1. It was attempted to clarify the mechanism of the pressor response to raised intracranial pressure in urethane-anesthetized rabbits. 2. Intraventricular clonidine markedly inhibited the pressor response to raised intracranial pressure. 3. Intraventricular regitine antagonized the above mentioned inhibitory effect of clonidine on the pressor response. 4. In reserpine-treated rabbits the pressor response to raised intracranial pressure was not observed, whereas after the intraventricular administration of norepinephrine the pressor response was observed. 5. Intraventricular clonidine inhibited the pressor response that could be observed in the reserpine-treated rabbits after the intraventricular norepinephrine. 6. It is inferred that raised intracranial pressure stimulated some part of the brain to cause the increase of norepinephrine release, resulting in the increase of the sympathetic outflow and the elevation of blood pressure.
Blood Pressure ; Brain ; Clonidine* ; Intracranial Pressure* ; Norepinephrine ; Phentolamine* ; Rabbits*

The purpose of this study is to evaluate the effects of Chu-ma therapy and to suggest that the therapy is an effective nursing intervention tool to reduce blood pressure. The research design employed was the non-synchronized research method with non- equivalent control group. A total of 30 people with essential hypertension, who were from forty to sixty five years old, participated in the study. The Chu-ma therapy was administered by every day for ten or fifteen minutes for eight weeks from 19, April to 13, June in 1999. In order to evaluate the effects of Chu-ma therapy, blood pressure of the two groups were measured once a week, and physiological parameters (epinephrine, norepinephrine, total cholesterol, HDL-cholesterol, triglycerides) were measured before and after the treatment. Collected data was analyzed by SAS package. The results of this study can be summarized as follows: 1) There were significant decrease in systolic blood pressure and diastolic blood pressure in the experimental group. 2) There were no significant changes in epinephrine, norepinephrine of the two groups. 3) There were significant decrease in total cholesterol and triglycerides, and HDL- cholesterol increased significantly in the experimental group. 4) The effect of Chu-ma therapy on the measured time on the blood pressure in experimental group was as follows: Both of systolic and diastolic blood pressures were significantly decreased after 5weeks. The result proved that Chu-ma therapy is an effective nursing intervention tool for clients with essential hypertenion. However further research is still necessary to compare the effect with the different periods and number of times for Chu-ma therapy.
Blood Pressure* ; Cholesterol ; Epinephrine ; Hypertension* ; Norepinephrine ; Nursing ; Research Design ; Triglycerides

The aim of the present study was to examine the effects of platycodin D and D3, which are active components derived from the roots of Platycodon grandiflorum A. DC., on the contractile force of the i3olated rat aorta and blood pressure of the anesthetized rat, and also to elucidate its mechanism of action. Both phenylephrine (an adrenergic alpha1-receptor agonist) and high potassium (a membrane- depolarizing agent) caused great contractile responses in the isolated aortic strips. Platycodin D at high concentration (24microgram/ml) inhibited contractile responses induced by phenylephrine (10 (-5) M) and high potassium (5.6x10 (-2) M), while low concentrations of platycodin D (4~8microgram/ml) did not affect those responses. However, platycodin D3 (8~32microgram/ml) did not alter the contractile responses evoked by phenylephrine and high K+. Interestingly, the infusion of platycodin D3 (1.0 mg/kg/30 min) significantly reduced the pressor responses induced by intravenous norepinephrine. However, platycodin D3 (1.0 mg/kg/30 min) did not affect them. Taken together, these results show that intravenously administered platycodin D depresses norepinephrine-induced pressor responses in the anesthetized rat, at least partly through the blockade of adrenergic alpha1-receptors. Platycodin D also caused vascular relaxation in the isolated aortic strips of the rat via the blockade of adrenergic alpha1-receptors, in addition to an unknown direct mechanism. However, platycodin D3 did not affect both norepinephrine-induced pressor responses and the isolated rat aortic contractile responses evoked by phenylephrine and high potassium. Based on these results, there seems to be much difference in the mode of action between platycodin D and platycodin D3.
Animals ; Aorta ; Blood Pressure ; Norepinephrine ; Phenylephrine ; Platycodon ; Potassium ; Rats* ; Relaxation

Serum epinephrine and norepinephrine concentrations were measured in 7 patients during fentanyl-oxygen anesthesia, who were undergoing elective open heart surgery(single valvular replacement operations) in Seoul National University Hospital. Sampling times and corresponding total fentanyl doses were as follows; 1) after arterial cannulation 2) 5 minutes after intubation(50 ug/kg of B. Wt) 3) 5 minutes after sternotomy(65 ug/ka) 4) after aortic dissection(75 ug/kg) 5) 15 minutes after initiating bypass 6) 60 minutes after initiating bypass [20 ug/kg of fentanyl was added to the priming solution before initiation of Cardio-pulmonary bypass(CP bypass)]. High Performance Liquid Chromatography(HPLC) was used to analyze hormones. Epinephrine concentrations(pg/ml) corresponding to the sampling times were as follows (mean+/-SE); 1) 213+/-59 2) 199+/-62 3) 246+/-83 4) 173+/-35 5) 270+/-70 6) 269+/-70 Norepinephrine concentrations(pg/ml) were as follows(mean+/-SE); 1) 609+/-107 2) 500+/-73 3) 645+/-152 4) 470+/-82 5) 494+/-65 6) 955+/-311 There were no significant hormonal changes except the 6th norepinephrine value. There were no significant hemodynamic changes except blood pressure decrease at the beginning of CP bypass. It is concluded that high dose fentanyl-oxygen anesthesia was limitedly effective to block the stress of open heart surgery, general anesthesia and CP bypass.
Anesthesia* ; Anesthesia, General ; Blood Pressure ; Catheterization ; Epinephrine ; Fentanyl* ; Heart* ; Hemodynamics ; Humans ; Norepinephrine ; Oxygen* ; Seoul ; Thoracic Surgery*

Hyperglycemia during either global or regional ischemia is widely known to be detrimental, and ischemia induced release of diverse neurotransmitters and the ensuing activation of specific postsynaptic receptors have been suggested to play a important role in the development of ischemic selective vulunerability. This study was undertaken to investigate the influence of blood glucose change on tissue concentration of some catecholamines ; dopamine, norepinephrine, serotonin, of the transient ischemic rat's brain, estimated by high performance liquid chromatography(HPLC) assay system, following transient bilateral forebrain ischemia in the rat's model subjected to 20 minutes of normothermic ischemia by two vesseles occulusion plus profound cortex, hippocampus and striatum respectively by HLPC. The concentrations of catecholamines were significantly decreased in all sampled areas in experimental groups compared with the control group(p<0.05), respectively(average decrease rate : norepinephrine 71%, dopamine 89%, serotonin 80% in frontal cortex ; norepinephrine 71%, dopamine 93%, serotonin 81% in hippocampus ; norepinephrine 33%, dopamine 35%, serotonin 78% in striatum). Dopamine was relatively decreased in concentration in frontal cortex and hippocampus, and serotonin was relatively decreased in striatum. But no statistic significancy(p>0.05) of catecholamines level between each experimental group(hyper-, hypo- and normoglycemic group) according to the change of blood sugar. The results suggested that blood glucose level did not influence the tissue concentration of dopamine, norepinephrine and serotonin in frontl cortex, hippocampus and striatum of transient ischemic rat's brain.
Blood Glucose* ; Brain* ; Catecholamines ; Dopamine* ; Frontal Lobe* ; Hippocampus* ; Hyperglycemia ; Ischemia ; Neurotransmitter Agents ; Norepinephrine* ; Prosencephalon ; Serotonin*

Ketamine produces an increase in the heart rate and blood pressure, but the precise mechanism is controversial. In order to obtain inslight into the mechanism by observing the influence of nitroglycerin (NTG) on the ketamine effect, ketamine was administered intravenously following sublingual administration of nitroglycerin in conscious patients. The results were as follows: 1) In the ketamine(2mg/kg) group(n=15), the heart rate and blood pressure increased significantly by as much as 25%. 2) In the nitroglycerin(1.2mg) group(n=12), the heart rate increased, but blood pressure decreased from 5 minutes after administration. 3) In the group which received ketamine(2mg/kg) 5min. after NTG(1.2mg)(N=15), the heart rate did not change, but the blood pressure increased significantly without attenuation by nitroglycerin. From the above results, it is suggested that in the ketamine effect control mechanism may also be participated in addition ot the peripheral mechanism involving norepinephrine release.
Administration, Sublingual ; Blood Pressure* ; Heart Rate* ; Heart* ; Humans ; Ketamine* ; Nitroglycerin* ; Norepinephrine

The reaction to stress, while vital to the conscious animal, may be detrimental to the surgical patient. To assess the stress-associated action of halothane and its doses, we studied the responses in plasma norepinephrine, epinephrine, blood pressure and heart rate to changes of halothane concentration from 0 MAC to 1.5 MAC in 8 healthy adults. Systolic blood pressure, diastolic blood pressure and mean blood pressure were decreased as the concentration of the halothane increased from 0 MAC 0.5 MAC, 1.0 MAC and 1.5 MAC, respectively. But norepinephrine and epinephrine show no statistic ally significant response to changes in the concentration of halothane.
Adult ; Anesthesia ; Animals ; Blood Pressure ; Epinephrine* ; Halothane* ; Heart Rate ; Humans ; Norepinephrine* ; Plasma*

1. The intracranial pressure (ICP) was raised by the extradural balloon method in urethane-anesthetized rabbits, and change of the arterial blood pressure (BP) with change of ICP was studied. 2. In the control rabbit group raising ICP resulted in marked increase in BP. 3. In the reserpine-treated group raising ICP did not induce the increase in BP but the decrease in BP. 4. In the tetrabenazine-treated group raising ICP did not cause change in BP. 5. After the administration of norepinephrine through the lateral ventricle to the reserpine-treated and tetrabenazine-treated rabbits, raising ICP resulted in marked increase in BP. 6. These results indicate that the existence of norepinephrine in the brain is essential for the BP increase by raising ICP.
Arterial Pressure ; Blood Pressure* ; Brain* ; Intracranial Pressure* ; Lateral Ventricles ; Norepinephrine* ; Rabbits

The effect of Pheniramine(Avil), a histaminergic-1 receptor blocking agent presently employed in treating various allergic diseases on pressor actions of norepinephring(NE) and tyramine (TR) was studied in the rabbit. Pheniramine, when given into a femoral vein with a dose(3mg/kg) enough to block H1-receptor, potentiated markedly the pressor responses of NE and TR. The pressor action of NE augmented by pheniramine was not affected by additional adminstration of debrisoquin (Drenergic neuron blocker) or phenelzine(monoamine oxidase inhibitor) or desipramine(U1-uptake blocker), or while potentiated by additional treatment with chlorisondamine(ganglionic blocker)or reserpine(catecholamine depleter). The hypertensive response of NE to phenelzine or desipramine was reinforced significantly by addition of pheniramine, but the response of NE in rabbits treated with reserpine or chlorisondamine or debrisoquin was not influenced by pheniramine-addition. Elevation of blood pressure to TR potentiated by pheniramine was attenuated significantly by reserpine treatment with chlorisondamine made the significant augmentation of pressor action to TR after pheniramine. Tyramine-induced response of blood pressure after pheniramine, but the response of blood pressure to TR caused by phenelzine or desipramine was enhanced markedly by pheniramine-treatment. From the above experimental results, it is thought that the pressor effect of NE and TR potentiated by pheniramine is similar to that of debrisoquin, i.e. the sensitization of effector cell, and that central action of pheniramine can not ruled out.
Blood Pressure ; Chlorisondamine ; Debrisoquin ; Desipramine ; Femoral Vein ; Neurons ; Norepinephrine* ; Oxidoreductases ; Phenelzine ; Pheniramine ; Rabbits ; Reserpine ; Tyramine*

Although the conclusion is controversial, there has long been an appealing notion that catecholamines may be involved in some way in the pathogenesis of primary hypertension and almost invariably most of hypotensive drugs involve at various sites of the neuron and produce their effect by depletion of norepinephrine in the sympathetic nerve ending. The authors undertook the comparative study on catecholamine depleting action of 3 most effective drugs available for the treatment of hypertension, reserpine, guanethidine and alpha-methyldopa, measuring the plasma catecholamine levels and urinary exceretion of caecholamine by the modified fluorometric method of Weil-Malherbe and Bone during the treatment of hypertension. The results are as follows: 1) Before the administration of hypotensive drugs, mean blood pressure was 180/110mmH, mean psalma epinephrine level was 0.36+/-0.23gamma%, mean plasma norepinephrine level was 0.48+/-0.35gamma%, 24 hours urinary excretion of epinephrine was 3.6+/-0.12gamma/day and 24 hours urinary excretion of norepinephrine was 68.9+/-0.34gamma/day. 2) In group 1 (reserpin administered group), the mean blood pressure was 190/110mmHg before the treatment and which was declined to 155/89mmHg on the last day of 4th week, in group 2 (guanethidine administered group), the mean blood pressure measured before the treatment was 185/110mmHg and which was declined to 150/85mmHg on the last day of 4th week, and in group 3 (alpha-methylodpa administered group), the mean blood measured pressure measured before the treatment was 182/110mmHg and which was declined to 153/88mmHg on the last day of 4th week. 3) After the treatment for 4 weeks with reserpin guanethidine and alpha-methyldopa, the mean plasma epinephrine levels were declined from 0.37+/-0.12gamma% to 0.11+/-0.08gamma% in group 1, from 0.38+/-0.16gamma% to 0.14+/-0.10gamma% in group 2 and from 0.33+/-0.23gamma% to 0.10+/-0.09gamma% in group 3. 4) The mean plasma norepinephrine levels were declined from 0.05+/-0.21gamma% to 0.22+/-0.12gamma% in group 1, from 0.51+/-0.25gamma% to 0.20+/-0.10gamma% in group 2 and from 0.51+/-0.21gamma% to 0.20+/-0.11gamma% in group 3 after the treatment of 4 weeks respectively. 5) Urinary exceretion of epinephine was declined from 32.3+/-0.16gamma/day to 10.4+/-0.10gamma/day in group 1, from 34.5+/-0.34gamma/day to 17.2+/-0.16gamma/day in group 2, and from 28.2+/-0.14gamma/day to 10.3+/-0.11gamma/day in group in group 3 after the treatment of 4weeks duration. 6) The mean value of 24 hours urinary excretion of norepinephrine was declined to from 72.2+/-0.35gamma/day to 28.5+/-0.14gamma/day in group1, from 69.2+/-0.34gamma/day to 22.6+/-0.21gamma/day in group 2 and from 68.6+/-0.34gamma/day to 18.2+/-0.10gamma/day in group 3 after the treatment of 4 weeks duration. 7) From the above result we can summarized as follows: Antihypertensive effect of each drugs was; guanethidine>alpha-methylodopa>reserpin in order but depressing action plasma norepinephrine levels was; alpha-methyldopa>guanethidine>reserpin and depressing effect of urinary norepinephrine excretion was; alpha-methyldopa>guanethidine>reserpin, in order.
Antihypertensive Agents* ; Blood Pressure ; Catecholamines ; Epinephrine ; Guanethidine ; Humans ; Hypertension ; Methyldopa ; Nerve Endings ; Neurons ; Norepinephrine ; Plasma* ; Reserpine