Effects of increased ventilation and improved pulmonary gas-exchange on maximal oxygen uptake and power output

Recent reports suggest that aerobic performance at very high levels may be limited by the pulmonary system. The purpose of the present study was to compare respiratory functions at rest and during graded maximal aerobic exercise (cycle ergometry) between well-trained (TR, n = 11) and untrained (UT, n = 14) individuals while breathing atmospheric air, normoxic helium (He) and oxygen-enriched mixture. When the subjects breathed air, TR exhibited lower exercise ventilatory reserve (MVV-VE_max), ratio between minute ventilation (VE) and oxygen uptake (V_o2) and SaO₂ than UT. Breathing HE resulted in an increase in VE and V_o2max in both groups but in an increased VE/V_o2 and SaO₂ and maximal mechanical cycle ergometer load, only in TR. Compared with air, breathing an oxygen-enriched mixture resulted in increased peak exercise SaO₂ and maximal mechanical load in both groups. It is concluded that arterial O₂ desaturation secondary to a relative hypoventilatory response may limit V_o2max and aerobic performance capacity at high work levels.     

Preservation of cerebral autoregulation in the unanesthetized hypoxemic newborn dog

Studies were conducted to determine the effects of hypoxemia on cerebral blood flow and the influence of hyperoxia and hypoxemia on autoregulation of cerebral blood flow in the unanesthetized newborn dog. Twenty-one newborn dogs less than 2 weeks of age were studied. Cerebral blood flow was measured using radioactive microspheres during successive periods of normotension, hypotension (produced by blood withdrawal) and normotension (produced by infusion of previously withdrawn blood). In the hyperoxic animals, arterial pO2 was maintained above 250 torr by having the animal breathe 100% oxygen, while in the hypoxemic animals arterial pO2 was maintained between 30 and 35 torr by having the animal breathe 12% O2. Cerebral blood flow increased significantly with hypoxemia. In both hypoxemic and hyperoxic animals cerebral blood flow was maintained constant in spite of a large fall in arterial blood pressure and cardiac output, demonstrating the presence of autoregulation. Calculated oxygen transport to the brain was constant during hypoxemia and hypotension in all animals. Thus autoregulation of cerebral blood flow is present in newborn animals and is preserved under conditions of moderate hypoxemia.     

Evidence for the role of dialysis hypoxemia in the pathogenesis of hemodialysis-induced rise in tissue-type plasminogen activator

It is well known that hemodialysis (HD) causes a rise in plasma tissue-type plasminogen activator (t-PA). Although there have been several suggested mechanisms responsible for this effect of HD, the precise cause has not been well understood yet. Another complication of HD, when performed with acetate-containing dialysate, is hypoxemia, which is commonly observed during the first hour of the session. The purpose of this study was to investigate the relationship between dialysis hypoxemia and HD-induced t-PA changes during the first two hours of HD.

HD caused significant increase in plasma t-PA antigen levels. When individual t-PA profiles versus time were examined, two patterns were observed. Whilst ten subjects (%56) experienced minimal or no increase, t-PA antigen level of the remaining eight subjects began to rise at 30 minutes and continued at that level up to 90 minutes, when the last samples were drawn. The courses of pO₂ were also different; whilst the former group had “early-onset and short-term” hypoxemia, the latter had “late-onset and prolonged” hypoxemia. The amount of increase in t-PA antigen and the amount of decrease in pO₂ were correlated at 60 and 90 minutes of the HD session.

Thus, it is concluded that dialysis hypoxemia may contribute to HD-induced rise in plasma t-PA levels. Further studies comparing different dialysates and dialyser membranes are required to confirm this hypothesis.     

Inequality of ventilation—Perfusion ratios in the lungs and arterial hypoxemia

A general analysis was made of the relationship between the degree of inequality of ventilation—perfusion ratios and the blood flow through poorly ventilated regions of the lungs, on the one hand, and arterial hypoxemia, on the other hand. Quantitative data on the onset of arterial hypoxemia during disturbance of ventilation—perfusion ratios were obtained.Laboratory of Experimental and Clinical Physiology, A. V. Vishnevskii Institute of Surgery, Academy of Medical Sciences of the USSR, Moscow. (Presented by Academician of the Academy of Medical Sciences of the USSR V. N. Chernigovskii.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 88, No. 10, pp. 406–408, October, 1979.     

Timing of injury in utero causing respiratory inhibition after crying

Background: The aim of this study was to clarify the timing of injuries in utero that cause respiratory inhibition after crying (RIAC). We evaluated infants with cranial ultrasound abnormalities diagnosed during hospitalization. Methods: We retrospectively examined the medical records of preterm infants who were treated in the neonatal intensive care unit at Nara Prefectural Hospital in Nara, Japan from January 2006 through December 2010. Inclusion criterion was gestational age less than 34 weeks. We evaluated the perinatal factors and cranial ultrasound abnormalities associated with RIAC, feeding hypoxemia, and prolonged apnea. We also evaluated the timing of appearance of cranial ultrasound abnormalities. Results: A total of 125 infants were examined. Mean gestational age was 30.6 ± 2.4 weeks and mean birthweight was 1465 ± 454 g. The numbers of infants who showed RIAC, feeding hypoxemia, and prolonged apnea were 44, 48, and 63, respectively. Among 91 infants who showed cranial ultrasound abnormalities, 67 had increased echogenicity in the ganglionic eminence (GE). There was a significant correlation between increased echogenicity and RIAC (P < 0.001). Of the infants who showed increased echogenicity in the GE, 19 had this finding during the course of hospitalization. In these 19 infants, however, gestational age of those with RIAC was less than 31 weeks. Conclusion: We speculate that the timing of intrauterine injury resulting in RIAC in infants is less than 31 gestational weeks.     

阻塞性睡眠呼吸暂停与心血管疾病的关系及发病机制探讨

阻塞性睡眠呼吸暂停的发病率有逐年增高趋势,越来越多的研究表明阻塞性睡眠呼吸暂停与心血管疾病（如高血压、肺动脉高压、冠心病、心律失常、心力衰竭等）的发生率与病死率关系密切;为有助于加深心血管病医生对阻塞性睡眠呼吸暂停与心血管疾病的认识,进一步探索阻塞性睡眠呼吸暂停的发病机制,从而提高疾病的防控水平;现就阻塞性睡眠呼吸暂停与心血管病的关系,导致疾病的可能发病机制作一综述。     

The effects of nocturnal home mechanical ventilation on daytime blood gas disturbances

INTRODUCTION: In chronic alveolar hypoventilation, previous studies of selected patient groups have shown that nocturnal home mechanical ventilation (HMV) may result in improvements in chronic blood gas disturbances during daytime spontaneous breathing. We wished to examine the effects of this treatment in a large sample of non-selected patients prospectively followed up, in a national multicentric register. MATERIAL: A total of 288 patients from a broad diagnostic spectrum were studied. We looked at the blood gases and vital capacity before the patients elected for initiation of HMV and at the first register-recorded follow-up after 6-24 months. RESULTS: We found statistically significant improvements in PO(2) and PCO(2) (approximately 1 kPa in both) and in base excess, but no changes in vital capacity or calculated alveolo-arterial gradient. All changes were independent of the observation period and only weakly diagnose-related. DISCUSSION: Our findings extend those of previous studies, showing a relatively early and apparently stable improvement in blood gases after starting and continuing nocturnal HMV. The equal extent of the improvements in blood gases among all the diagnostic groups including the neurological patients with progressive diseases was unexpected. CONCLUSION: In 288 patients starting nocturnal HMV electively we found significant improvements in daytime blood gases after 6-24 months. There were no changes in vital capacity or calculated alveolo-arterial gradient.     

Hyperhydration prior to a simulated second day of the 3-day moderate intensity equestrian competition does not cause arterial hypoxemia in Thoroughbred horses

Dehydration and the associated impairment of cardiovascular and thermoregulatory function comprise major veterinary problems in horses performing prolonged exercise, particularly under hot and humid conditions. For these reasons, there is considerable interest in using pre-exercise hyperhydration to help maintain blood volume in the face of the excessive fluid loss associated with sweat production during prolonged exertion. However, recently it was reported that pre-exercise hyperhydration causes arterial hypoxemia in horses performing moderate intensity exercise simulating the second day of an equestrian 3-day event competition (E3DEC) which may adversely affect performance (Sosa Leon et al. in Equine Vet J Suppl 34:425–429, 2002). These findings are contrary to data from horses performing short-term maximal exertion, wherein hyperhydration did not affect arterial O₂ tension/saturation. Thus, our objective in the present study was to examine the impact of pre-exercise hyperhydration on arterial oxygenation of Thoroughbred horses performing an exercise test simulating the second day of an E3DEC. Control and hyperhydration studies were carried out on seven healthy Thoroughbred horses in random order, 7 days apart. In the control study, horses received no medications. In the hyperhydration experiments, nasogastric administration of NaCl (0.425 g/kg) 5 h pre-exercise induced a plasma volume expansion of 10.9% at the initiation of exercise. This methodology for inducing hypervolemia was different from that of Sosa Leon et al. (2002). Blood-gas tensions/pH as well as plasma protein, hemoglobin and blood lactate concentrations were measured pre-exercise and during the exercise test. Our data revealed that pre-exercise hyperhydration neither adversely affected arterial O₂ tension nor hemoglobin-O₂ saturation at any time during the exercise test simulating the second day of an E3DEC. Further, it was observed that arterial blood CO₂ tension, pH, and blood lactate concentrations also were not affected by pre-exercise hyperhydration. However, hemodilution in hyperhydrated horses caused an attenuation of the expansion in the arterial to mixed-venous blood O₂ content gradient during phases B and D of the exercise protocol, which was likely offset by an increase in cardiac output. It is concluded that pre-exercise hyperhydration of horses induced in the manner described above is not detrimental to arterial oxygenation of horses performing an exercise test simulating the second day of an E3DEC.