• The Korean Journal of Physiology and Pharmacology
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• v.2 no.1
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• pp.77-84
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• 1998

Ureteral obstruction causes increase in renal blood flow (RBF) and partial impairment of the autoregulation of RBF. Although increased renal prostaglandin production is responsible for the former, it is not clear whether or not it is also responsible for the latter. Therefore, we investigated the role which prostaglandins play in the autoregulation of RBF during an ureteral pressure elevation (40 $cmH_2O$). Since the major mechanism of RBF autoregulation is the tubuloglomerular feedback, studying the interaction between ureteral pressure and RBF autoregulation may reveal the role of prostaglandin in tubuloglomerular feedback. To pursue the purpose, six anesthetized dogs were prepared for the measurements of RBF, mean sytemic and renal arterial pressure (RAP) and the manipulation of ureteral pressure. The autoregulation curves were determined during both control and elevation of the ureteral pressure, before and after the pretreatment with indomethacin, a cyclooxygenase inhibitor. The desired ureteral pressure was achieved by vertically elevating the water-filled reservoir connected to the ureteral catheter to 40 cm above the kidney level. In response to the elevation of the ureteral pressure, RBF increased from $170{\pm}8 ml{\cdot}min^{-1}\;to\;189{\pm}8$, and the systemic arterial pressure didn't change significantly. During spontaneous urine flow, RBF autoregulation was abolished when RAP was reduced to $59{\pm}3$ mmHg. On the other hand, during the ureteral pressure elevation, the autoregulation curves shifted upward and rightward from control, and the pressure when RBF autoregulation was abolished was $74{\pm}3$ mmHg. The pretreatment of the dogs with indomethacin failed to affect the lower limit of RBF autoregulaion during both control ($63{\pm}5$ mmHg) and the elevated ureteral pressure ($77{\pm}5$ mmHg). Since RBF failed to increase in response to the elevated ureteral pressure, RBF autoregulation curves obtained during the elevated ureteral pressure shifted only rightward from indomethacin control. The results indicate that the increased intrarenal level of prostaglandin or prostaglandin-induced vasodilation does not appear to bear any relation to the reduction in the autoregulatory capacity during partial ureteral obstruction. It seems that the partial impairment of the autoregulation during acute ureteral obstruction is due to the consumption of tubuloglomerular feedback mechanism at spontaneous RAP and that prostaglandin is neither mediator nor effector of tubuloglomerular feedback mechanism.

• Journal of Chest Surgery
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• v.29 no.1
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• pp.1-6
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• 1996

We developed an experimental model of brain death using dogs. Brain death was induced by increasing the intracranial pressure (ICP) gradually by continuous Infusion of saline through an epidural Foley catheter in 5 mongrel dogs (weight, 18~22kg). Hemodynamic and electrocardiographic changes were evaluated continuously during the process of brain death and obtained the following results. 1. The average volume and time required to induce brain death was 4.8$\pm$1.0ml and 143.0$\pm$30.9minutes respectively. 2. There was a steady rise of the ICP after starting the constant infusion of saline, and ICP rised continuously until the brain death (122.0$\pm$62.5mmHg). After reaching to the maximal value (125.0$\pm$47.7mmHg) at 30 minutes after brain death, the ICP dropped and remained approximately constant at the slightly higher level than the mean arterial pressure (MAP). 3. MAP showed no change until the establishment of brain death and it declined gradually. The peak heart rate reached to 172.6$\pm$35.3/min at 30 minutes after the brain death. 4. Even though the body temperature and all hemodynamic variables, such as cardiac output, mean pulmonary arterial pressure, left ventricular (LV) end-diastolic pressure and LV maximum + dp/dt, were slightly greater than those of basal state, at the point of brain death, there was no statistically significant change during t e process of brain death. 5. There was no remarkable arrhythmias during the experiment except ventricular premature beats which was observed transiently in one dog at the time of brain death. Hemodynamic changes in the brain death model induced by gradual ICP increment were inconspicuous, and arrhythmias were rarely seen. Hyperdynamic state, which was observed at the point of brain death in another brain death model caused by abrupt ICP increase, was not observed.

• The Korean Journal of Physiology
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• v.2 no.1
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• pp.47-52
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• 1968

Twenty white rabbits anesthetized with nembutal (30 mg/kg) were employed in this experiment. Five of them served as controls; the remaining rabbits as experimental group were subjected to irreversible hemorrhagic shock. Shock was induced by bleeding the animals until mean blood pressure decreased to a level of 50-40 mmHg. This level of pressure was maintained for 3-4 hours, after which the drawn blood was reinfused. The reinfusion of blood caused the elevation of arterial pressure almost the control level for some minutes, after which a gradual and progressive decline of blood pressure became evident. This decline was thought to be the result from irreversible hemorrhagic shock. When mean blood pressure declined to less than 50 mmHg, chest was opened and samples of arterial blood and left ventricular muscle were taken. Left ventricular muscle and blood plasma were analyzed for potassium, sodium, chloride and water content. Blood glucose concentration was determined by Somogyi-Nelson's method. Extracellular and intracellular myocardial water and electrolyte content were calculated on the basis that electrolytes are distributed between plasma water and interstitial water according to Gibbs-Donnan equilibrium. In this calculation extracellular water was substituted for Na space. The findings obtained were as follows: 1. The concentration of blood glucose was 87mg% in the controls and it rose to 222 mg% in shock (P<0.01). 2. Plasma potassium elevated significantly from 3.3 mEq/l in controls to 8.0 mEq/l in shock (P<0.01), while small decreases in sodium (151-146 mEq/l) and chloride (102-96 mEq/l) were observed (P<0.3, P<0.1), 3. The changes of blood water content (83.1-84.3%) and cardiac water content (77.5-78.3 gm/100gm WT) were observed. 4. In control animals myocardial potassium levels which averaged 30.2 mEq/100 gmDT rose significantly to 40.3 mEq/100 gmDT in shock (P<0.01), while moderate decreases in sodium(16.3-14.3 mEq/100 gmDT) were observed in shock. 5. The calculated transmembrane resting potential of left ventricular muscle of control animals averaged 95 mV, while rabbits in shock averaged 77 mV. (P <0.01). The findings of this experiment do not correspond with the conclusions that myocardial depression seems to be the cause of irreversible hemorrhagic shock, because the excitability of heart muscle is elevated. From the point of view that the lowered transmembrane resting potential, the cause of death in terminal stage of irreversible hemorrhagic shock may be ventricular fibrillation. It can't be said, however, that the lowered transmembrane resting potential is responsible for the transition from reversible to irreversible hemorrhagic shock. The marked increase in blood glucose suggested that glycogenolysis in the liver is favorably active in shock.

• Journal of Trauma and Injury
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• v.32 no.2
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• pp.101-106
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• 2019

Purpose: The purpose of this study was to determine the essential factors for prompt arrangement of angio-embolization in patients with pelvic ring fractures. Methods: A total of 62 patients with pelvic ring fractures who underwent angio-embolization in Dankook University Hospital from March 2013 to June 2018 were retrospectively reviewed. There were 38 men and 24 women with a mean age of 59.8 years. The types of pelvic ring fractures were categorized according to the Tile classification. Patient variables included sex, initial hemoglobin concentration, initial systolic blood pressure, transfused packed red blood cells within 24 hours, Injury Severity Score (ISS), mortality rate, length of hospital stay, and time to angio-embolization. Results: The most common pelvic fracture pattern was Tile type B (n=34, 54.8%). The mean ISS was $27.3{\pm}10.9$ with 50% having an $ISS{\geq}25$. The mean time to angio-embolization from arrival was $173.6{\pm}89minutes$. Type B ($180.1{\pm}72.3minutes$) and type C fractures ($174.7{\pm}91.3minutes$) required more time to angio-embolization than type A fractures ($156.6{\pm}123minutes$). True arterial bleeding was identified in types A (35.7%), B (64.7%), and C (71.4%). Conclusions: It is important to save time to reach the angio-embolization room in treating patients with pelvic bone fractures. Trauma surgeons need to consider prompt arrangement of angio-embolization when encountering Tile type B or C pelvic fractures due to the high risk of true arterial bleeding.

• Journal of Chest Surgery
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• v.32 no.11
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• pp.1004-1008
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• 1999

Background: Total anomalous pulmonary venous return is a relatively rare disease which has a very high mortality(80% within a year) if not properly corrected surgically. Material and Method: Twenty-six infants with total anomalous pulmonary venous return underwent repair between May, 1991 and February, 1996. Result: There were 19 boys and 7 girls. The mean age at operation was 2.6 months(range: 5 day to 11 month) and the mean body weight was 4.3kg(range:2.8 to 6.7 kg). Preoperative stabilization included ventilator for 5 patients and inotropic support for 6 patients. There were 6 hospital mortalities. Significant risk factors of operative mortality were preoperative ventilator care(p<0.03) and preoperative inotropic support(p<0.05). Age, body weight at operation, pulmonary venous obstruction, high pulmonary arterial pressure, spurasystemic right ventricular pressure or emergency operation did not affected the operative outcome. Postperative pulmonary venous obstruction occurred in three patients 2 or 3 months later, among them one patient was reoperated. The actuarial survival was 76% at 40 months. Conclusion: Although early mortality was high, repair of total anomalous pulmonary venous return should be attempted in early life, but the patients receiving ventilator care or inotropic support need special attention.

• Sleep Medicine and Psychophysiology
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• v.9 no.1
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• pp.24-33
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• 2002

Objectives: Nasal continuous positive airway pressure (CPAP) corrected elevated blood pressure (BP) in some studies of obstructive sleep apnea syndrome (OSAS) but not in others. Such inconsistent results in previous studies might be due to differences in factors influencing the effects of CPAP on BP. The factors referred to include BP monitoring techniques, the characteristics of subjects, and method of CPAP application. Therefore, we evaluated the effects of one night CPAP application on BP and heart rate (HR) reactivity using non-invasive beat-to-beat BP measurement in normotensive and hypertensive subjects with OSAS. Methods: Finger arterial BP and oxygen saturation monitoring with nocturnal polysomnography were performed on 10 OSAS patients (mean age $52.2{\pm}12.4\;years$; 9 males, 1 female; respiratory disturbance index (RDI)>5) for one baseline night and another CPAP night. Beat-to-beat measurement of BP and HR was done with finger arterial BP monitor ($Finapres^{(R)}$) and mean arterial oxygen saturation ($SaO_2$) was also measured at 2-second intervals for both nights. We compared the mean values of cardiovascular and respiratory variables between baseline and CPAP nights using Wilcoxon signed ranks test. Delta ($\Delta$) BP, defined as the subtracted value of CPAP night BP from baseline night BP, was correlated with age, body mass index (BMI), baseline night values of BP, BP variability, HR, HR variability, mean $SaO_2$ and respiratory disturbance index (RDI), and CPAP night values of TWT% (total wake time%) and CPAP pressure, using Spearman's correlation. Results: 1) Although increase of mean $SaO_2$ (p<.01) and decrease of RDI (p<.01) were observed on the CPAP night, there were no significant differences in other variables between two nights. 2) However, delta BP tended to increase or decease depending on BP values of the baseline night and age. Delta systolic BP and baseline systolic BP showed a significant positive correlation (p<.01), but delta diastolic BP and baseline diastolic BP did not show a significant correlation except for a positive correlation in wake stage (p<.01). Delta diastolic BP and age showed a significant negative correlation (p<.05) during all stages except for REM stage, but delta systolic BP and age did not. 3) Delta systolic and diastolic BPs did not significantly correlate with other factors, such as BMI, baseline night values of BP variability, HR, HR variability, mean SaO2 and RDI, and CPAP night values of TWT% and CPAP pressure, except for a positive correlation of delta diastolic pressure and TWT% of CPAP night (p<.01). Conclusions: We observed that systolic BP and diastolic BP tended to decrease, increase or remain still in accordance with the systolic BP level of baseline night and aging. We suggest that BP reactivity by CPAP be dealt with as a complex phenomenon rather than a simple undifferentiated BP decrease.

• Tuberculosis and Respiratory Diseases
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• v.45 no.5
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• pp.1022-1030
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• 1998

Background : In volume-controlled ventilation, the use of inspiratory pause increases the inspiratory time and thus increases mean airway pressure and improves ventilation. But under the same I : E ratio, the effects of inspiratory pause on mean airway pressure and gas exchange are not certain. Moreover, the effects may be different according to the resistance of respiratory system. So we studied the effects of inspiratory pause on airway pressure and gas exchange under the same I : E ratio in volume-controlled ventilation. Methods: Airway pressure and arterial blood gases were evaluated in 12 patients under volume-controlled mechanical ventilation with and without inspiratory pause time 5%. The I : E ratio of 1 : 3, $FiO_2$, tidal volume, respiratory rate, and PEEP were kept constant. Results: $PaCO_2$ with inspiratory pause was lower than without inspiratory pause ($38.6{\pm}7.4$ mmHg vs. $41.0{\pm}7.7$ mmHg. p<0.01). P(A-a)$O_2$ was not different between ventilation with and without inspiratory pause $185.3{\pm}86.5$ mmHg vs. $184.9{\pm}84.9$ mmHg, p=0.766). Mean airway pressure with inspiratory pause was higher than without inspiratory pause ($9.7{\pm}4.0\;cmH_2O$ vs. $8.8{\pm}4.0\;cmH_2O$, p<0.01). The resistance of respiratory system inversely correlated with the pressure difference between plateau pressure with pause and peak inspiratory pressure without pause (r=-0.777, p<0.l), but positively correlated with the pressure difference between peak inspiratory pressure with pause and peak inspiratory pressure without pause (r=0.811, p<0.01). Thus the amount of increase in mean airway pressure with pause positively correlated with the resistance of respiratory system (r=0.681, p<0.05). However, the change of mean airway pressure did not correlated with the change of $PaCO_2$. Conclusion: In volume-controlled ventilation under the same I : E ratio of 1 : 3, inspiratory pause time of 5% increases mean airway pressure and improves ventilation. Although the higher resistance of respiratory system, the more increased mean airway pressure, the increase in mean airway pressure did not correlated with the change in $PaCO_2$.

• Journal of Biomedical Engineering Research
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• v.29 no.5
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• pp.371-375
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• 2008

In blood pressure measurement, the oscillometric method detects and analyzes the pulse pressure oscillation while deflating the cuff around the arm. For its principle, one has to inflate cuff pressure above the subject's systolic pressure and deflate below the diastolic pressure. Most of the commercialized devices inflate until the fixed target pressure and deflate until the fixed completion pressure because there is no way to know the systolic and diastolic pressure before measurement. Too high target pressure makes stress to the subject and too low target pressure makes big error or long measurement time because of re-inflation. There are similar problems for inadequate completion pressure. In this study, we suggest new algorithm to set proper target and completion pressure for each subject by analyzing pressure waveform while inflating period. We compared our proposed method and auscultation method to see the errors of estimation. The differences between the two measurements were -4.02$\pm$4.80mmHg, -10.50$\pm$10.57mmHg and -0.78$\pm$5.l7mmHg for mean arterial pressure, systolic pressure and diastolic pressure respectively. Consequently, we could set the target pressure by 30 mmHg higher than our estimation and we could stop at 20mmHg lower than our estimated diastolic pressure. Using this method, we could reduce the measurement time.

• Journal of Chest Surgery
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• v.35 no.4
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• pp.267-273
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• 2002

Background: We performed a phase IV clinical trial to examine the usefulness of a continuous infusion of nicardipine hydrochloride to control hypertension in patients with acute aortic dissection. material and Method: Systolic/diastolic blood pressure, and heart rate were monitored before and after the intravenous administration of nicardipine in 31 patients with aortic diseases. The period of nicardipine administration in each patient was from 3 to 14 days. Efficacy was evaluated by determining the average amount of blood pressure reduction on the 3rd day of drug administration. The dosage of another antihypertensive agent was slowly tapered down, and ultimately replaced by the test drug. Result: 28 patients were diagnosed as acute aortic dissection, 2 patients as rupture of the aortic arch aneurysm, and 1 patient as traumatic aortic rupture. Mean age was 53.9 $\pm$ 14.9(29~89) years, and 21 patients(67.7%) were male. 14 patients(32.3%) had complications associated with underlying aortic disease: aortic insufficiency in 7, hemopericardium in 6, acute renal failure in 1, paraplegia in 1, lower extremity ischemia in 1, and hemothorax in 1. The time needed to reach the target blood pressure was within 15 minutes in 16, from 15 to 30 minutes in 10, from 30 to 45 minutes in 3 and from 45 to 60 minutes in 2, and their baseline average systolic, diastolic, and mean arterial blood pressures(mmHg) were 147$\pm$23, 82.3$\pm$ 18.6, and 104 $\pm$ 18, respectively. Average systolic, diastolic, and mean arterial blood pressures(mmHg) on the third day of nicardipine infusion were 119$\pm$ 12, 69$\pm$9, and 86$\pm$8, and they all showed statistically significant decrease(p<0.05). The average systolic, diastolic, and mean arterial blood pressure(mmHg) after the discontinuation of the nicardipine infusion were 119 $\pm$ 15, 71 $\pm$ 14, and 86$\pm$ 13, respectively. No significant difference was observed between the average pressures measured on the third day and those measured after the discontinuation of the nicardipine infusion, and no definite side effects were observed during the study period. Conclusion: Nicardipine hydrochloride was both effective and safe at controlling blood pressure in patients with acute aortic dissection.

• Journal of Trauma and Injury
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• v.21 no.1
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• pp.46-52
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• 2008

Purpose: This study was to evaluate the effect of arterial embolization on survival in patients with pelvic bone fractures and arterial bleeding. Methods: From January 2001 to December 2007, in all, 18 patients with pelvic bone fractures that had been treated with interventional arterial embolization were included in this retrospective study. The Injury Severity Score (ISS), the Revised Trauma Score (RTS), the initial hemodynamic status, the blood gas analysis, blood transfusion data, and mortality were the main outcome measurements. Results: Pelvic bone fractures were classified into lateral compression (LC), antero-posterior compression (APC), vertical shear (VS), and combined (CM) type according to the Young-Burgess classification. The Survivor group included 11 patients (61.1%), and the non-survivor group included 7 patients (38.9%). The mean ages for the survivor and the non-survivor groups were 40.0 and 45.6 years (p=0.517). The types of pelvic bone fractures were LC 11 (61.1%), APC 6 (33.3%), and VS 1 (5.6%): LC 7 (63.6%), and APC 4 (36.4%) in the survivor group and LC 4 (57.1%), APC 2 (28.6%), and VS 1 (14.3%) in the non-survivor group. The internal iliac artery was the predominant injured vessel among both the survivors (n = 5, 45.5%) and the non-survivors (n = 4, 57.1%). No differences in initial blood pressures, ISS, and RTS existed between the two groups, but the arterial pH was lower in the non-survivor group (pH 7.09 (${\pm}0.20$) vs 7.30 (${\pm}0.08$), p=0.018). The number of transfused 24-hour units of packed RBC was greater in the non-survivor group ($24.1{\pm}12.5$ vs $14.4{\pm}6.8$, p=0.046). Conclusion: No differences in initial blood pressure and trauma scores existed between survivors and non-survivors with pelvic bone fractures, who had been treated with arterial embolization, but arterial pH was lower the in non-survivors.