We assessed the effect of pressure support ventilation (PSV) on breathing patterns and the work of breathing in 10 postoperative patients. Minute ventilation (VE) increased by 8% with 5 cm H2O PSV and 10% with 10 cm H2O PSV compared to 0 cm H2O PSV. The increase in VE was achieved by increased mean inspiratory flow (24% with 5 cm H2O PSV and 67% with 10 cm H2O PSV) and a decrease in duty cycle (13% with 5 cm H2O PSV and 39% with 10 cm H2O PSV). The decrease in duty cycle along with a decrease in respiratory frequency allowed a greater expiratory time including a rest period for the respiratory muscles, which might minimize the risk of muscle fatigue. Furthermore, the inspiratory work added by the ventilator was near zero with 5 cm H2O PSV and 10 cm H2O PSV. Oxygen consumption also decreased significantly with 5 cm H2O PSV. We conclude that PSV improves the breathing patterns and minimizes the work of breathing spontaneously via a ventilator.

We have developed a functional vegetative model by an 18-min clamping of the ascending aorta combined with a bypass formation between the aorta to right atrium and the aorta to femoral vein. Complete global brain ischemia (CGBI) induced for 18 min with this model provided the following distinct advantages: cardiopulmonary functions were well preserved during postischemic recirculation, and all dogs survived without serious extracerebral complications. Neuronal damage in vegetative dog induced by an 18-min CGBI was studied by light and electron microscopy. The Purkinje cells and the hippocampal CA1 pyramidal cells showing clumping of nuclear chromatin and slightly increased stainability were observed after CGBI without recirculation. All these neurons showed transient increased stainability with microvacuolation 15 min after recirculation. Over 50% of these neurons showed virtually normal features 1 h after recirculation. Damage to these neurons progressed again slowly up to 6 h after recirculation. However, all these neurons had disintegrated 2-3 days after recirculation. A decrease in synaptic vesicles was observed in many presynaptic terminals in the molecular layers of the cerebellum after CGBI without recirculation. These changes in the presynaptic terminals progressed 15 min after recirculation. These results indicated that the damage to the Purkinje cells and the CA1 pyramidal cells induced by CGBI consisted of two phases, and that the change in the early phase was reversible. We speculate that the damage to the Purkinje cells in the early stage is related to the decrease of the synaptic vesicles in the presynaptic terminals.

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