• Journal of Chest Surgery
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• v.2 no.1
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• pp.85-104
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• 1969

This experiment was carried out to study the effect of rapid hemorrhage on cardiopulmonary hemodynamics of the cooled dogs. Hypothermia was induced by means of body surface cooling with ice water. Lowest esophageal temperatures ranged from 24 to 26 degree. Dogs were bled via the femoral artery into a reservoir in amount of the equivalent blood volume of 3% of body weight of the dogs. Some dogs were reinfused with the same amount of blood which they lost and others infused with 5% dextrose solution. Fourty adult mongrel dogs were divided into three groups: group I[15 dogs]; dogs were bled in normothermic state. Five dogs had no further treatment, but five dogs were reinfused with blood and five infused with 5% dextrose solution 30 minutes after bleeding. GroupII[10 dogs]; dogs were bled as group I after having been cooled. Five dogs were reinfused with blood as group I. Group III[15 dogs]; dogs were first bled and then cooled. Reinfusion procedures were the same as in group l Results were as follow: 1. The heart rate showed a slight decrease after bleeding in group I and then increased over the control level after 60 minutes. After reinfusion and infusion, the heart rate was also increased gradually and after three hours almost returned to the control level. In group II and groupIll, the heart rate decreased remarkably and after reinfusion showed a light increase but after infusion tended to decrease cotinually. 2. The stroke volume showed remarkable decrease after bleeding in group I., and recovered to control level after reinfusion and infusion,and then gradually decreased again. In group III, the stroke volume showed no remarkable change after hypothermia, and tended to decrease after reinfusion. In group III, the stroke volume decreased remarkably after bleeding and hypothermia,and clearly increased after reinfusion and infusion and then returned to control level. 3. Femoral mean pressure declined very rapidly and significantly right after bleeding and showed a remarkable prompt rise after reinfusion and infusion in group I [67% recovery]. On the other hand, it declined remarkably after hypothermia and bleeding and showed a slight rise after reinfusion and infusion in group II[46% recovery] and III [41% recovery]. 4. Venous pressure declined slightly after bleeding and tended to return to the control level after reinfusion and infusion,in group I. In group II, it did not change significantly during hypothermia but showed a slight decline after bleeding and returned toward control level after reinfusion. In group III, it declined slightly after bleeding and showed no significant change after hypothermia and rose over the control level after reinfusion and infusion. 5. Right ventricular systolic pressure decreased markedly after bleeding and then increased progressively after 30 minutes. It increased after reinfusion and infusion as well, approaching the control level in group I. In group II, it showed no significant change during hypothermia, but decreased remarkably after bleeding and then returned to near control level after reinfusion. In group III, it was decreased markedly after bleeding but did not change significantly during hypothermia and showed a slight increase after reinfusion. 6. The respiratory rate increased gradually after bleeding and decreased gradually after reinfusion but did not return to the control level, whereas it decreased near to the control level after infusion,and tended to increase in group I. In group II, it decreased significantly after hypothermia and bleeding but returned near to the control level after reinfusion. In group III, it showed a remarkable decrease after hypothermia and increased slightly after reinfusion and infusion but did not returned to the control level. In group I, the tidal volume decreased slightly after hemorrhage, and increased gradually to near the control level after 3 hours following reinfusion.

• Tuberculosis and Respiratory Diseases
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• v.53 no.4
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• pp.409-419
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• 2002

Background : The therapeutic effects of surfactant on acute lung injury derive not only from its recruiting action on collapsed alveoli but also from its anti-inflammatory effects. Pro-apoptotic action on alveolar neutrophils represents one of the important anti-inflammatory mechanisms of surfactant. In the present study, we evaluated the effects of sufactant on the apoptosis of human peripheral and rat alveolar neutrophils. Methods : In the (Ed- the article is not definitely needed but it helps to separate the two prepositions 'in') in vitro study, human neutrophils were collected from healthy volunteers. An equal number of neutrophils ($1{\times}10^6$) (Ed-confirm) was treated with LPS (10, 100, 1000ng/ml), surfactant (10, 100, $1000{\mu}g/ml$), or a combination of LPS (1000ng/ml) and surfactant (10, 100, $1000{\mu}g/ml$). After incubation for 24 hours, the apoptosis of neutrophils was evaluated by Annexin V method. In the in vivo study, induction of acute lung injury in SD rats by intra-tracheal instillation of LPS (5mg/kg) was followed by intra-tracheal administration of either surfactant (30mg/kg) or normal saline (5ml/kg). Tenty-four hours after LPS instillation, alveolar neutrophils were collected and the apoptotic rate was evaluated by Annexin V method. In addition, changes of the respiratory mechanics of rats (respiratory rate, tidal volume, and airway resistance) were evaluated with one chamber body plethysmography before, and 23 hours after, LPS instillation. Results : in the in vitro study, LPS treatment decreased the apoptosis of human peripheral blood neutrophils (control: $47.4{\pm}5.0%$, LPS 10ng/ml; $30.6{\pm}10.8%$, LPS 100ng/ml; $27.5{\pm}9.5%$, LPS 1000ng/ml; $24.4{\pm}7.7%$). The combination of low to moderate doses of surfactant with LPS promoted apoptosis (LPS 1000ng/ml + Surf $10{\mu}g/ml$; $36.6{\pm}11.3%$, LPS 1000ng/ml +Surf $100{\mu}g/ml$; $41.3{\pm}11.2%$). The high dose of surfactant ($1000{\mu}g/ml$) decreased apoptosis ($24.4{\pm}7.7%$) and augmented the anti-apoptotic effect of LPS (LPS 1000ng/ml + Surf $1000P{\mu}g/ml$; $19.8{\pm}5.4%$). In the in vivo study, the apoptotic rate of alveolar neutrophils of surfactant-treated rats was higher than that of normal saline-treated rats ($6.03{\pm}3.36%$ vs. $2.95{\pm}0.58%$). The airway resistance (represented by Penh) of surfactant-treated rats was lower than that of normal saline-treated rats at 23 hours after LPS injury ($2.64{\pm}0.69$ vs. $4.51{\pm}2.24$, p<0.05). Conclusion : Surfactant promotes the apoptosis of human peripheral blood and rat alveolar neutrophils. Pro-apoptotic action on neutrophils represents one of the important anti-inflammatory mechanisms of surfactant.

• The Sea:JOURNAL OF THE KOREAN SOCIETY OF OCEANOGRAPHY
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• v.10 no.3
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• pp.154-163
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• 2005

Irregular discharges of freshwater through the water gates of the Keum River Estuarine Weir, Korea, whose construction had been completed in 1998 with its water gates being operated as late as August 1994, drastically modified the estuarine environment. Sharp decrease of salinity along with the altered concentrations of inorganic nutrients are accompanied with the irregular discharges of freshwater into the estuary under the influence of regular semi-diurnal tidal effect. Field sampling was carried out on the time of high tide at 2 fixed stations(St.1 near the Estuarine Weir and St.2 off Kunsan Ferry Station) every other day for 4 months from mid-February 2004 to investigate into the semi-weekly variation of spring phytoplankton community in relation to the freshwater discharges from Keum River Estuarine Weir. CV(coefficient of variation) of salinity measurements was roughly 2 times greater in St.1 than that in St.2, reflecting extreme salinity variation in St.1 Among inorganic nutrients, concentrations of N-nutrients($NO_3^-,\;NO_2^-$ and $NH_4^+$) were clearly higher in St.1, to imply the more drastic changes of the nutrient concentrations in St.1. than St.2 following the freshwater discharges. As a component of phytoplankton community, diatoms were among the top dominants in terms of species richness as well as biomass. Solitary centric diatom, Cyclotella meneghiniana, and chain-forming centric diatom, Skeletonema costatum, dominated over the phytoplankton community in order for S-6 weeks each (Succession Interval I and II), and the latter succeeded to the former from the time of <$10^{\circ}C$ of water temperature. Cyanobacterial species, Aphanizomenon Posaquae and Phormidium sp., which might be transported into the estuary along with the discharged freshwater, occupied high portion of total biomass during Succession Interval III(mid-April to late-May). During this period, freshwater species exclusively dominated over the phytoplankton community except the low concentrations of the co-occurring 2 estuarine diatoms, Cyclotella meneghiniana and Skeletonema costatum. During the 4th Succession Interval when the water temperature was over $18^{\circ}C$, the diatom, Guinardia delicatula, was predominant for a week with the highest dominance of $75\%$ in discrete samples. To summarize, during all the Succession Intervals other than Succession Interval III characterized by the extreme variation of salinity under cooler water temperature than $18^{\circ}C$, the diatoms were the most important dominants for species succession in spring. If the scale and frequency of the freshwater discharge could have been adjusted properly even during the Succession Interval III, the dominant species would quite possibly be replaced by other estuarine diatom species rather than the two freshwater cyanobacteria, Aphanizomenon flosaquae and Phormidium sp.. The scheme of field sampling every other day for the present study was concluded to be the minimal requirement in order to adequately explore the phytoplankton succession in such estuarine environment as in Keum River Estuary: which is stressed by the unpredictable and unavoidable discharges of freshwater under the regular semi-diurnal tide.