• Journal of Biomedical Engineering Research
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• v.12 no.3
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• pp.177-184
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• 1991

Characteristics of the lung inflation and deflation reflexes were measured at various temperatrues on the cervical vagi in five anesthetized mongrel dogs. Nerve temperature was maintained at the body temperature, and $2-14^{\circ}C$ with $2^{\circ}C$ apart using a specially designed automated vagal cooling apparatus with an accuracy to within ${\pm}0.1^{\circ}C$ at each temperature. The inflation reflex was blocked abruptly at $8-10^{\circ}C$. The deflation reflex started weakened at $14^{\circ}C$, thereafter showed a gradual blockade with the temperature decreased with a substantial variance among the animals. It was approximately 75% blocked at $2-6^{\circ}C$. These differences in temperature characteristics made it hard to differentiate the deflation reflex from the inflation reflex. In one animal, however, the inflation reflex was completely blocked with the deflation reflex almost alive at $6-8^{\circ}C$. This suegests that differential cold blockade of the vagal reflexes can be done only in selected subjects. Fur- thermore, the fact that these two reflexes were blocked at different temperatures may be due to the differences in the nerve fiber size and the changes in the conduction velocity with temperature.

• Journal of Biomedical Engineering Research
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• v.4 no.1
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• pp.3-8
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• 1983

Characteristics of the lung inflation and deflation reflexes were measured at various temperatures on the cervical vagi in five anesthetized mongrel dogs. Nerve temperature was maintained at the body temperature, and 2-14˚C with 2˚C apart using a specially designed automated vagal cooling apparatus with an accuracy to within $\pm$ 0.1˚c at each temperature. The inflation reflex was blocked abruptly at 8-10˚C. The deflation reflex started weakened at 14˚C, thereafter showed a gradual blockade with the temperature decreased with a substantial variance among the animals.It was approximately 75% blocked at 2-5˚C. These differences in temperature characteristics made it hard to differentiate the deflation reflex from the inflation reflex. In one animal, however, the inflation reflex was completely blocked with the deflation reflex almost alive at 6-8˚C. This suggests that differential cold blockade of the vagal reflexes can be done only in selected subjects. Furthermore, the fact that these two reflexes were blocked at different temperatures may be due to the differences in the nerve fiber size and the changes in the conduction velocity with temperature.

• The Korean Journal of Physiology
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• v.17 no.1
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• pp.23-28
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• 1983

In order to clarify the effect of steroid on the pulmonary pressure-volume curve in the pneumonectomized rabbit, the right side pneumonectomy was performed under general anesthesia with pentobarbital sodium and the remaining lung was excised on the fifth day after surgery. The intrapulmonic pressure in the excised left lung was measured at 20, 25, and 30 ml lung volume during inflation and deflation period. In the steroid treated group, the intrapulmonic pressure at 20, 25, and 30 ml lung volume during inflation was significantly decreased compared with intrapulmonic pressure of the control group. But in the pneumonectomy group the decreasing tendency of the pressure was observed. During deflation, the intrapulmonic pressure at 25 ml and 20 ml was not significantly different from the control group in pneumonectomy and steroid treated pneumonectomy group. And the lung weight was measured in each experimental group and also the lung weightbody weight ratio(L/B) was calculated. The lung weight was significantly increased in both pneumonectomy and steroid treated pneumonectomy group. Calculated L/B was increased significantly in both group. Above results suggest that steroid increases the secretion of pulmonary surfactant or affects the catabolic effect on protein metabolism of connective tissue in lung parenchyma.

• The Korean Journal of Physiology
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• v.27 no.1
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• pp.37-49
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• 1993

Ventilatory responses to inhaled $CO_2$ were measured during continuous negative pressure breathing (CNPB) in awake dogs. End expiratory lung volume (EELV) decreased linearly with pressure level during CNPB (correlation coefficient= 0.81, p<0.005) during air breathing. When CNPB was applied during 5% $CO_2$ inhalation, the decrease in EELV was not significantly different (p<0.5) from that during air breathing. As a result of a lowered EELV, tidal volume ($V_T$) significantly decreased by 22% and breathing frequency ($f_B$) increased by 68% in the steady state during air breathing (p<0.0001). These responses were similar during 5% $CO_2$ inhalation, thus the $CO_2$ response curve measured during CNPB shifted upward without a change in sensitivity (p>0.05). These results indicate additive effects of CNPB and $CO_2$ inhalation. The degree of hyperventilation during CNPB at eupnea was estimated to be 63% of that during control ventilation and was significantly greater than zero (p<0.0001), which suggests an alveolar hyperventilation due to CNPB. These results suggest that the mechanical alterations associated with n decrease in lung volume could play an important role in ventilatory control independently of chemical regulation of breathing. Thus, exercise hyperpnea, which is associated with a lowered functional residual capacity (FRC), may in part be explained by this mechanical stimulation of breathing.

• Journal of Chest Surgery
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• v.7 no.1
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• pp.1-8
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• 1974

Acute pulmonary edema was induced by intravenous injection of epinephrine, intravenous infusion of dextran and intratracheal instillation of acid solution index was determined from pressure volume curves in excised lungs. Surface activity was also investigated with measurements of maximum and minimum surface tension and stability index on saline extracts of same lungs. The results were as follows. 1. The expansion index of excised lung in which pulmonary edema was induced by intravenous injection of epinephrine, intravenous infusion of dextran and intratracheal instillation of acid solution was ignificantly decreased as compared with the normal control of $0.86{\pm}0.017$ to $0.74{\pm}0.03$, $0.71{\pm}0.081$and $0.76{\pm}0.02$, respectively. 2. The deflation curves of excised lungs in which pulmonary edema was induced were significantly decreased as compared with the normal controls. 3. The minimum surface tension of excised lung in which pulmonary edema was induced was significantly increased in each groups and stability index was significantly decreased as compared with the normal controls 0.78 to $0.35{\pm}0.039$, $0.29{\pm}0.02 $ and $0.31{\pm}0.083$, respectively. 4. The decrease of pulmonary surface activity in acute pulmonary edema was in proportion to the degree of pulmonary edema regardless of their etiology.

• The Korean Journal of Physiology
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• v.8 no.2
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• pp.49-53
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• 1974

A single dose of pilocarpine was subcutaneously injected into the rabbit in order to clarify the effects of cholinergic activities on the secretion of the pulmonary surfactant. The animal was sacrificed four hours after the injection, and the pressure-volume curve of the excised lung was obtained. The surfactant activities of the lung washings were also measured, and a comparison was made with the normal. The pressure-volume curve of the excised lung by the injection and ejection of air formed a loop (hysteresis) and the mean intra-alveolar pressure at 35 ml of air was 220 $mmH_20$ in the normal. The mean deflation curve of the pilocarpine treated rabbit lungs was shifted to the left compared with the normal. The surfactant activities were slightly increased than the normal. The above results suggest that pilocarpine stimulates the secretion of the pulmonary surfactant from the Type II alveolar epithelial cell.

• The Korean Journal of Physiology
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• v.15 no.1
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• pp.27-36
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• 1981

Relatively little has been done on the metabolic changes of the lung produced by the excessive alcohol ingestion to the point of the acute alcohol intoxication. In the present study, an effort was made to clarify the possible changes of the pulmonary surfactant system by the acute alcohol ingestion. The dynamic pulmonary compliance and the levels of protein and inorganic phosphorus (Pi) of both lung lavage and extract were chosen as the parameters of the pulmonary surfactant activities. The albino rats of both sexes were used, and 1.5 ml of 50% ethanol per 100 g body weight was given by oral intubation, and the experiment was performed at 1, 3, 6, 12, and 24 hours after the alcohol ingestion. The rat was sacrificed by cutting the carotid arteries, and blood sample for the determination of hematocrit(Hct) and the blood alcohol concentration was obtained. Both lungs were completely removed without dammage to the lung tissue, and the pulmonary compliance was measured by the changes of pressure-volume(P-V) curves by inflating or deflating the lung with air. Immediately after the P-V curves were recorded, the lung lavage was obtained by washing the lobes with 15ml of isotonic saline 3 times with a syringe. Next, total lungs were homogenized and filtered to obtain the lung extract. The protein and Pi levels were measured using the lung lavage and extract as the samples, and the lung/body weight ratio(L/B ratio) was also calculated. The results thus obtained were compared with the normal values and summarized as follows. The blood alcohol concentration reached the highest level of $0.71{\pm}0.02\;g\;%$ at 1 hr and gradually decreased until 24 hrs$(0.36{\pm}0.02\;g%)$ after the alcohol ingestion, but all the experimental groups showed significant increase comparing with the normal. The highest Hct value was obtained at 1hr$(64.86{\pm}2.45%)$ and significantly elevated value was continued throughout the experiment. The L/B ratio was significantly lowered from 3hrs until 24hrs after the alcohol ingestion but from 6 th hr on, a generally elevated value was observed with a significant value at 12 hrs and gradual recovery to the normal value at 24 hrs after the alcohol ingestion. The pulmonary compliance at inflation and deflation did not change appreciablly from the normal until 3 hrs after the alcohol ingestion but from 6 th hr on, a generally elevated value was observed with a significant value at 12 hrs and gradual recovery to the normal value at 24 hrs after the alcohol ingestion. The protein level of the lung lavage stowed a significantly increased value of $12.36{\pm}0.35\;mg/gm(3rd hr)$, $12.70{\pm}0.74\;mg/gm(12 th hr)$, and $12.65{\pm}0.88\;mg/gm(24 th hr)$, respectively, comparing with the normal value of $10.65{\pm}0.62\;mg/gm$, and the Pi level also showed a similar tendency of significant increase at 12th hr $(7.65{\pm}0.63\;{\mu}mol/gm)$ and 24 th hr$(6.70{\pm}0.36\;{\mu}mol/gm)$ comparing with the normal value of $5.32{\pm}0.20\;{\mu}mol/gm$. The protein level of the lung extract in the alcohol group was generally similar to the normal value with a slight decrease at 1st and 3 rd hr, tut the Pi level of the lung extract was generally increased in the alcohol group, and a significant increase was observed at 6 th hr$(17.77{\pm}1.54\;{\mu}mol/gm)$, 12 th hr$(13.92{\pm}0.78\;{\mu}mol/gm)$ and 24 th hr$(14.57{\pm}0.53\;{\mu}mol/gm)$ of the alcohol ingestion comparing with the normal value of $10.34{\pm}0.37\;{\mu}mol/gm$. From the above, it may be concluded that the acute alcohol intoxication produces the metabolic changes of the lungs by the increased surfactant activities and elevated pulmonary compliance.