was administered i.v. over 5 min. Vascular variables were recorded before (control), after 150 min of endotoxaemia and 5, 15 and 30 min after glibenclamide infusion. Glibenclamide transiently (within 5 min) increased systemic arterial pressure, reduced by LPS administration, without an effect on cardiac output. Our data indicate that ATP-sensitive K+ channels may play a partial role in the vascular changes due to endotoxaemia.
Pulmonary lymphatic vessels extend within the connective tissue sheets surrounding airways and blood vessels. Frequently in this location they also border the lobular parenchyma, but not lymphatic vessels have been found within intralobular compartments between blood capillaries and alveoli. The presence and distribution of lymphatic vessels in pulmonary tissue are consistent with an important role for the lymphatic system in the clearance of interstitial fluids in the lung. Pulmonary lymphatic channels have structural characteristics of initial lymphatics; their walls are formed only by an endothelial layer, and no muscular cells are present. A network of anchoring filaments and collagen and elastic fibers surrounds the vessel walls. Because the lung is a mobile organ the tissue undergoes compression and distension during respiratory phases. These modifications could have a role in the mechanisms for lymph formation and flow.
SUMMARYThe aim of the study was to evaluate the effects of nitric oxide (NO) on diaphragmatic fatigue in fifteen anaesthetized, mechanically ventilated pigs, divided into three groups. The animals were pre-treated with indomethacin (3 mg kg-', I.V.) to block the cyclo-oxygenase pathway. To group 1 pigs (n = 6) NG-nitro-L-arginine methyl ester (L-NAME, 5 mg kg-' I.V.) was administered as a bolus to block endogenous NO production, while group 2 pigs (n = 6) were infused with sodium nitroprusside (SNP, 0 023 mg kg-' min-', I.v.), a donor of NO. Group 3 pigs (n = 3) were used as the controls. We evaluated diaphragmatic strength by measuring the transdiaphragmatic pressure (Pdi) generated during bilateral phrenic nerve stimulation at 10, 20, 30 and 50 Hz, 15 V, while the diaphragmatic endurance was assessed by a 30 s stimulation at 10 Hz, 15 V. Diaphragmatic index was assessed as the ratio of peak force between single twitches performed before and after the 30 s stimulation test. We also evaluated mean systemic (MAP) and pulmonary (MPAP) arterial pressures, pulmonary wedge pressure (Pw), systemic (SVR) and pulmonary vascular resistances (PVR) and cardiac output (CO). L-NAME increased MAP, MPAP, Pw, SVR and PVR, but decreased CO. SNP caused a decrease in MAP, MPAP, Pw and SVR, while PVR and CO did not change. The main finding of this study was that diaphragmatic strength was not significantly weakened after L-NAME administration, except at 10 Hz, while it did not change after SNP infusion. However, both L-NAME and SNP caused significant decreases in diaphragmatic endurance capacity. The fatigue appearing after L-NAME is probably correlated with a decline in diaphragmatic blood flow, as evidenced by the increase in SVR and the decrease in CO, and consequently in oxygen supply. In contrast, the decrease in endurance capacity after SNP infusion can be attributed to a direct action of NO on skeletal muscle.
In six dogs trained to wear a mask and to swallow an esophageal balloon, the dynamic work of breathing (Wdyn) was measured while the animals ran on a treadmill at different intensities (7-13 km.h-1,+10%). Wydn (kg.m.min-1) increased with ventilation (VE, 1.min-1) according to Wdyn = 0.308.10(-2) VE2 + 0.0098.10(-2).VE3. However, if the exercise was prolonged so that the body temperature rose above approximately 39 degrees C, Wdyn, for a given ventilation, decreased; and hence Wdyn = 0.253.10(-2).VE2 -- 0.0011.10(-2).VE3. Similar observations have been made on another dog heated from an external source. From this finding it seems that during exercise, when the temperature rises and the ventilation increases to dissipate heat, the airway size, at least in some portion of the respiratory tract, increases markedly and therefore the cost of breathing is greatly diminished. This mechanism would save oxygen for the exercising limb muscles when exercise has to be continued for an extended time.
SUMMARYLaryngeal airflow resistance was measured in anaesthetized pigs during stimulation of lung vagal reflexes by injection of phenylbiguanide and of capsaicin, before and during pulmonary microembolism due to intravenous injection of hardened red blood cells; the microembolism caused pulmonary hypertension. The Breuer-Hering reflex was also assessed before and after pulmonary microembolism. Phenylbiguanide and capsaicin caused apnoea followed by rapid shallow breathing, hypertension, bradycardia and laryngeal constriction in inspiration and expiration. Most of these effects were abolished by bilateral cervical vagotomy. Pulmonary microembolism caused only small changes in breathing pattern, mainly a decrease in inspiratory time. After microembolism the Breuer-Hering reflex was enhanced, and injections of phenylbiguanide and capsaicin caused longer apnoeas by a vagal reflex. The changes in pattern of breathing and in lung reflexes after lung microembolism and during the associated pulmonary hypertension are consistent with an enhancement of pulmonary stretch receptor activity in this condition, but do not indicate any important role for C fibre reflexes.
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