Although extracorporeal circulation (ECC) has been routinely used for cardiovascular surgery, hyperoxemia during ECC may produce oxygen toxicity and cellular injury. This study was performed to investigate the clinical influences of hyperoxemic ECC during cardiovascular operation. 40 adult patients scheduled for elective cardiovascular surgery were classified into normoxemic (arterial oxygen tension: 115 mmHg, n=20) and hyperoxemic (arterial oxygen tension: 380 mmHg, n=20) ECC. At preoperative and postoperative period, total leukocyte and neutrophil counts, platelet counts, iron, glucose, aspartate aminotransferase (AST), alanine aminotransferase (ALT), blood urea nitrogen (BUN), and creatinine in peripheral arterial blood, malondialdehyde (MDA) and troponin-T concentration (TnT) in coronary sinus blood, pulmonary vascular resistance (PVR), and postoperative blood loss volume (BLS) were measured and compared between groups. Hyperoxemic group had postoperatively higher total leukocyte and neutrophil counts, MDA, TnT, PVR total BLS, iron, glucose, AST, ALT, BUN, and creatinine than normoxemic group (p<0.05).0 conclusion, hyperoxemic ECC results in greater inflammatory response and oxidative damaging effects on the heart lung, liver and kidney, probably being adverse to postoperative patient recovery. For reducing these deleterious effects and improving postoperative outcomes, management lowering oxygen tension during ECC is recommended.
Cardiovascular effects of propofol, were assessed after premedication with xylazine(1.0 mUkg, IM) under oxygen supply(200 ml/kg/min) via a endotracheal tube. Twelve adult mixed-breed dogs were divided into four groups; 0.2(Group 1), 0.4(Group 2), 0.6(Group 3) and 0.8 mg/kg/min(Group 4) of propofol respectively. Arterial blood pressure and electrocardiogram were monitored with a physiograph after an arterial catheter was inserted into the femoral artery. pH, arterial carbon dioxide tension($PaCO_2$and arterial oxygen tension($PaO_2$) were evaluated with arterial blood collected through the inserted catheter. Diastolic arterial pressure, systolic arterial pressure and mean arterial pressure were decreased slightly in Group I IIand III, but decreased significantly in Group IV. They were increased rapidly after stopping propofol infusion in Group IV pH was maintained in normal range in Group I, II and m, but was decreased in proportion to time passing in Group IV. $PaCO_2$ was increased significantly only in Group IV but $PaO_2$ was maintained in normal range in all groups Although heart rate was recorded in normal range for 90 minutes, arythmia was noted after stopping propofol infusion in all groups. It was concluded that propofol depressed the cardiovascular system in proportion to infusion dosage, and 0.8 mg/kg/min of propofol infusion rate was not appropriated in canine anesthesia with xylazine premedication.
Plasma protein concentration, plasma albumin concentration, hematocrit, and arterial blood gas tension were measured in 15 mongrel dogs undergoing heart transplantation with cardiopulmonary bypass. The hemodilution due to priming solution resulted in a 49% decrease in plasma protein concentration, a 57% decrease in plasma albumin concentration, a 46%a decrease in hematocrit. The measurements had returned to preperfusion values 1 hour after the end of cardiopulmonary bypass. The intraoperative changes in plasma protein and albumin concentration did not correlate with changes in alveolar-arterial oxygen tension gradients[D[A\ulcorner PO2]]. It is concluded that, in the absence of an increase in left atrial pressure, marked decrease in plasma protein concentration can be tolerated without the occurrence of pulmonary edema. And further study should be done to determine how to prepare an ideal priming solution.
Pulmonary function is the determinant of blood gas tension. However, Acid-Base disturbances can also alter partial pressures of oxygen and carbon dioxide in arterial blood. During respiratory acidosis $PO_2$ will be lowered and reverse changes will be produced during respiratory alkalosis. On the other hand, in metabolic acidosis $PO_2$ will be elevated and $PCO_2$ will be lowered by the respiratory compensation, and reverse response will be induced in metabolic alkalosis. Urinary gas tension has many influencing factors than arterial blood and difficult to estimate the tendency of its alterations. Urinary $PO_2$ and $PCO_2$ are not always identical level as venous blood. It is to be altered by blood gas tension, flow rate of urine, metabolic rate of kidney, and Acid-Base status of blood. Particularly countercurrent exchange of oxygen and carbon dioxide in the renal medulla will make larger alteration of gas tension than venous blood. After induction of Acid-Base disturbances [disturbances] arterial and urinary $PCO_2$, $PO_2$, urinary volume, and osmolarity were determined in dogs, and the relationships between arterial and urinary $PCO_2$ , $PO_2$ Acid-Base disturbances, urinary volume, and osmolarity were investigated. 1. During the acute Metabolic and Respiratory disturbances urinary pH did not respond on respiratory origin. However, there were immediate urinary response in pH on metabolic origin. 2. Urinary $PO_2$, $PCO_2$, did not always follow arterial or venous gas tension and Acid-Base disturbance. Urinary $PCO_2$, correlate well with the urinary volume. The larger the urinary volume, $PCO_2$ lowered to the venous level. The smaller the urinary volume, urinary $PCO_2$ tends to be higher. However urinary $PO_2$ did not have any particular correlation with urinary volume. 3. Correlation between urinary $PCO_2$ and $PO_2$ were inversely proportional to arterial blood. Differences of $PCO_2$ between arterial blood and urine also did not have any particular correlation with urinary volume. This may suggest that changes on blood gas tensions can influence on urinary $PCO_2$. 4. There were eminent clear inverse correlation between urinary $PCO_2$ and osmolar concentrations of urine. Above results strongly suggest that partial pressure of gas in urine primarily depend upon counter-current exchanges in renal medullary tissues.
Extracorporeal circulation by hemodilution technique has been currently used with its clinical safety and good peripheral tissue perfusion in open heart surgery. There is no doubt that $O_{2}$ carrying capacity of the blood is disturbed by decreased hemoglobin level resulting from hemodilution of the circulating blood. From the view point of the blood gas exchange, these experimental studies were undertaken to determined the sate limit of hemodilution in the condition of cardiopulmonary bypass with a constant perfusion flow rate. Twelve adult mongrel dogs weighing 10 to 13 Kg. were anesthetized with pentobarbital and then respiration was controlled with Harvard volume respirator using room air. The cardiopulmonary by pass was performed by use of Sarns heart lung machine (console 5000, 5 head and 2 roller pumps) and Travenol pediatric bubble oxygenator. The perfusion rate during bypass was maintained at a constant rate of 80 ml/min/Kg of body weight. The ratio of oxygen gas flow to blood flow was kept in 3 to 1 constantly. International hemodilution was attained by serial blood withdrawals and immediate infusion of equal volumes of diluants composed of Ringer's lactate, 5% dextrose in water and 25% mannitol solution, proportionally 60%, 30%, and 10%. Arterial and venous blood samples were obtained between 15 and 20 minutes following each hemodilution. Hematocrits and hemoglobin values, $PO_{2}$, $PCO_{2}$ and pH were measured. Oxygen and carbon dioxide contents oxygen consumption and carbon dioxide elimination were calculated groups according to different hematocrit values and the correlations were evaluated. Result were as follows. 1. the arterial $O_{2}$ tension and $O_{2}$ saturation were maintained at the physiological level irrespective of the hematocrit value. 2. The venous $O_{2}$ tension and $O_{2}$ saturation showed a tendency to decline with the decrease in hematocrit value and positive correlation between them (r = +0.49, r = +0.76), The mean values of venous $O_{2}$ tension and $O_{2}$ saturation, however, were not decreased when the hematocrit levels were lower than 20%. 3. The arterial $O_{2}$ content declined lineally in proportion to the fall of hematocrit level with a positive correlation between them (r = +0.95). 4. The venous $O_{2}$ contents were decreased gradually as the hematocrit value decreased with positive correlation between them ( r =+0.89). The trend of diminution of venous $O_{2}$ content, however, was became low according to progressive decrease of hematocrit level. 5. Systemic oxygen consumption was in higher range than $O_{2}$ requirement of basal metabolism when the hematocrit value was above 20%, but abruptly decreased when the hematocrit value became to below 20%. 6. The arterial $CO_{2}$ tension and $CO_{2}$ content showed trend of increasing with progressive decrease of hematocrit value but exhibited a rather broad range and there was no relationship between those value and the hematocrit value. 7. The venous $CO_{2}$ tension and $CO_{2}$ content have also no correlation with change of Ht. value but related directly to those value of arterial blood with positive correlation between them (r = +0.78, r = +0.95_. 8. A-V difference of $CO_{2}$ content and $CO_{2}$ elimination wasnot significantly influenced by Ht. value. From the results, we obtained that feasible limit in inteneional hemodilution is above the hematocrit value of 20% under the given experimental condition.
We investigated the interaction between nitric oxide and the renin angiotensin system in regulating isolated pulmonary arterial tension and pulmonary arterial pressure (PAP) in renal hypertensive rats (RHR) made by complete ligation of left renal artery. Losartan induced a depressor response that was smaller in RHR than in normotensive rats (NR) (3.3 and 7.0 mmHg, respectively, at 3.0 mg/kg, p<0.05), and the response was significantly reduced by $N^{G}$-nitro-Larginine methyl ester (L-NAME). Angiotensin II elevated the PAP (7.6 and 10.8 mmHg at $0.1 {\mu}g/kg$; 20.3 and 23.6 mmHg at $1.0{\mu}g/kg$, respectively) and contracted the isolated pulmonary artery ($pD_2$: 8.79 and 8.71, respectively) from both NR and RHR with similar magnitude, and these effects were significantly enhanced by L-NAME in NR, but not in RHR. Acetylcholine lowered the PAP slightly less effectively in RHR than in NR (3.8 and 6.0 mmHg at 10 .mu.g/kg, respectively) and relaxed the pulmonary artery precontracted with norepinephrine in both rats with similar magnitude ($E_max$: 60.8 and 63.6%, respectively), and the effect being completely abolished after pretreatment.with L-NAME or removal of endothelial cells. These results suggest that nitric oxide interacts with renin angiotensin system to control the pulmonary vascular tension and pulmonary arterial circulation of RHR.R.
Background: Hyperinflation during lung ischemia has been known to improve pulmonary functions after reperfusion which may be exerted through a pulmonary vasodilation and avoidance of atelectasis by an increased surfactant release and been known whether the improvement of pulmonary function was the effect of hyperinflation itself or the oxygen content in inflation gas. Therefore we attempted to clarify the effect of hyperinflation with oxygen in pulmonary inflation gas during warm ischemia on pulmonary function after reperfusion to solve the problem of ischemia-reperfusion injury after lung transplantation. Material and Method: sixteen mongrel dogs were randomly divided into two groups: the left lung was inflated to 30-35 cm H2O with 100% oxygen in oxygen group and 100% nitrogen in nitrogen group. The inflated left lung was maintained with warm ischemia for 100 minutes. Arterial and mixed venous blood gas analysis and hemodynamics were measured before ischemia and 30, 60, 120, 180 and 240 minutes afer reperfusion. Lung biopsy was taken for the measurement of lung water content after the end of reperfusion. Result: In oxygen group arterial oxygen tension the difference of arterial and mixed venous oxygen tension and the difference of alveolar-arterial oxygen tension at 30-minute after reperfusion were not significantly different from those before ischemia and were stable during the 40hour reperfusion. However in nitrogen group these values were significantly deteriorated at 30-minute after reperfusion. there was no significant difference between two groups in hemodynamic data peak airway pressure and lung water content. Conclusion : The results indicated that the oxygenation one of the most important pulmonary functions was improved by pulmonary inflation with 100% oxygen during warm ischemia but the hemodynamics were not. Oxygen as a metabolic substrate during warm ischenia was believed to make the pulmonary tissues to maintain aerobic metabolism and to prevent ischemic damage of alveoli and pulmonary capillary.
The purpose of this study was to analyze the Rhizoma on the blood pressure, heart rate and to define the mechanism of Notopterygii Rhizoma-induced relaxation in rabbit common carotid arterial contracted by agonists. Method : In order to explore the effect of Notopterygii Rhizoma on the blood pressure and heart rate, Notopterygii Rhizoma extract was injected in vein of rabbit ear. In order to investigate the effect of Notopterygii Rhizoma on norepinephrine(NE)-induced contracted rabbit carotid arterial strips, transverse strips with intact or damaged endothelium were used for the experiment using organ bath. To analyze the mechanism of Notopterygii Rhizoma-induced relaxation, Notopterygii Rhizoma extract infused into NE-induced contracted strips induced by agonists after treatment of methylene blue, propranolol, ouabain and it infused into serotonin, potassium chloride-induced contracted strips. Result : The blood pressure was significantly decreased by Notopterygii Rhizoma, but heart rate was insignificantly. In addition, Notopterygii Rhizoma significantly relaxed the norepinephrine, serotonin, potassium-induced contracted strips with intact endothelium or damaged endothelium. The relaxing effect of Notopterygii Rhizoma In NE-induced contracted strips with damaged endothelium by pretreatment of methylene blue, propranolol was not changed, but Ouabain was significantly decreased. Conclusion : These results were shown that Notopterygii Rhizoma affected the NE -induced contracted smooth muscle without the participation of endothelium, and demonstrated that the mechanism of NotoDtervgii Rhizoma-induced relaxation was the obstruction of receptor-operated Ca2+ channel.
It has been suggested that mixed venous $O_{2}$ tension is a predicor of cardiac output especially in a critically ill patient after an open heart surgery. From April 1988 through September 1989, we monitored mixed venous $O_{2}$ tension and pulmonary arterial pressure in 48 patients with acyanotic congenital heart disease at postoperative 1 hour, 6 hour, 12 hour, 24 hour, and 48 hour respectively. They were divided into Group I, with severe pulmoary hypertension, and Group II, without severe pulmonary hypertension. In Group I, mixed venous $O_{2}$ tension and cardiac index showed significant increase with time (p<0.05), but the ratio of pulmonary-aortic systolic pressure didn't show significant change. The increase was significant only 24 hour after operation, and so this low cardiac performance in early postoperative period should be considered when postoperative management is being planned in the risky patient. In Group II, all of the three variables didn't show any significant change with time. The correlation coefficient between mixed venous $O_{2}$ tension and cardiac index was significantly different from zero in both Group I (p<0.001) and group II (p<0.05) at each imeperiod, but the ratio of pulmonary-aortic systolic pressure didn't correlated well with the other 2 variables. Our study showed that serial determination of mixed venous $O_{2}$ tension in acyanotic congenital heart disease could be used as a guide in estimating the cardiac index postoperatively.
Ventilatory functions and arterial respiratory gases were studied in 24 patients who underwent resectional surgery for pulmonary tuberculosis. Postoperative measurements were made 24 hours, 72 hours and 7 days after surgery and the results were compared to preoperative values. Twenty-four hours postoperatively, there occurred striking increase in respiratory rate, minute ventilation, dead space ventilation and dead space tidal volume ratio, and the increase in minute ventilation was caused primarily by the increase in respiratory rate. However, alveolar ventilation, oxygen consumption, carbon dioxide elimination and respiratory quotient showed no significant postoperative changes although two of the last values showed slight decreases 24 hours after surgery. The lowest arterial oxygen saturation level was obtained 24 hours postoperatively followed by gradual rises but not to the preoperative levels until 7 days after surgery. A decreased arterial carbon dioxide tension with elevated pit was noted 24 hours after surgery, which returned to the preoperative level on the following measurement.
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