Cardiovascular effects of high frequency ventilation--the possible involvement of thromboxane

Recent studies with high frequency ventilation (HFV) have noted that HFV-induced increases in mean airway pressure leads to a marked cardiovascular depression, especially in cardiac output (CO). Aside from mechanical events a negative inotropic agent possibly prostaglandin in nature may also be involved. This study examined the possible involvement of thromboxane A2 (TXA2) in the HFV-induced cardiovascular deterioration. Chloralose-anesthetized mechanically-ventilated dogs were subjected to HFV 4, 10, and 20 mm Hg for 30 min. Some animals were also treated with imidazole (25 mg/Kg/hr) prior to HFV. Arterial levels of TXB2 (stable metabolite of TXA2) where monitored by radioimmunoassay. During HFV, tracheal pressure-related decreases in both CO and stroke volume (SV) were noted. Imidazole treatment significantly reduced the decrement in SV. Application of HFV resulted in variable changes in circulating TXB2 levels. Overall, application of HFV did not result in a significant change from baseline levels. Furthermore there was no correlation between changes in CO and SV with changes in arterial TXB2 concentration. These results do not support the hypothesis that hyperexpansion of the lungs during HFV causes the release of a cardiodepressant prostanoid.