6-ketoprostaglandin-f1-alpha and Burns--Inhalation

A prospective study was carried out on 57 patients with total burned surface area (TBSA) over 30%. It was found that myocardial damage occurred early postburn, which was one of the major causes of cardiac dysfunction and failure. The postburn respiratory failure (RF) might be classified into three patterns. The etiology of each pattern varied. The imbalance between thromboxane and prostacyclin in plasma and visceral tissues played important roles in the genesis and development of postburn MOF as well as the causes of pathophysiological alterations in the main factors (including inhalation injury, severe shock and systemic infection) which contributed to occurrence of visceral damage and MOF.

Topics: 6-Ketoprostaglandin F1 alpha; Adolescent; Adult; Burns; Burns, Inhalation; Child; Female; Humans; Male; Multiple Organ Failure; Prospective Studies; Shock, Traumatic; Thromboxane B2

In the majority of clinical cases, smoke inhalation results in a self-limited lung injury mostly confined to the airways. In this study, an animal model of inhalation injury was developed that reflected similar pathophysiology. Cardiopulmonary parameters were studied in awake, instrumented goats following spontaneous inhalation of characterized Douglas fir smoke. Peak carboxyhemoglobin levels averaged 37% during a mean exposure time of 33 minutes. All animals survived the 24-hour study period, and showed only transient abnormalities in lung fluid balance and gas exchange, with no change in lung mechanics or plasma eicosanoid (TxB2 and 6-keto-PGF1 alpha) levels. However, extravascular lung water at 24 hours was increased 33%, suggesting the presence of some airway edema and retained secretions. We feel this model fairly represents the majority of clinical smoke inhalation cases. This model is compared to other large animal inhalation injury models producing more severe lung injury.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Body Water; Burns, Inhalation; Carboxyhemoglobin; Disease Models, Animal; Goats; Hemodynamics; Lung; Pulmonary Gas Exchange; Thromboxane B2

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Body Water; Burns, Inhalation; Hydrochloric Acid; Lung; Lung Injury; Lymph; Proteins; Sheep; Thromboxane B2; Vascular Resistance

Inhalation injury was induced in chronically instrumented sheep (n = 9) by insufflating them with smoke from burning cotton cloth. Sham animals (n = 9) were insufflated with air. There were no temporal changes in any measured parameter of the sham animals. Smoke induced a depression in PaO2. There was a threefold elevation in protein-rich pulmonary lymph which was sustained for over 48 hours. The lymph-to-plasma oncotic pressure ratio was increased. The cardiac index, left atrial pressure, and pulmonary arterial pressure remained unchanged in both groups. After smoke inhalation, the interstitial levels of neutrophils increased while interstitial antiprotease activity was depressed. The lung lymph concentration of 6-keto prostaglandin F1a, the major metabolite of prostacyclin, was increased. These data suggest that the pulmonary injury following smoke inhalation is the result of an increase in lung microvascular permeability to protein with resultant pulmonary edema. The mechanisms responsible for these changes appear to be related to direct injury to the tracheobronchial tree by cytotoxic agents in the smoke; polymorphonuclear leukocytes; and, possibly, eicosanoids.

Topics: 6-Ketoprostaglandin F1 alpha; alpha-Macroglobulins; Animals; Burns, Inhalation; Capillary Permeability; Cardiac Output; Female; Lung; Lung Injury; Lymph; Neutrophils; Pulmonary Edema; Sheep; Smoke; Thromboxane B2; Time Factors