Comparing Lung Odema In Diabetic And Non Diabetic Rats

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Comparing Lung Odema In Diabetic And Non Diabetic Rats

During hydrostatic pulmonary edema, active Na+ transport and alveolar fluid reabsorption are decreased. Dopamine (DA) and isoproterenol (ISO) have been shown to increase active Na+ transport in rat lungs by upregulating Na+-K+-ATPase in the alveolar epithelium. We studied the effects of DA and ISO in isolated rat lungs with increased left atrial pressure (Pla = 15 cmH2O) compared with control rats with normal Pla (Pla = 0). Alveolar fluid reabsorption decreased from control value of 0.51 ± 0.02 to 0.27 ± 0.02 ml/h when Pla was increased to 15 cmH2O (P < 0.001). DA and ISO increased the alveolar fluid reabsorption back to control levels. Treatment with the D1antagonist SCH-23390 inhibited the stimulatory effects of DA (0.30 ± 0.02 ml/h), whereas fenoldopam, a specific D1-receptor agonist, increased alveolar fluid reabsorption in rats exposed to Pla of 15 cmH2O (0.47 ± 0.04 ml/h). Propranolol, a ß-adrenergic-receptor antagonist, blocked the stimulatory effects of ISO; however, it did not affect alveolar fluid reabsorption in control or DA-treated rats. Amiloride (a Na+ channel blocker) and ouabain (a Na+-K+-ATPase inhibitor), either alone or together, inhibited the stimulatory effects of DA. Colchicine, which disrupts the cellular microtubular transport of ion-transporting proteins to the plasma membrane, inhibited the stimulatory effects of DA, whereas the isomer ß-lumicolchicine did not block the stimulatory effects of DA. These data suggest that DA and ISO increase alveolar fluid reabsorption in a model of increased Pla by regulating active Na+ transport in rat alveolar epithelium. The effects of DA and ISO are mediated by the activation of dopaminergic D1receptors and the ß-adrenergic receptors, respectively.

Pulmonary edema (American English), or oedema (British English; both words from the Greek ??d?µa), is fluid accumulation in the lungs.[1] It leads to impaired gas exchange and may cause respiratory failure. It is due to either failure of the heart to remove fluid from the lung circulation ("cardiogenic pulmonary edema") or a direct injury to the lung parenchyma ("noncardiogenic pulmonary edema").[2] Treatment depends on the cause, but focuses on maximizing respiratory function and removing the cause.

Pulmonary edema is a condition in which there is an accumulation of fluid in the lungs, which makes it difficult or even impossible to breathe effectively. Acute pulmonary edema is a form of pulmonary edema that occurs suddenly, is a life-threatening emergency, and can be rapidly fatal if not treated immediately.

In most cases, pulmonary edema is due to heart failure, a condition in which the heart muscle has been damaged and is too weak to pump sufficient amounts of oxygen-rich blood to and from the lungs and the rest of the body. This increases blood pressure in the lungs and leads to a back-up and build-up of fluid in the lungs.

Less commonly, pulmonary edema can result from acute mountain sickness, a condition brought on by the lower air pressure and reduced oxygen levels that occur at high altitudes. Pulmonary edema can also occur due to pneumonia and in infants who are given ...