The buffering behaviour of blood during hypoxemia and respiratory exchange: theory.
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Biomedical subjects
Publications and source records attributed to C C Michel.
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1. Isolated lung lobes of the dog perfused through the pulmonary circulation only with atropinized autologous blood obtained by bleeding out the animal under general anaesthesia or following premedication with morphine hydrochloride were subjected to repetitive tests of ventilation hypoxia, the control and test gas mixtures containing similar concentrations of CO(2).2. The pulmonary vasomotor response to ventilation hypoxia depended upon the temperature of the perfusate and the time which had elapsed from the death of the animal to the start of perfusion, termed the ;ischaemic period'. The higher blood temperatures and shorter ischaemic periods favoured a pulmonary vasopressor response to hypoxia, and the lower temperatures and longer ischaemic periods a vasodepressor response or an absence of response.3. The vasopressor responses to hypoxia were associated with a rise in the pH (average, 0.09 in 5 experiments) and a fall in the P(CO2) of the blood. There were no consistent changes in the pH and P(CO2) of the blood accompanying vasodepressor responses.4. The vasopressor responses could be obtained over periods of perfusion lasting 4 hr or longer.5. It is suggested that changes in the composition of blood equilibrated in the isolated perfused lung cannot be predicted from in vitro dissociation curves.
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Microvascular permeability to fluid and hydrophilic solutes is restricted to channels between the endothelial cells and through the fenestrations when these are present. The channels have a molecular filter which appears to be a lattice of fibrous molecules reinforced by plasma proteins. The quantitative description of blood-tissue fluid movements is complicated by plasma protein permeation which leads to a non-linear steady state relation between fluid filtration and microvascular pressure. When fluid filtration is low it can be balanced by lymph flow but at high pressures oedema develops. Microvascular pressure rises less than expected with increments of venous pressure owing to local vasoconstriction of the arterioles. The sluggish flow which results from this vasoconstriction and high venous pressure leads to a haemoconcentration which reduces oedema formation but favours leucocyte and platelet sequestration within the microcirculation.