Cardiovascular and respiratory effects of apnea in humans

Detta är en avhandling från Animal Physiology

Sammanfattning: This thesis deals with cardiovascular and respiratory effects of apneas in humans. During apnea (breath-holding), a number of interacting cardiovascular reflexes are initiated, and together these reflexes are called the “diving response”. The main cardiovascular characteristics of the human diving response are reduced heart rate, decreased cardiac output, peripheral vasoconstriction, and increased arterial blood pressure. The diving response of some diving mammals has been shown to have an O2-conserving effect. I.e., some species perform dives that are longer than expected considering their tissue O2 stores. A shift from aerobic to anaerobic metabolism is probably the major cause of the O2-conservation, and a reduced O2-delivery to the tissues by means of the peripheral vasoconstriction is the mechanism by which this shift is attained. Whether or not the human diving response has an O2-conserving effect has not been elucidated. The main focuses of this study have been the initiation and effects of the human diving response. Involvement of splenic contraction in the human diving response and mechanisms for the O2-conserving effect of the human diving response are suggested. The results show that mechanical effects and possibly also input from pulmonary stretch receptors influence the development of the diving response, resulting in a non-linear relationship between the magnitude of the diving response and the lung volume in the near-vital capacity range. Studies on interactions between thermoregulatory and exercise reflexes and the diving response indicate that the human diving response has priority over other cardiovascular responses in the threat of asphyxia, which appears to be a functional quality of an O2-conserving response. Increases in hematocrit during apneas were observed in intact but not in splenectomized subjects. Therefore it is suggested that the changes in the intact subjects are due to splenic contraction and an associated release of sequestered erythrocytes. Contraction of the spleen is thus a part of the human diving response, just as in some diving mammals. Increased blood gas storage capacity and facilitated recovery from apneas following splenic emptying are probably involved in prolonging repeated apneas, since a delay of the physiological breaking point of apneas was only observed in the intact subjects. Apneas reduced the rate of O2 uptake from the lung compared to the O2 uptake during eupnea, and with a more pronounced diving response, i.e., during apneas with face immersion, the reduction in O2 uptake was augmented. This suggests that the human diving response, through reductions in cardiac output and peripheral blood flow, reduce the alveolar-to-capillary O2 uptake and prolong the turnover time of peripheral O2 stores during apneas. Thus, the lung O2 store is preserved while the peripheral (venous) O2 stores are relatively more reduced with a more pronounced diving response. In addition, an increase in plasma lactate concentration indicates that the anaerobic metabolic rate increases as a consequence of a reduced peripheral O2 delivery, thereby to some extent reducing the total tissue O2 consumption during apneas. Therefore, it is concluded that the human diving response has an O2-conserving effect, similar to the response of some diving mammals.

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