In this study, pulse waves were measured at radial artery using non-invasive tonometric pulse pressure measurement system, SphygmoCor(AtCor, Australia), according to subject's posture. Then it was analysed whether the pulse wave parameters, which contain heart activities, change among three different postures (upright stand, sit, and supine). And it was also verified that the pulse wave parameters change among blood pressure level groups(hypotensive, normotensive, and hypertensive). As a results, posture effects were verified in time information of pulse wave rather than amplitude. But some parameters calculated by ratio of two amplitude, such as augmented index(AI) and ratio of central aortic pulse and radial artery pulse, showed significant difference according to postures. In post hoc test, time to the $1^{st}$ and $2^{nd}$ pulse peak(P_$T_1$, and P_$T_2$), ED(ejection duration), and HR(heart rate) showed significant difference among posture groups with each other. In comparison of blood pressure groups, it was verified that the parameters related to amplitude of pulse wave showed significant difference rather than time information.
Recent studies have shown that a GABAergic mechanism in the brain modulates arterial blood pressure (BP) through alterations of sympathetic activity in the brain. The purpose of the present study was to determine if this modulation is involved in the pressor response to raised intracranial pressure (ICP). The pressor response to raised ICP was abolished by pretreatment of anesthetized rabbits with intracerebroventricular (icv) muscimol (a GABA agonist) as well as with icv clonidine $(an\;{\alpha}_2-agonist)$. Raising ICP in the hypertensive state after icv yohimbine $(an\;{\alpha}_2-antagonist)$ did not cause an additional increase in the BP, whereas raising ICP in the hypertensive state following icv bicuculline (a GABA antagonist) produced a further increase. Bicuculline produced an increase of the BP which had been lowered by muscimol or by clonidine, whereas it failed to increase the hypertensive state induced by either previous yohimbine or raised ICP. Yohimbine reversed the BP which had been made low by clonidine but was incapable of raising the hypotensive state after muscimol. Yohimbine failed to increase the heightened BP due to raised ICP, whereas bicuculline-induced pressor state was further elevated by yohimbine. Muscimol, besides the bicuculline-antagonizing property, inhibited the pressor response to yohimbine, suggesting participation of a GABAergic mechanism in the pressor action of yohimbine. From these results it was inferred that there were three ways in which BP could be increased via raised ICP: inactivation of the inhibitory sympathetic activity through (1) ${\alpha}_{2}-adrenoceptors$, (2) bicuculline-sensitive GABA receptors, (3) yohimbine-sensitive, clonidine-acting GABAergic sites.
To evaluate GC-rhEPO, human erythropoietin produced by recombinant DNA technique, its general pharmacological properties were investigated in experimental animals administering intravenously and in vitro test system. GC-rhEPO at doses of 70,700 and 7,000 IU/kg body weight had no influence on general behavior, spontaneous motor activity, thiopental-inducted sleeping time, writhing syndrome induced by acetic acid, strychnine-induced convulsions, charchoal meal propulsion in mice, and body temperature, gastric juice secretion, urine and electrolyte excretion in rats. In anesthetized rabbits, GC-rhEPO (70, 700 and 7,000 lU/kg, i.v.) did not alter respiratory rate, blood pressure, heat rate. In in vitro experiments, GC-rhEPO did not affect the contractions of the isolated ileum of guinea pigs and the muscle twitchs of isolated neuromuscular junction of the rats. In addition, GC-rhEPO did not affect the blood coagulation time and ADP-induced platelet aggregation in plasma of rabbits. Taken together, these results indicate that GC-rhEPO does not induce any adverse effects in the experimental animals.
Cold $(0^{\circ}C)$ or warm $(25^{\circ}C)$ fresh and sea water were flooded into the lungs of rabbits through tracheal canule. Respiratory arrest ensued in 19.5 minutes in the warm fresh water flooded rabbits and was the longest survival time among the experimental groups. The survival times in the other groups were: 2.32 minutes in cold fresh water group, 2.75 minutes in .warm sea water group, and 4.57 minutes in cold sea water group. Cardiac output was measured by means of T-1824 dilution technique after 2 or 3 minutes of flooding in 27 rabbits. Blood pressure was observed by mercury manometer throughout the survival time in 40 rabbits. The following results were obtained. 1. Cardiac output in the warm fresh water flooded and sea water flooded animal was smaller than that of control rabbits. In the cold fresh water flooded animal cardiac output was greater than that of the control animal. 2. Time constants of T-1824 dilution curve of experimental group were elongated than the normal curve. 3. Central blood volume showed an increase in the fresh water group, a decrease in cold sea water group and no change in warm sea water group. 4. In all of the experimental groups arterial blood Pressure showed an abrupt and great variations after flooding of lungs and lasted about 30 seconds. Thereafter, arterial pressure remained at a plateau level until the sudden fall to zero and this was almost coincided with the time of respiratory arrest. The Plateau level of arterial Pressure in fresh water group was about 10 mmHg higher than the control value, and it was lower than the control value in warm sea water group. In cold sea water group the plateau was made up by fluctuations around the control value. 5. Osmosis of water through the lung alveolar membrane occured in all animals. Fresh water caused hemodilution and sea water caused hemoconcentration. 6. In sea water flooded animal more volume of water was recovered through the tracheal canule than the volume injected into trachea. This was interpreted as the consequence of the shift of water from plasma to alveolar sac. 7. Relative freight of lung was greater in fresh water group than sea water group. In all animal lung edema ensued. 8. The mechanisms of cardiac output variations were discussed.
Objective: To examine the relationship between hypertension prevalence and the four commonest anthropometric measurements for obesity(body mass index(BMI), wasit-hip ratio(WHR), waist circumference(WC) and body fat in Korean adults. Methods: We studied the cross-sectional association of the anthropometric indices and blood pressure in 1,197 individuals(who were participants in the population-based cohort study). Hypertension was defined as blood pressure $\geq160/95\;mmHg$ or current use of antihypertensive medication. Informations on life-style factors were obtained from personal interview. Results: There were close associations between BMI, WHR and WC with blood pressure in both men and women. After age adjustment, BMI and WC showed significantly positive correlation with systolic and diastolic blood pressure levels in both men and women. Odds ratio(ORs) of being hypertensive were estimated comparing the highest to the lowest quantile, adjusting for age, smoking status, alcohol intake levels, education attainment. The simultaneously adjusted ORs of being hypertensive, comparing the highest vs the lowest categories, was for BMI 2.0(95% confidence interval(CI)=0.9-3.2) in men and 3.2 (95% CI=1.7-6.1) in women, for WC 2.1(95% CI=1.0-4.4) in men and 3.1 (95% CI=1.6-5.9) in women, for fat(%) 4.2(95% CI=1.9-9.5) in men and 2.1(95% CI=1.2-3.6) in women. Conclusion: In addition to measures of overall obesity(BMI) as well as central obesity(WHR, WC), body fat(%) was independently associated with prevalence of hypertension. Among obesity indices, body fat was the most predictor variable in hypertensive state in male and BMI was in female.
Clinical perfusion data on 16 cases of cardiopulmonary bypass using Sigmamotor pump and RyggKyvsgaard Oxygenator which performed at Seoul National University Hospital during the period of Aug. 1968 to Aug. 1970 was analized. AIl cases were hemodiluted and the perfusion was carried out under the normothermic condition. The age of the patients ranged between 6 and 43 years. The b:dy weight varied between 18.3 and 54.0 kg and the body surface area between 0.78 and 1. 59$M^2$. The priming solution was consiste:I with fresh ACD blood. Hartmann solution and Mannitol. The average amount of priming was approximately 2242 ml. The average hemodilution rate was 17%. The flow rate ranged from 1.7L to 3.5L/Min/$M^2$ and averaged 2.4L/Min/$M^2$ or 78mI/Min/kg. The duration of perfusion varied from 22 to 110 min with average of 56.9 minutes. Some hemodynamic responses were observed. The arterial pressure dropped immediately after the initiation of partial perfusion and was more marked after the total perfusion foIlowed by gradual increase to the safety level. The central venous pressure reflected the reduced blood volume especially in the cases of prolonged perfusion which lasted over 60 min. In most of the cases, red blood cell count decreased and white blood ceIl count increased after the perfusion. Hemoglobin level was decreased, averaging of 12.5mg%, Hct 3.3% and platelets count of 18% postoperatively. Plasma hemoglobin increased mildly, from pre-perfusion average value of 4. 06mg% to postperfusion value of 22.5mg%. Serum potassium was 4.4mEq/L pre-operatively and was decreased to 3.7mEq/L postoperatively. Five cases showed definite hypopotassemia immediately after the operation. Sodium and chloride decreased mildly. These electrolyte changes are thought to be related with hemodilution. diuretics and reduced blood volume during and after the perfusion. Arterial blood pH value revealed minimal to moderate elevation from preperfusion average value of 7.376 to 7.461 during perfusion and then 7.365 after perfusion. The pC02 and hicarbonate showed minimal to moderately lowered values. The total CO2 was decreased. Buffer base decreased during perfusion (Av. 42.6mEq/L) and further decreased after the perfusion (Av. 40.8mEq/L). These arterial blood acid base changes suggested that the metabolic acidosis was accompanied by respiratory alkalosis during and immediately after the perfusion. Authors belived that the acidosis could more effectively be corrected with the more additional dose of bicarbonate than we used by this study. The chest tune drainage during the first 24 hours following operation was 1158 ml in average. One case (Case No. 15) showd definite bleeding tendency and it was believed that the cause might be due to the defect of heparin and protamine titration. The average urinary out put during 24 hours post-perfusion was 1291ml. One case (Case No. ]) showed definite post perfusion oliguria. As conclusion hemodilution using fresh ACD blood. Hartmann and Mannitol solution added with Bivon and high flow rate unler normothermia. was thought to amelioratc the severity of mctabolic acidosis during and after perfusion with relatively satisfactory effect on the diuresis and bleeding tendency.
Clinical experience on 16 cases of open heart surgery under the extracorporeal circulation with mild or moderate hypothermia and partial hemodilution technique at the National Medical Center during the period from June 1976 to October 1977. Nine of sixteen were congenital heart disease and seven were acquired heart disease. The age of the patient ranged between 6 and 48 years. The body weight varied from 18.5kg to 60kg and body surface area 0. 79-1.70m2. The average priming volume of pump oxygenator was 2080 ml, which was consisted fresh ACD blood, buffered Hartmann`s solution, Mannitol, 50% dextrose in water and Vit. C. The average hemodilution rate was 27%. The average flow 2.3 L/min/m2 or 80 ml/min and the duration of perfusion varied from 31 min to 270 min with average of 107 min. The perfusion was carried out under the mild or moderate hypothermia using core cooling alone in 10 cases, core cooling and local myocardial cooling with $0-4^{\circ}C$ physiologic saline in 2 cases. From a hemodynamic point of view, the blood pressure dropped down around 80 mmHg after the initiation of perfusion follwed by increase to safety level and stable during the perfusion. The central venous pressure remained within normal limits. In most cases, hemoglobin and hematocrit decreased during and after the perfusion. Hemogiobin level was decreased, average of 20.6 %, hematocrit 18.6%, pletelets 55% postoperatively. Plasma hemoglobin increased moderately, from preperfusion average valve of 7.79 mg % to post-perfusion value of 54.7 mg %. Electrolytes changes during cardiopulmonary bypass showed definite hypokalemia but changes of Na, Ca were not definite. Arterial blood gas analysis during cardiopulmonary bypass suggested that the metabolic acidosis which was accompanied by respiratory alkalosis which was corrected postoperatively. As the opera tive complication, transient hemoglobinuria in 4 cases and neurological signs in 2 cases were all cured. There were 2 death cases and operative mortality rate was 12.5%.
The renoprotective activities of white ginseng radix and rootlet were compared in spontaneously hypertensive rat (SHR) with diabetes. During oral administration of white ginseng radix (Ginseng Radix Alba, GRA) and white ginseng rootlet (Ginseng Radix Palva, GRP) for four weeks, arterial blood pressure and blood glucose levels were determined at every 10 days. In both GRA- and GRP-treatment groups, arterial blood pressures started to go down after 10 days of administration and maintained throughout the study period. After four weeks administrations of GRA and GRP, diastolic blood pressures were significantly decreased with 17% and 9%, respectively. GRA treatment also decreased blood glucose levels after 10 days of administration when compared with diabetic SHR group. At the end of the experiment, serum creatinine (Scr) and blood urea nitrogen (BUN) were not significantly different between the groups, except 62% higher value of BUN in diabetic SHR group when compared with SHR group. In the diabetic SHR group, the excretion of urinary albumin was increased significantly when compared with SHR. The level of urinary albumin in GRA treated group was markedly reduced when compared with diabetic SHR group $(67.8{\pm}4.7\;vs.\;131.3{\pm}13.5\;mg/24\;h).$ To examine the effects of ginseng radices on an overt diabetic nephropathy, index of kidney hypertrophy and transforming growth $factor-{\beta}1\;(TGF-{\beta}1)$ protein levels were evaluated. The glomerular and tubular cells stained positive for $TGF-{\beta}1$ seemed to be more abundant in diabetic SHR than in those with SHR, and GRA treated rats showed somewhat less $TGF-{\beta}1$ protein in glomerular and tubular cells when compared with diabetic SHR. Our results suggest that GRA might be a useful antihypertensive and antidiabetic agent with renoprotective effect.
Studies of cardiopulmonary function and acid-base balance were performed on 29 dogs during control period, during oligemic hypotension and following return of blood to the animals. Intravenous morphine and local anesthesia were used. Fifteen of the 29 animals survived the complete experiment. The 14 animals that failed to survive the experimental period died between 15 to 90 minutes after the onset of bleeding. The results were as follows. 1. The heart rate increased after the onset of bleeding and failed to return to control level following reinfusion. Stroke volume decreased markedly after bleeding and failed to recover after return of blood from the reservoir. Cardiac output also decreased during oligemic hypotension and was maintained at this level after re-infusion. Total peripheral resistance decreased significantly immediately after bleeding, however it increased soon over the pre-bleeding level. Central venous pressure decreased after the onset of bleeding and remained at lower level for the rest of the experimental period. Arterial blood pressure, clown to 40-45 mmHg by acute hemorrhage, was elevated near to control level. Left ventricular work decreased tremendously during oligemic hypotension and failed to return to control level with the re-infusion of blood. Hematocrit value showed no significant decrease after bleeding and increased after re-infusion. Hemoglobin decreased after the onset of bleeding and recovered to control value after re-infusion. 2. The respiratory rate fell rapidly after bleeding from 124 to 29 and remained at this lower level for the remainder of the experiment. The tidal volume increased after bleeding and was maintained at this level for the remainder of the experiment. The respiratory minute volume showed no significant changes throughout the experimental period. Oxygen consumption fell lightly in all animals during oligemic hypotension and returned to normal levels following re-infusion. Arterial oxygen content and arterial oxygen saturation decreased following bleeding and the values returned to normal levels after the return of blood from the reservoir The arterio-venous oxygen difference increased after the onset of bleeding. It failed to return to normal values following re-infusion. Arterial $Pco_2$ decreased in all animals after the beginning of the bleeding. Partial pressure of $Co_2$ continued to fall until re-infusion, after which the values returned toward normal. Animals became acidotic. The pH fell to lower level following bleeding. Lactic acid and lactate: pyruvate ratio also increased during same period. Arterial pH and lactic acid failed to return to control value and lactate: pyruvate ratio increased more after re-infusion. Sodium bicarbonate decreased after bleeding and returned to control value following re-infusion.
To delineate the relationship between subtypes of central alpha-adrenoceptor and central calcium channel, influences of intracerebroventricular (icv) diltiazem and nifedipine on the changes of blood pressure and heart rate by icv methoxamine and clonidine were investigated in urethane-anesthetized rabbits. 1) Methoxamine (1mg, icv) produced pressor and bradycardiac effect and clonidine $(30\;{\mu}g,\;icv)$ produced hypotension and bradycardia. 2) Icv diltiazem and nifedipine elicited dose-dependent deprcssor and bradycardiac responses. The depressor response to nifedipine was more prominent than that to diltiazem but the bradycardiac effect of nifedipine was smaller than that of diltiazem. The depressor responses to icy nifedipine $(35{\mu}g)$ and icv diltiazem $(400{\mu}g)$ were persistent but those to intravenous (iv) nifedipine $(35{\mu}g/kg)$ and diltiazem $(200{\mu}g/kg)$ were transient. 3) The pressor response to methoxamine was little affected by pretreatment with in diltiazem $(400{\mu}g)$ or icv nifedipine $(35,\;350{\mu}g)$ but the bradycardiac response to methoxamine was significantly attenuated by the same pretreatment. 4) The depressor response to clonidine was markedly attenuated by pretreatment with icv diltiazem $(400{\mu}g)$ or icv nifedipine $(35,\;350{\mu}g)$ but not affected by pretreatment with iv diltiazem $(200{\mu}g/kg)$ or iv nifedipine $(20{\mu}g/kg)$. Pretreatment with icv and iv diltiazem or nifedipine reduced the bradycardiac effect of clonidine. 5) Pretreatment with icv clonidine had no effect on the depressor and bradycardiac responses to in diltiazcm or icv nifedipine. These results indicate that diltiazem and nifedipine have no effect on icv methoxamine-induced pressor response elicited by the activation of central alpha-l adrenoceptors whereas the icv clonidine-induccd depressor and bradycardiac effects which result from the activation of central alpha-2 adrenoceptors are inhibited by the calcium antagonists.
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