The purpose of this study was 1) to answer whether the reduction in spleen size in breath-hold apnea is an active contraction or a passive collapse secondary to reduced splenic arterial blood flow and 2) to monitor the spleen response to repeated breath-hold apneas. Ten trained apnea divers and 10 intact and 7 splenectomized untrained persons repeated five maximal apneas (A1-A5) with face immersion in cold water, with 2 min interposed between successive attempts. Ultrasonic monitoring of the spleen and noninvasive cardiopulmonary measurements were performed before, between apneas, and at times 0, 10, 20, 40, and 60 min after the last apnea. Blood flows in splenic artery and splenic vein were not significantly affected by breath-hold apnea. The duration of apneas peaked after A3 (143, 127, and 74 s in apnea divers, intact, and splenectomized persons, respectively). A rapid decrease in spleen volume ( approximately 20% in both apnea divers and intact persons) was mainly completed throughout the first apnea. The spleen did not recover in size between apneas and only partly recovered 60 min after A5. The well-known physiological responses to apnea diving, i.e., bradycardia and increased blood pressure, were observed in A1 and remained unchanged throughout the following apneas. These results show rapid, probably active contraction of the spleen in response to breath-hold apnea in humans. Rapid spleen contraction and its slow recovery may contribute to prolongation of successive, briefly repeated apnea attempts.
1. The human spleen sequesters 200-250 mL densely packed red blood cells. Up to 50% of this viscous blood is actively expelled into the systemic circulation during strenuous exercise or simulated apnoea (breath-hold) diving. The contribution of splenic contraction to changes in the circulating volume of red blood cells (RBCV), as well as the venous concentration of white blood cells (WBC) and platelets (PLT), was investigated following repeated breath-hold apnoeas. 2. Eighteen trained apnoea divers and 18 intact and six splenectomized subjects without diving experience repeated five maximal apnoeas with face immersion in cold water, with 2 min intervals between successive attempts. Venous blood samples were taken before and between consecutive apnoeas, as well as at 0, 10 and 20 min after the last breath hold. Arterial pressure, heart rate and transcutaneous partial pressure of oxygen and carbon dioxide were monitored continuously. 3. Plasma protein concentration decreased by 5.8, 2.2 and 9% in apnoea divers, untrained and splenectomized subjects, respectively, indicating an expansion of plasma volume. The RBCV and venous concentration of WBC, corrected for changes in plasma volume, increased in both trained apnoea divers (4.9+/-1.0 and 14.9+/-3.1%, respectively) and intact subjects (1.7+/-0.8 and 7.2+/-1.8%, respectively), whereas in splenectomized subjects there was no change in RBCV and a delayed increase in WBC concentration. Furthermore, an initial lymphocytosis detected during repeated breath holds in divers and intact subjects was completely absent in splenectomized subjects. None of the groups showed significant changes in PLT concentrations. The well-recognized diving response to apnoea (bradycardia and increased blood pressure) was seen during all breath-hold attempts in all subjects. 4. Repeated breath-holds (apnoeas) contribute to increased RBCV and venous blood concentrations of WBC through splenic contraction.
These findings indicate that, in moderately trained athletes, postexercise hypotension is associated primarily with reduced cardiac output because of reduced stroke volume, suggesting venous pooling. In addition, the occurrence of hypotension is more frequent in trained subjects with lower cardiopulmonary fitness level or higher resting SBP.
We investigated the spleen volume changes as related to the cardiovascular responses during short-duration apneas at rest. We used dynamic ultrasound splenic imaging and noninvasive photoplethysmographic cardiovascular measurements before, during, and after 15-20 s apneas in seven trained divers. The role of baroreflex was studied by intravenous bolus of vasodilating drug trinitrosan during tidal breathing. The role of lung volume was studied by comparing the apneas at near-maximal lung volume with apneas after inhaling tidal volume, with and without cold forehead stimulation. In apneas at near maximal lung volume, a 20% reduction in splenic volume (P = 0.03) was observed as early as 3 s after the onset of breath holding. Around that time the heart rate increased, the mean arterial pressure abruptly decreased from 89.6 to 66.7 mmHg (P = 0.02), and cardiac output decreased, on account of reduction in stroke volume. Intravenous application of trinitrosan resulted in approximately 6-mmHg decrement in mean arterial pressure, while the splenic volume decreased for approximately 13%. In apneas at low lung volume, the early splenic contraction was also observed, 10% without and 12% with cold forehead stimulation, although the mean arterial pressure did not change or even increased, respectively. In conclusion, the spleen contraction is present at the beginning of apnea, accentuated by cold forehead stimulation. At large, but not small, lung volume, this initial contraction is probably facilitated by downloaded baroreflex in conditions of decreased blood pressure and cardiac output.
HBO therapy reduced the frequency of wound complications in patients with Gustilo type III wounds and shortened the time to granulation formation. HBO therapy was more effective in non-NATO than in NATO treated patients for the prevention of deep soft-tissue infection but not flap necrosis.
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