Appreciation of the large volume deficits which may occur in surgical or trauma patients due to blood loss has led to vigorous transfusion techniques designed to overt hypovolemic shock and ischemic damage to vital organs which may develop in minutes during the hypovolemic state. In a significant proportion of patients treated with massive rapid blood or fluid transfusion, hypervolemia occurs and life threatening pulmonary edema may develop. Especially, hypervolemia may occur during transfusion for preventing development of the so-called low output syndrome following cardiac surgery. However, the most effective indicator which reveals the adequate level of transfusion is not settled yet. The present study was aimed to compare the effectiveness of the indicators suggested thus far and to determine the most sensitive one. Eight dogs were experimentally studied in terms of left atrial pressure, pulmonary arterial systolic pressure, central venous pressure, mean systemic arterial pressure and heart rate before and after induced hypervolemia with infusion of 600ml heparinized homologous blood. Immediately after induced overtransfusion of the blood, pulmonary arterial systolic pressure increased 75.0%, in omparison with the control before transfusion, left atrial pressure 58.8%, central venous pressure 44.6%, and mean systemic arterial pressure 10.1%, one hour after transfusion, pulmonary arterial systolic pressure 40.0%, left atrial pressure 21.2%, central venous pressure 14.5%, and mean systemic arterial pressure 3.2%, central venous pressure 14.5%, and mean systemic arterial pressure 3.2%, respectively. Heart rate showed no significant change throughout the experiment. These result suggested that the changes of the pulmonary arterial systolic pressure is the most sensitive indicator for detection of hypervolemia during blood transfusion.
Nam, Ki Yeul;Yang, Byung Wook;Shin, Wang Soo;Park, Jong Dae
Korean Journal of Pharmacognosy
/
v.48
no.2
/
pp.97-107
/
2017
There is no doubt that the effect of ginseng on blood pressure could be different depending upon the type of ginseng employed for the experiment and methodology, thereby can exert bilateral modulatory activity on blood pressure. It has been reported that ginseng induced no significant change in blood pressure in those subjects with normal blood pressure, but had a normalizing effect on the subjects with abnormal blood pressure. Especially, experimental evidence indicates that ginsenoside Rg3, a major component of red ginseng, has been found to lower blood pressure, which is mediated by release of endothelium-derived NO, enhancing the accumulation of cGMP in the rat aorta. This clinical results further support the beneficial effect of Korean ginseng on blood pressure elucidated by animal experiment. As expected, a multicentric non-controlled clinical study shows that the effect of ginseng consumption has been found to normalize blood pressure in hypertensive or hypotensive individuals as compared to virtually no effect in normotensives. In addition, ginseng has been known to exhibit blood pressure decreased with no significant side effect and deteriorated QOL during the combination therapy of ginseng and anti-hypertensive drugs. This review provides a comprehensive overview on the effects of Korean ginseng on blood pressure.
As the importance of cardiovascular health is highlighted, research on its correlation with blood pressure, the most important indicator, is being actively conducted. Therefore, extensive clinical data is essential, but the measurement of the central arterial blood pressure waveform must be performed invasively within the artery, so the quantity and quality are limited. This study suggested a mock circulatory robot and artificial aorta to reproduce the blood pressure waveform generated by the overlap of forward and reflected waves. The artificial aorta was fabricated with biomimetic silicone to mimic the physiological structure and vascular stiffness of the human. A pressurizing chamber was implemented to prevent distortion of the blood pressure waveform due to the strain-softening of biomimetic silicone. The reproduced central arterial blood pressure waveforms have similar magnitude, shape, and propagation characteristics to humans. In addition, changes in blood pressure waveform due to aging were also reproduced by replacing an artificial aorta with various stiffness. It can be expanded to construct a biosignal database and health sensor testing platform, a core technology for cardiovascular health-related research.
Captopril, an inhibitor of angiotensin converting enzyme, is also known to inhibit the degradation of bradykinin. We examined the effects of intracerebroventricular (ICV) captopril on the central pressor response to bradykinin in normotensive, 2-kidney, 1 clip Goldblatt (GHR) and deoxycorticosterone acetate (DOCA)-salt hypertensive rats. Captopril (1 mg) and bradykinin (5 nmol) were administered into the right lateral cerebral ventricle, and blood pressure and heart rate were continuously monitored throughout the experiment. ICV captopril alone did not affect the blood pressure within 10 minutes but it significantly augmented the central pressor response to bradykinin in GHR. On the contrary, captopril was without effect on the pressor response to bradykinin in normotensive and DOCA-salt rats. These findings indicate that endogenous kinins are not critical in regulating arterial pressure in normotensive and DOCA hypertensive rats. However, in GHR, an enhanced activity of the brain kallikrein-kinin system in maintaining the high blood pressure is suggested.
Kim, Seong-Yun;Sung, Ki-Wug;Koh, Hyun-Chul;Lee, Sang-Bok
The Korean Journal of Physiology and Pharmacology
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v.1
no.6
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pp.639-645
/
1997
The purpose of the present study is to determine the role of muscarinic cholinergic receptors of posterior hypothalamus in the central blood pressure regulation when respiration is controlled. In anesthetized and artificially ventilated rats, vasodepressor response was evoked by injection of L-glutamate(10 nmol) neuroexcitatory amino acid into the posterior hypothalamic area. The injection of $carbachol(0.5{\sim}8\;nmol)$ into the same area induced dose-dependent vasodepressor and bradycardic responses. Pretreatment with atropine(4 nmol) completely blocked the vasodepressor response to carbachol(2 nmol). In contrast, in spontaneously breathing rats, the injection of carbachol(8 nmol) into the posterior hypothalamic area induced the vasopressor and tachycardic responses. These results suggest that the muscarinic cholinergic receptors in the posterior hypothalamic area primarily play an inhibitory role in the central regulation of blood pressure and heart rate.
Park, Jae-Sik;Lee, Zee-Ihn;Jang, Jae-Hee;Ahn, Dong-Kuk
The Korean Journal of Physiology and Pharmacology
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v.6
no.3
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pp.149-154
/
2002
The blood pressure (BP) is regulated by the nervous system and humoral factors, such as renin- angiotensin system, vasopressin and others. In the present study, we examined the central effects of glutamate and GABA on the cardiovascular regulation by injection of these substances into the lateral ventricle and also investigated the relationship between these central effects and the action of angiotensin II (Ang). Male Sprague Dawley rats, $350{\sim}400$ g, were anesthetized with urethane and instrumented with an arterial catheter for direct measurement of BP and heart rate (HR), and an guide cannula in the lateral ventricle for drug injection. A glass microelectode was inserted into the rostral ventrolateral medulla (RVLM) for recording single unit spikes. Barosensitive neurons were identified by changes of single unit spikes in RVLM following intravenous injection of nitroprusside and phenylephrine. The effects of GABA and glutamate injected into the lateral ventricle were studied in single neuronal activity of the RVLM in addition to changes in BP and heart rate, and compared the results before and after treatment with intravenous losartan, nonpeptide Ang II-type 1 receptor antagonist (1 mg/100 g BW). Intracerebroventricular administration of GABA decreased systolic blood pressure (SBP) and HR, but increased the firing rates in the RVLM. However, intracerebroventricular glutamate injection produced effects opposite to GABA. After pretreatment of intravenous losartan, the central effects of GABA on BP and firing rate in the RVLM were significantly attenuated and that of glutamate showed a tendency of attenuation. These results suggested that central GABA and glutamate regulated BP and firing rates in RVLM were inversely related to BP change. The central effects of GABA or glutamate on the autonomic nervous function were modulated by humoral factor, Ang II, by maintaining BP.
This study was undertaken to hemodynamically determine the differences of myocardial protective effect between crystalloid and blood cardioplegic solution. Twenty nine children undergoing cardiac operations due to cyanotic congenital heart diseases were randomized into two groups receiving crystalloid or blood cardioplegia. Cardiac indices and other hemodynamic datum were examined postoperatively. Although there was no statistical differences between groups, postoperative stroke volume indices and left ventricular stroke work indices were slightly better with blood cardioplegia. We also found that postoperative left atrial pressures[p=0.0003], central venous pressures[p=0.004], and heart rates[p=0.014] were significantly lower with blood cardioplegia. The fact that relatively lower ventricular preloads [left atrial pressure and central venous pressure] were required to provide adequate cardiac output in blood cardioplegia group suggested superior myocardial protective effect of blood cardioplegic solution.
Kim, Kyu-Soo;Oh, Sang-Yu;Choi, Byung-Ok;Lee, Joong-Kil
The Korean Journal of Physiology
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v.3
no.2
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pp.25-31
/
1969
Effects of graded increase of positive lung inflation upon heart rates and arterial blood pressure were observed in the anesthetized dogs to analyze the mechanical and neural regulatory factor in response to the positive inflation of the lung. The results obtained were summarized as followings: 1) When the low grade of positive lung inflation was employed under the mild to moderate anesthesia, central venous pressure was linearly increased while heart rate was decreased. After bilateral vagotomy, central venous pressure was obviously increased while heart rate was constant. 2) When the high degree of positive lung inflation was employed, changes of central venous pressure and heart rate were not significant. 3) The low grade of intrapulmonary pressure increase caused reflex tachycardia in phase 2 and overshooting in phase 4 in response to the systemic arterial blood pressure change. 4) On the other hand, the high degree of intrapulmonary pressure increase caused paradoxical bradycardia in phase 2 and lack of overshooting in phase 4 in response to the systemic arterial blood pressure change. 5) It may be noted that the experimental model employed in the present study is a useful tool to evaluate and analyze the neural and mechanical regulatory factor in response to the graded increase of the positive lung inflation.
Various factors influencing the lymph flow from thoracic duct were investigated in an attempt to evaluate their contributing degree and the mechanisms. Sixteen mongrel dogs weighing between 10 and 16 kg were anesthetized and polyethylene catheters were inserted into the thoracic duct and femoral veins. Arterial blood pressure, heart rate, central venous pressure, lymph pressure and lymph flow were measured under various conditions. Electrical stimulation of left sciatic nerve, stepwise increase of central venous pressure, manual application of rhythmical depressions onto abdomen, injection of hypertonic saline solution and histamine infusion were employed. Measurement of cental venous pressure was performed through the recording catheter inserted into abdominal inferior vena cava. Changes in central venous pressure were made by an air-ballooning catheter located higher than the tip of the recording catheter in the inferior vena cava. Lymph flow from thoracic duct was measured directly with a graduated centrifuge tube allowing the lymph to flow freely outward through the inserted cannula. The average side pressure of thoracic lymph was $1.1\;cmH_2O$ and lymph flow was 0.40 ml/min or 1.9 ml/kg-hr. Hemodynamic parameters including lymph flow were measure immediately before and after (or during) applying a condition. Stimulation of left sciatic nerve with a square wave (5/sec, 2 msec, 10V) caused the lymph flow to increase 1.4 times. The pattern of lymph flow from thoracic duct was not continuous throughout the respiratory cycle, but was continuous only during Inspiration. Slow and deep respiration appeared to increase the lymph flow than a rapid and shallow respiration. Relationship between central venous pressure and the lymph flow revealed a relatively direct proportionality; Regression equation was Lymph Flow (ml/kg-hr)=0.09 CVP$(cmH_2O)$+0.55, r=0.67. Manual depressions onto the abdomen in accordance with the respiratory cycle caused the lymph flow to increase most remarkably, e.g,. 5.5 times. The application of manual depressions showed a fluctuation of central venous pressure superimposed on the respiratory fluctuation. Hypertonic saline solution (2% NaCl) administered Intravenously by the amount of 10 m1/kg increased the lymph flow 4.6 times. The injection also increased arterial blood pressure, especially systolic Pressure, and the central venous pressure. Slow intravenous infusion of histamine with a rate of 14-32 ${\mu}g/min$ resulted in a remarkable increase in the lymph flow (4.7 times), in spite of much decrease in the blood pressure and a slight decrease in the central venous pressure.
Anesthetized dogs were tilted from horizontal to the upright and head down position. Tilting to the upright position was followed by an increase in heart rate. In the head down position a decreased heart rate was obtained. The arterial blood pressure was decreased in the upright position and was decreased markedly in the head down position. The central venous pressure was decreased in the upright position and was markedly decreased down to the negative pressure in the head down position. The respiratory rate was slightly increased in the upright position comparing to that in the horizontal position. No remarkable changes were noted in the head down position. From the above results the following factors were discussed The decreased arterial blood pressure during the upright position was supposed to be the secondary effect from the diminished venous return that was suggested by the decreased central venous pressure. The decreased arterial blood pressure in the head down position was also supposed as the above reason as the diminished central venous pressure during the tilt. In addition the cardioinhibitory effects originated from the baroreceptors might have been operated during head down tilting. In the heart rate there was slight tachycardia in the upright position this was assumed as the abolished cardioinhibitory impulses from the baroreceptor in the upright position. On the contrary, despite of the decrease of arterial blood pressure in the head down position as well as in the upright, the bradycardia have been appeared. This was suggestive of cardioinhibitory impulses from the baroreceptors which was stretched during head down tilting. From the above findings there is a possibility of continous cardioinhibitory responses during head down tilting for this kind of the short period of 10 minutes which was chosed in this study.
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