Mechanisms of pulsus paradoxus in airway obstruction.

To assess the mechanisms of pulsus paradoxus (i.e., inspiratory decline of greater than or equal to 10 Torr in systolic pressure) in airway obstruction, we studied 12 patients with chronic airflow obstruction before and during breathing through an external resistance that provided loads during both inspiration and expiration. Esophageal pressure (Ppl) and brachial artery pressure, relative to either atmospheric (Pa) or esophageal pressure (Patm), were measured simultaneously during normal and loaded breathing. It was assumed that changes in intrathoracic systemic arterial transmural pressure were adequately represented by Patm. During control, no significant difference between systolic fluctuation (delta Pa) and pleural swings (delta Ppl) was found. Concurrently, inspiratory and expiratory Patm were nearly identical. By contrast, under maximally loaded conditions, higher magnitudes of delta Ppl than delta Pa were found and consequently Patm rose with inspiration. In this connection, the plot of delta Pa against delta Ppl showed that the slopes for delta Ppl less than or equal to 15 Torr (1.2 Torr delta Pa/delta Ppl) and delta Ppl greater than 15 Torr (0.4 Torr delta Pa/delta Ppl) were significantly different. Under all experimental conditions we found during inspiration a rise in diastolic Patm that is consistent with an increase in left ventricular afterload.(ABSTRACT TRUNCATED AT 250 WORDS)

Prevention by fructose-1,6-bisphosphate of cardiac oxidative damage induced in mice by subchronic doxorubicin treatment.

An experimental model of mild, subchronic doxorubicin cardiotoxicity in mice was investigated by monitoring changes of biochemical parameters related to cell response against oxidative stress in both liver and heart. A specific increase of the lactate dehydrogenase isoenzyme typical of the heart was observed for doxorubicin-treated mice. Lipid peroxidation, as evaluated by malondialdehyde determination, and catalase activity were greatly increased in heart and unaffected in liver. On the other hand, these changes can be considered as indicative of early heart damage induced by doxorubicin. Glutathione, glutathione peroxidase, and 6-phosphogluconate dehydrogenase values were not significantly altered by the treatment and glucose-6-phosphate dehydrogenase increased in both liver and heart. Administration of fructose-1,6-bisphosphate strongly reduced the increase of plasma lactate dehydrogenase, heart lipid peroxidation, and heart catalase while no effect on the diagnostically irrelevant increase of glucose-6-phosphate dehydrogenase was observed. The inhibitory effect on the onset of biochemical modification typical of early subchronic doxorubicin cardiotoxicity may be related to stimulation of ATP synthesis by fructose-1,6-bisphosphate and is therapeutically promising in view of the lack of toxicity of fructose-1,6-bisphosphate as a drug.