Tatsuya Shiga

Alterations in autonomic nervous control of heart rate among tourists at 2700 and 3700 m above sea level.

OBJECTIVES Many travelers who are not specially trained for activities at high altitude are at risk of physical problems, including cardiovascular disorders, when exposed to high-altitude environments. In the present study, we investigated how actual acute exposure to altitudes of 2700 and 3700 m affected the autonomic nervous control of heart rate in untrained office workers. METHODS Physiological parameters (heart rate, respiratory rate, arterial blood oxygen saturation, and end-expiratory carbon dioxide tension) were measured at sea level, 2700 m, and 3700 m. The power of heart rate variability was quantified by determining the areas of the spectrum in 2 component widths: low frequency (LF; 0.04-0.15 Hz) and high frequency (HF; 0.15-0.5 Hz). The ratio of LF power to HF power (LF:HF), which is considered to be an index of cardiac sympathetic tone, was also assessed. RESULTS Both HF and LF heart rate variability decreased according to the elevation of altitude. High- and low-frequency powers at 3700 m were significantly lower than those at sea level (P < .01 for HF, P < .05 for LF). The LF:HF ratio at 2700 m was not significantly different from that at sea level. However, it was significantly increased at 3700 m (P < .01). CONCLUSIONS At 2700 and 3700 m, the activity of the autonomic nervous system measured by heart rate variability was decreased in untrained office workers. The sympathetic nervous system was dominant to the parasympathetic at 3700 m. These alterations in the autonomic nervous system might play some role in physical fitness at high altitudes.

Exercise-induced cerebral deoxygenation among untrained trekkers at moderate altitudes.

The pathophysiology of altitude-related disorders in untrained trekkers has not been clarified. In the present study, the effects of workload on cardiovascular parameters and regional cerebral oxygenation were studied in untrained trekkers at altitudes of 2700 m and 3700 m above sea level. We studied 6 males and 4 females at each altitude, and their average ages were 31.3+/-7.1 y at 2700 m and 31.2+/-6.8 y at 3700 m, respectively. The resting values of heart rate and mean blood pressure were not significantly different at 2700 m and 3700 m than at sea level. However, increases in these values after exercise were more prominent at high altitudes (heart rate increase = 51.6% at 2700 m and 70.4% at 3700 m; mean blood pressure increase: 19.0% at 2700 m and 17.2% at 3700 m). In addition, post-exercise blood lactate concentration was significantly higher at 3700 m than at sea level or at 2700 m (i.e., 7.6 mM at 3700 m, 3.8 mM at 2700 m, and 4.17 mM at 0 m, respectively). Exercise induced an acute reduction in the arterial oxygen saturation value (SpO2) at 2700 m and 3700 m (i.e., 11.2% reduction at 2700 m and 9.4% at 3700 m), whereas no changes were observed at sea level. The resting values of regional oxygen saturation (rSO2)--measured by a near infra-red spectrophotometer at sea level, 2700 m, and 3700 m-were nearly identical. Exercise at sea level did not reduce this value. In contrast, we observed a decrease in rSO2 after subjects exercised at 2700 m and 3700 m (i.e., 26.9% at 2700 m and 48.1% at 3700 m, respectively). The rSO2 measured 2 min and 3 min after exercise at 3700 m was significantly higher than the preexercise value. From these observations, we concluded that alterations in cardiovascular parameters were apparent only after an exercise load occurred at approximately 3000 m altitude. Acute reduction in cerebral regional oxygen saturation might be a primary cause of headache and acute mountain sickness among unacclimatized trekkers.

Hyperventilation after tourniquet deflation prevents an increase in cerebral blood flow velocity

PurposeIn this study we examined whether normocapnia maintained by hyperventilation after lower limb tourniquet deflation prevents an increase in cerebral blood flow velocity.MethodsThirteen patients, undergoing elective orthopedic surgery, requiring a pneumatic tourniquet around the lower extremity, were divided into two groups. In group I, ventilation was controlled at tidal volume of 10 mL·kg−1 and respiratory rate of eight per minute after tourniquet release. In group 2, ventilation was controlled to maintain PETCO2 between 30 and 35 mmHg after tourniquet release. Arterial blood pressure, heart rate, peak and mean middle cerebral artery (MCA) flow velocity, and arterial blood gas were measured every minute for ten minutes after tourniquet release. The MCA blood flow velocity was measured using Transcranial Doppler ultrasonography (TCD).ResultsIn group I, the maximum peak MCA flow velocity was 53 ± 6 cm·sec−1 (50 % ± 6% increase compared with pre-release value), and achieved 3 ± 0.4 min after tourniquet release. In group 2, there was no increase either in mean or peak MCA velocity after tourniquet release.ConclusionsNormocapnia maintained by hyperventilation after tourniquet deflation prevents an increase in cerebral blood flow velocity.RésuméObjectifVérifier si la normocapnie maintenue par l’hyperventilation après le dégonflage d’un garrot autour du membre inférieur empêche l’augmentation de la vitesse du flux sanguin cérébral.MéthodeTreize patients, admis pour une chirurgie orthopédique nécessitant un garrot pneumatique autour du membre inférieur, ont été répartis en deux groupes. Après le relâchement du garrot, on note que: dans le Groupe I, la ventilation était maintenue au volume courant de 10 ml·kg−1 et la fréquence respiratoire à huit par minute; dans le Groupe 2, la ventilation était contrôlée pour maintenir la PETCO2.entre 30 et 35 mmHg: la tension artérielle, la fréquence cardiaque, la vitesse moyenne et maximale du flux de l’artère cérébrale moyenne (ACM) et les gaz du sang artériel étaient mesurés à chaque minute pendant dix minutes. La vitesse du flux de l’ACM a été mesurée par échographie-Doppler transcrânienne (DTC).RésultatsDans le Groupe I, la vitesse maximale du flux de l’ACM a été de 53 ± 6 cm·sec−1 (50 % ± 6 % d’augmentation en comparaison des valeurs précédant la libération du garrot), et a été atteinte 3 ± 0,4 min après le garrot. Dans le Groupe 2, il n’y a pas eu d’augmentation de la vitesse moyenne ou maximale du flux de l’ACM après le garrot.ConclusionLa normocapnie maintenue par l’hyperventilation après le dégonflage du garrot peut empêcher une augmentation de la vitesse du flux sanguin cérébral.

Platelet-activating factor receptor antagonist attenuates endotoxin-induced vascular hyporeactivity in the pithed rat.

The role of platelet activating factor (PAF) and nitric oxide (NO) in the endotoxin-induced hyporeactivity to noradrenaline was studied in the pithed rat. Pressor dose-response curves to noradrenaline (0.01-10 microg/kg, i.v.) were made starting 1 h after the administration of endotoxin (0.5 mg/kg, i.v.) to the rats. Saline was administered to the control rats. The PAF receptor antagonist, TCV-309 (3-bromo-5-[N-phenyl-N-[2-[[2-(1,2,3,4-tetrahydro-2-isoquinolylcarbon yloxy)ethyl]carbamoyl]ethy]carbamoyl]-1-propylpyridinium nitrate, 100 microg/kg, i.v.), or the NO synthase inhibitor, N(G)-monomethyl-L-arginine (L-NMMA, 30 mg/kg, i.v.), was administered to the endotoxin-treated rats 20 or 10 min before the noradrenaline challenge. L-NMMA reversed endotoxin-induced hyporeactivity completely. TCV-309 produced a significant, but partial attenuation of the hyporeactivity to noradrenaline (P < 0.01). There was still significant hyporeactivity when compared with the control rats (P < 0.01) and the L-NMMA-treated endotoxin-administered rats (P < 0.05). These data suggest that endogenous PAF contributes to the vascular hyporeactivity to noradrenaline induced by endotoxin and that NO plays a major role in the endotoxin-induced hyporeactivity.

Experimental use of a transportable hyperbaric chamber durable for 15 psi at 3700 meters above sea level

A transportable hyperbaric chamber durable for 15 psi of pressure was used to treat a patient suffering from moderate acute mountain sickness at 3700 m above sea level. The symptoms were ameliorated a few minutes after pressurization in the chamber. After a 20-minute stay in the chamber, the patient was completely free of symptoms. Since the chamber can be inflated by using compressed air from a cylinder, no strenuous work was required of the operators. This transportable chamber seems to be useful for the treatment of high-altitude disorders at around 3000 m above sea level.

Change in plasma endotoxin titres and endotoxin neutralizing activity in the perioperative period

PurposeTo elucidate whether endotoxaemia detected during major surgery was a specific or non-specific reaction.MethodsProspective clinical study in the operating theatre and multidisciplinary intensive care unit in a university hospital. A series of plasma samples was obtained from 21 patients, including eight after cardiopulmonary bypass (CPB), until 48 hr after surgery. The endotoxin titres in these samples were compared by the two chromogenic limulus amebocyte lysate (LAL) assays; one is factor C containing and the other factor G-free, endotoxin-specific test. The endotoxin neutralizing activity of the plasma was determined by adding the endotoxin to the plasma (1,000 pg · ml−1), and by assaying how much the potency of the endotoxin to activate LAL was lost during incubation for 120 min at 37°C.ResultsAlthough endotoxin litres measured using the test including factor G showed a marked elevation during and after surgery, which were 3 ± 5 (4 ± 10), 14 ± 13 (20 ± 17**), 133 ± 13* (46 ± 29*), 89 ± 72* (48 ± 35*), 62 ± 40** (37 ± 29*), 50 ± 54 (39 ± 36) pg · ml−1 in patients with CPB (without CPB), mean ± SD, at 0, 3, 6, 9, 24, and 48 hr after start of surgery (*P < 0.01, **P < 0.05 compared with 0 hr), those measured by the endotoxin-specific test did not show any changes. Plasma neutralized 95% of endotoxin potency after five minutes incubation at 37°C.ConclusionUsing an endotoxin-specific assay, endotoxin could not be deleted in the blood stream during or after major surgery.RésuméObjectifDéterminer si l’endotoxémie décelée pendant une chirurgie majeure constitue une réaction spécifique ou non spécifique.MéthodesÉtude prospective réalisée au bloc opératoire et à l’unité des soins intensifs d’un hôpital universitaire. Une série d’échantillons de plasma a été prélevée chez 21 patients dont huit après une circulation extracorporelle (CEC) jusqu ’à la 48e h après la chirurgie. Les concentrations d’endotoxine déterminées dans ces échantillons ont été comparés grâce à deux épreuves chromogènes au limulus amébocyte lysate (LAL), une contenant du facteur G et l’autre sans facteur G, l’épreuve spécifique pour l’endotoxine. L’activité neutralisante de l’endotoxine par le plasma a été déterminée en additionnant de l’endotoxine au plasma (1 000 pg ml−1), et en estimant l’importance de la perte de puissance de l’endotoxine nécessaire à l’activation du LAL pendant une incubation de 120 min à 37°C.RésultatsBien que les titrages d’endotoxine déterminés par l’épreuve la facteur G aient révélé une élévation importante pendant et après la chirurgie, 3 ± 5 (4 ± 10), 14 ± 13 (20 ± 17**), 133 ± 13* (46 ± 29*), 89 ± 72* (48 ± 35*), 62 ± 40** (37 ± 29*), 50 ± 54 (39 ± 36) pg · ml−1 chez les opérés sous CEC (sans CEC), moyennes ± SD, à 0, 3, 6, 9, 24 et 48 h après le début de la chirurgie (*P < 0,01, **P < 0,05 comparativement à l’heure 0), les titrages déterminés par le test spécifique de l’endotoxine n’ont pas révélé de changement. Le plasma a neutralisé 95% de la puissance de l’endotoxine après cinq minutes d’incubation à 37°C.ConclusionL’endotoxine n’a pas été décelée dans le sang pendant et après une chirurgie majeure.

Platelet-activating factor-induced loss of vascular responsiveness to noradrenaline in pithed rats: involvement of nitric oxide

The role of nitric oxide and cyclo-oxygenase products in the platelet-activating factor (PAF)-induced hyporesponsiveness to noradrenaline was investigated in pithed rats. Infusion of PAF (30 ng/kg/min) for 60 min reduced the mean arterial blood pressure and impaired the pressor responses to noradrenaline (10 ng/kg, 100 ng/kg, 1 microgram/kg). Administration of NG-monomethyl-L-arginine (L-NMMA, 30 mg/kg) restored the reduced MABP and the impaired responses to their original levels. Indomethacin (5 mg/kg) had no significant effect on the PAF-induced hyporesponsiveness. Administration of 30 mg/kg L-NMMA caused hypertension in the PAF vehicle-treated animals and reduced the pressor response to 1 microgram/kg noradrenaline. Administration of 3 mg/kg L-NMMA had no significant effect on the responsiveness to noradrenaline. These results suggest that nitric oxide contributes to the PAF-induced hyporesponsiveness to noradrenaline and that cyclo-oxygenase products do not play a major role in this hyporesponsiveness.