No abstract available.
Animals ; Enalapril* ; Nicardipine* ; Nitroprusside* ; Rats* ; Skin*

The antihypertensive effect and side reactions of perdipine was studied in 22 cases of essential hypertension using 20mg 3 times daily regimen for average period of 5 weeks. 1) Average reduction of 20mmHg in systolic and 17mmhg in diastolic pressure was observed and percentile reduction was 11.90% and 14.92%, respectively. The overall effect rate was 81.82%. The blood pressure lowered significantly after 2 weeks of treatment both in systolic and diastolic pressure. 2) There was no significant change in heart rates before and after treatment. 3) No specific side reaction was observed except 1 case in which discontinued the medication because of severe headache and fatigability on the 1st day of medication.
Blood Pressure ; Headache ; Heart Rate ; Hypertension ; Nicardipine*

The effect of nicardipine was investigated on hypertension due to raised intracranial pressure, pressor response of alpha-adrenoceptor agonists in the dissected thoracic aorta. Intracerebroventricular(icv) and intravenous(iv) nicardipine produced dose-dependent depressor response and bradycardiac effect, especially marked response was observed following iv injection. The pressor response to raised intracranial pressures was potentiated following iv injection of 50 microgram/kg nicardipine but was markedly inhibited following iv 100 microgram/kg injection, and was not affected following icv 50 microgram/kg administration but was markedly inhibited following icv administration of 100-200 microgram/kg nicardipine. The nicardipine inhibited contractile effect of KCI 35 mM in a dose-dependent fashion but did not affect that of Ne and ME. These data suggest that nicardipine caused hypotensive effect by blocking calcium influx in the peripheral vessels and that direct effect of nicardipine on central nervous system involves the hypotensive action. Conclusively, the inhibitory effect of nicardipine on the pressor response to the intracranial pressure elevation may be induced by these two mechanisms.
Aorta, Thoracic ; Calcium ; Central Nervous System ; Hypertension ; Intracranial Pressure* ; Nicardipine*

Pheochromocytoma stems from the chromaffin cell and mostly is located in the adrenal medulla. It is an important cause of secondary hypertension due to correction of hypertension by a resection of the tumor. Because it produces and secretes catecholamine, it bothers anesthesiologists with excessive hypertension, tachycardia and arrhythmia during the anesthetic period. Therefore, anesthetic management is directed to avoid these conditions. We report a case of bilateral pheochromocytoma successfully managed intraoperatively with an infusion of nicardipine and an intermittent esmolol injection.
Adrenal Medulla ; Arrhythmias, Cardiac ; Chromaffin Cells ; Hypertension ; Nicardipine* ; Pheochromocytoma* ; Tachycardia

The antihypertensive effect of nicardipine was studied in 31 cases of essential hypertension and following results were obtained. 1) Daily dose was 30-60mg for 10 weeks. 2) Mean systolic and diastolic pressure were decreased by 39.5mmHg 921%) and 17.2mmHg(15%) respectively(P<0.005) and in 84% of cases, good or fair control of blood pressure was proved. 3) There was no significant change in heart rates before and after treatment. 4) There were no significant side effects except two cases of mild headache and facial flushing which subsided spontaneously.
Blood Pressure ; Flushing ; Headache ; Heart Rate ; Hypertension ; Nicardipine*

Nicardipine is a potent coronary and systemic vasodilator without depression of ventricular function. We investigated the changes in local myocardial perfusion (LMP) according to the nicardipine administration after coronary reperfusion in a beating canine model. A Doppler probe was placed around the left anterior descending coronary artery (LAD) and thermal diffusion microprobe was implanted in the myocardium perfused by the exposed LAD. To define the nicardipine effects, we compared the two groups (control group, n=7 vs nicardipine group, n=7). In nicardipine group, 5 microgram/kg/min nicardipine was infused continuously. After the release of the LAD occlusion, LAD blood flow were increased compared to the baseline of both groups. However, there was no difference between groups in the LAD blood flow. The LMP after LAD reperfusion did not recover to the baseline level until 30 min after LAD reperfusion in control group (74%, 52% and 70% at 10, 20 and 30 min after LAD reperfusion, respectively). In nicardipine group, however, the LMP recovered to the baseline level at 20 min (99%), and increased more than the baseline level at 30 min (141%) after LAD reperfusion. Our findings suggest that the nicardipine augments the LMP following the release of a coronary occlusion.
Animals ; Coronary Circulation/drug effects* ; Dogs ; Drug Evaluation, Preclinical ; Myocardial Reperfusion* ; Myocardial Reperfusion Injury/prevention & control* ; Nicardipine/pharmacology* ; Nicardipine/therapeutic use ; Vasodilator Agents/pharmacology* ; Vasodilator Agents/therapeutic use

OBJECTIVE: The purpose of the study is to determine the effectiveness and safety of nicardipine infusion for controlling blood pressure in patients with subarachnoid hemorrhage (SAH). METHODS: We prospectively evaluated 52 patients with SAH and treated with nicardipine infusion for blood pressure control in a 29 months period. The mean blood pressure of pre-injection, bolus injection and continuous injection period were compared. This study evaluated the effectiveness of nicardipine for each Fisher grade, for different dose of continuous nicardipine infusion, and for the subgroups of systolic blood pressure. RESULTS: The blood pressure measurement showed that the mean systolic blood pressure / diastolic blood pressure (SBP/DBP) in continuous injection period (120.9/63.0 mmHg) was significantly lower than pre-injection period (145.6/80.3 mmHg) and bolus injection period (134.2/71.3 mmHg), and these were statistically significant (p < 0.001). In each subgroups of Fisher grade and different dose, SBP/DBP also decreased after the use of nicardipine. These were statistically significant (p < 0.05), but there was no significant difference in effectiveness between subgroups (p > 0.05). Furthermore, controlling blood pressure was more effective when injecting higher dose of nicardipine in higher SBP group rather than injecting lower dose in lower SBP group, and it also was statistically significant (p < 0.05). During the infusion, hypotension and cardiogenic problems were transiently combined in five cases. However, patients recovered without any complications. CONCLUSION: Nicardipine is an effective and safe agent for controlling acutely elevated blood pressure after SAH. A more systemic study with larger patients population will provide significant results and will bring solid evidence on effectiveness of nicardipine in SAH.
Aneurysm ; Blood Pressure ; Humans ; Hypertension ; Hypotension ; Nicardipine ; Prospective Studies ; Subarachnoid Hemorrhage

BACKGROUND: Myocardial calcium overload during reperfusion may contribute to myocardial stunning. The protective effect of nicardipine against post-ischemic myocardial dysfunction was investigated. METHODS: Twenty-two halothane-anesthetized dogs were subjected to 15 minutes of left anterior descending coronary artery (LAD) occlusion and subsequent 3 hour reperfusion. One group of dogs (n=11) received nicardipine (1 microgram/kg/min) and another group (n=11) received saline (0.5 ml/kg/h) through intracoronary catheter for 1 hour beginning 15 minutes before LAD occlusion. Systolic shortening (%SS) and preload recruitable stroke work slope (Mw), as an index of regional myocardial contractility, and IMP-tau (time constant of myocardial relaxation based on intramyocardial pressure (IMP)) and post-systolic shortening (%PSS), as an index of regional diastolic function, were evaluated. LAD blood flow was measured by Doppler flowmeters as well. RESULTS: Regional systolic as well as diastolic functions during acute myocardial ischemia were similar between the two groups. However, Mw recovered to the baseline value with the onset of reperfusion in the nicardipine group but was significantly decreased throughout the reperfusion period in the controls. After 3 hours of reperfusion, the nicardipine group had recovered 67% of %SS, compared with 20% of the control group. IMP-tau was restored to the baseline value by 60 min of reperfusion in the control group but was significantly prolonged in the nicardipine group throughout the reperfusion period. CONCLUSIONS: Intracoronary nicardipine enhances the recovery of regional contractile function but prolongs myocardial relaxation in the canine model of myocardial stunning.
Animals ; Calcium ; Catheters ; Coronary Vessels ; Dogs* ; Flowmeters ; Myocardial Ischemia ; Myocardial Stunning* ; Nicardipine* ; Relaxation ; Reperfusion ; Stroke

The author investigated the cerebral circulatory and metabolic effects of systemic and intracisternal administration of nicardipine in a canine model of chronic cerebral vasospasm. Twenty-one dogs were assigned to one of three groups; control, intravenous nicardipine, and intracisternal nicardipine. All animals received a total of 12 ml of fresh unheparinized autologous blood via three cisternal injections. Sequential measurements of cerebral blood flow(CBF), cerebral metabolic rate of oxygen(CMRO2), and cerebral metabolic rate of glucose(CMRG) were chacked four times in nine days. Animals were sacrificed at Day 9 and amount of clot remained in brainstem and basal cistern was graded accordingly. Significant improvement of cerebral blood flow was noted in Day 6, Day 9 of intracisternal group and in Day 3, Day 6 of intravenous group(each, p<0.05) with slight better results seen in intracisthernal group. Results of sequential changes of CMRO2 and CMRG indicated possible role of nicardipine in protective effects on deleterious neuronal damage following ischemic changes after vasospasm, but definitive statements on this subject matter should be reserved until further study, espedially on morphologic examinations is carried on, Significantly less amount of clot remained in intracisthernal group may be due to effects of nicardipine in its inhibitory action on platelet aggregation, and/or stimulatory effect on prostacyclin production. These factors along with other possible factors should be speculated.
Animals ; Brain Stem ; Calcium* ; Dogs ; Epoprostenol ; Neurons ; Nicardipine ; Platelet Aggregation ; Vasospasm, Intracranial

BACKGROUND: Pneumoperitoneum for a gynecologic laparoscopic surgery induces hemodynamic changes. We evaluated the effects of nicardipine on induction, maintenance, and recovery. METHODS: Thirty patients scheduled for gynecologic laparoscopic surgery were randomly allocated to two groups: control group (placebo group, n = 15), group N (nicardipine group, 10 microgram/kg followed by 0.5-2.0 microgram/kg/min). The systolic arterial pressure, mean arterial pressure, and heart rate were measured at preinduction, induction, intubation and 5, 10, 15, 20 min after insufflation. Loss of consciousness, induction dose, effective site concentration, propofol maintenance dose (the maintenance dose of propofol from intubation to end of anesthesia, PMD) were also measured. Propofol was titrated to maintain a bispectal index value of 40-60. RESULTS: There was a significant difference in PMD between two groups. The PMD of group N was significantaly less than group C. Nicardipine adminstration attenuated increase in the blood pressure, but did not affect on heart rates during CO2 insufflation. CONCLUSIONS: Co-administration of nicardipine was effective in attenuating the hemodynamic changes after pneumoperitoneum during gynecologic laparoscopic surgery, without changes of induction and recovery.
Anesthesia ; Arterial Pressure ; Blood Pressure ; Heart Rate ; Hemodynamics ; Humans ; Insufflation ; Intubation ; Laparoscopy* ; Nicardipine* ; Pneumoperitoneum ; Propofol ; Unconsciousness