Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.16.2 (PCP)
 3,761 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Knowledge of osmotic pressure has long existed and its practical use in the treatment of patients under intensive care has been widely developed over the past few years following the introduction of simple electronic osmometers. It is related more to plasma albumin than to globulins. It varies in relation with a certain number of physiological factors and in different pathological circumstances. The value of OP and above all of the difference OP--PCP in the prevention, diagnosis, treatment and prognosis of pulmonary oedema has been clearly demonstrated in several recent studies. Its value in relation to total serum proteins is that it takes into account any possible dysproteinaemia and that it is directly expressed in units of pressure which makes possible the calculation of the OP--PCP difference which represents the difference between the only OP--PCP difference which represents the difference between the only two intravascular forces which participate in fluid exchanges at the level of the pulmonary capillary.
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PMID:[Osmotic colloidal pressure: measurement and clinical importance]. 3 8

A total of 237 patients with AIDS have been observed in the infectious Disease Division of the United Hospitals of Bergamo during the past six years. Five patients (4.21%), suffering from TB and PCP, revealed PNX which was characterised by being bilateral and recurrent; it was a concomitant cause of death in 2 patients. The complications which occurred included acute pulmonary heart, pulmonary edema due to reexpansion and irreversible shock.
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PMID:[Pneumothorax in AIDS]. 158 30

We studied the formation of pulmonary edema on 9 patients with paraquat poisoning using thermal-sodium double indicator dilution method for the measurement of lung water. In survivors group (n = 4) extravascular thermal volume (EVTV) was not almost changes. In non-survivors group (n = 5) EVTV increased about three times as much as that in survivors group on 32 hours after admission. EVTV was correlated with PCP-PCOP in both survivors group and non-survivors group (n = 64, r = 0.665, p less than 0.01). But EVTV in non-survivors group was higher than that in survivors group within same PCP-PCOP. In non-survivors group delta EVTV/delta (PCP-PCOP) in 24 hours after admission was correlated with initial PCP-PCOP (r = 0.984, p less than 0.01). We propose that the formation of pulmonary edema on paraquat poisoning is mainly due to the increased capillary permeability, influenced by the increased pressure gradient of capillary barrier.
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PMID:[A clinical study of pulmonary edema on paraquat poisoning by double indicator dilution method using heat and sodium]. 266 31

The inhalation of toxic gases or vapours is capable of resulting in pulmonary oedema (P.O.), the mechanism of which corresponds, on the basis of a number of hemodynamic studies carried out, to that which characterises the so-called "lesional" pulmonary oedema, which is different from so-called "hemodynamic" oedema. Classically PAP, PCP and P wedge pressure have virtually normal values (normalisation of pulmonary arterial hypertension by correction of hypoxemia). CI and SWILV are normal or increased and pulmonary resistances are virtually normal. The origin of the oedema is thus related to an increase in alveolo-capillary permeability. The inhalation of toxic gases or vapours with a caustic or irritant action, or containing particles, however, usually adds on an obstructive syndrome, similar to a severe asthmatic attack. Under such conditions, the marked reduction in intrathoracic pressure during inspiration definitely favours pulmonary oedema by decreasing intra-alveolar pressure and by the accumulation of blood in the pulmonary circulation, and is capable of masking pulmonary arterial hypertension. Raised pressure, related to expiratory effort, on the contrary, decreases venous return and may result in collapse of the capillaries. Whilst the principal mechanism of PO by the inhalation of toxic gases or vapours is related to an increase in alveolo-capillary permeability, it is nevertheless important not to under-estimate the role of variations in intra-thoracic pressures which may constitute a provoking or at least aggravating element.
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PMID:[Pulmonary edema of toxic origin. Hemodynamic data]. 611 Dec 79

The role of nitric oxide (NO) in precipitating pulmonary oedema in acute lung injury remains unclear. We have investigated the mechanism of involvement of NO in the maintenance of liquid balance in the isolated rabbit lung. Thirty pairs of lungs were perfused with colloid for up to 6 h, during which pulmonary vascular resistance (PVR) and capillary pressure (PCP) were measured frequently, and time to gain 5 g in weight (t5) was recorded. Four protocols with different perfusate additives were studied: (i) none (control, n = 11); (ii) 10 mmol NG-nitro-L-arginine methyl ester (L-NAME) (n = 6); (iii) 10 mmol L-NAME with 100 mumol lodoxamide, an inhibitor of mast cell degranulation (n = 7); (iv) 10 mmol L-NAME with 10 mumol 8-bromo-3',5'-cyclic guanosine monophosphate (8Br-cGMP), an analogue of cGMP that may reduce vascular permeability by relaxing contractile elements in endothelial cells (n = 6). Neither PVR nor PCP differed between protocols. L-NAME markedly reduced t5 from 248 (27) min (mean (SEM)) in protocol (i) to 144 (5) min in protocol (ii) (P < 0.05). Both lodoxamide (t5 = 178 (7) min) and 8Br-cGMP (t5 = 204 (10) min) substantially corrected the effect of L-NAME (P < 0.005). Results suggest that maintenance of a low permeability by NO may involve mast cell stabilization and endothelial cell relaxation.
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PMID:Inhibition of nitric oxide synthesis augments pulmonary oedema in isolated perfused rabbit lung. 1106 16