The purpose of this study was to assess the iron nutritional status of college women residing in the Kyungin area. The anthropometric parameters, nutrient intake, and biochemical status of iron were measured for 102 college women. The mean height and weight were 160.3 cm and 52.4 kg, respectively. The proportion of subjects whose BMI was less than 20 was 41.3%. The proportion of subjects assessed as overweight(25 or =25%) assessed by the fat percent(FP) was 53.9%. The mean daily intake of iron was 13.90mg(77.1% of RDA), composed of 0.97mg of heme iron and 12.93mg of nonheme iron. the iron intake computed with the chemical analysis of food was 12.44mg(69.0% of RDA). When the sources of iron were grouped as rice(including bread), noodle, soup, side dish, and snack, noodle provided, 3.95mg of iron regarded as the highest amount. Subjects were taking 6.72mg(51.4% of RDA) of iron per day from main dishes(rice, bread and noddle). The fifty percent of the subjects showed iron depletion(serum ferritin<20ng/ml) and 33.4% showed suppressed erythropoiesis with iron deficiency(serum ferritin<10ng/ml). The anemic subjects assessed with transferrin saturation(<155) represented 33.3% of the test population, whereas 11.8% of the subjects possessed less than 12g/dl of hemoglobin. Subjects not satisfed with their body shape were having significantly lower amount of energy intake(p<0.05) than the subjects satisfied with their body shape. College women having mothers who graduated from university had a significantly decreased amount of energy, carbohydrates, fat and vitamin C(p<0.05). The mean RBC and serum iron of the subjects who were on a diet more than one mouth were lower than those of the subjects who were not on a diet(p<0.05).
Bread ; Carbohydrates ; Diet ; Erythropoiesis ; Female* ; Heme ; Humans ; Iron* ; Mothers ; Mouth ; Nutritional Status* ; Overweight ; Prevalence ; Snacks ; Transferrin ; Vitamins

Randomly selected 193 patients who received elective operation under general anesthesia and were able to communicate with anesthesiologists and follow up for 5 days between May and September 1994 at Chonnam University Hospital, were interviewed and evaluated on the night before, 2 and 5 days after their operation. Distribution of physieal status by ASA was that more than half the total patients belongs to class I and 36.8% of patients were under class II. Sedation scores did not chang between on the night before and the day of operation. A significant correlation existed among the visibility of pharyngeal structures, the exposure of glottis by laryngoscopy, and the degree of difficulty with intubation. About 83% of patients was readily intubated, and none of patient was impossible to intubate. All of the patients lost consciousness during induction of anesthesia, and did not recall during operation. Postanesthetic complications were sore throat(30%), nausea and vomiting(28%), lumbago(15%), urticaria(3%), and dizziness(3%).
Anesthesia ; Anesthesia, General ; Consciousness ; Follow-Up Studies ; Glottis ; Humans ; Incidence* ; Intraoperative Awareness* ; Intubation* ; Jeollanam-do ; Laryngoscopy ; Nausea

Intravenous lidocaine has been used for attenuating cardiovascular responses to endotracheal intubation. To determine the optimal time of administration of lidocaine for attenuating hemodynamic changes induced by intubation, 100 patients were allocated randomly to a control group (without lidocaine) or four treated groups (with lidocaine). Lidocaine 1.5 mg/kg was administered intravenously at 60 (Group 2), 90 (Group 3), 120 (Group 4) and 180 seconds (Group 5) before intubation. Arterial pressure (systolic, mean and diastolic), heart rate and rate-pressure product (RPP) were measured before induction, after lidocaine injection, immediatly before intubation, immediately and 5 minutes after intubation. After intubation, arterial pressure, heart rate and RPP increased significantly in every study groups. In group 2 and 3, however, such changes were attenuated significantly, Postintubation elevation of systolic blood pressure, mean arterial pressure and RPP were effectively prevented in group 2 and 3. Lidocaine effect on diastolic pressure was observed only in group 3. Changes of heart rate were not affected with lidocaine adminiistration. In Group 4 and Group 5, this effect was not observed. In diastolic pressure, suppressive effect of lidocaine in increasing of blood pressure and RPP was observed in Group 3 significantly, but not in Group 2, Group 3 and Group 5. Changes of heart rate show that in all groups injected lidocaine (Group 2,3,4,5) significantly suppressive effect was not observed as compared with control group. These results suggest that intravenous lidocaine (1.5 mg/kg), 60-90 second prior to intubation attenuate hemodynamic responses induced by intubation.
Arterial Pressure ; Blood Pressure ; Heart Rate ; Hemodynamics ; Humans ; Intubation ; Intubation, Intratracheal* ; Lidocaine*

Ketamine, a dissociative anesthetic, produces an increase in heart rate and blood pressure, but the precise mechanism of the cardiovascular stimulating affects of ketamine is not understood clearly. Clonidine, an antihypertensive agent, is an alpha-2 agonist that appears to act primarily on the CNS, where it apparently produces a decrease in the sympathetic outflow from the brain. Prazosin is antihypertensive agent that appears to evert its vasodilator action through the blockade of postsynaptic alpha-1 receptors. In order to investigate the effects of clonidine and prazosin on the heart rate and blood pressure increased by ketamine, ketamine was administered intravenously following administration of clonidine or prazosin in conscious patients. The results were as follows : 1) Intravenous ketamine (2 mg/kg) produced significant increases in heart rate and blood pressure by as much as 25%. 2) Intravenous clonidine (1.25 ug/kg) produced a decrease in the heart rate by 5 beats per minute and decreased blood pressure significantly. 3) In the clonidine pretreated group (1.25 ug/kg, lV), intravenous ketamine (2 mg/kg/kg, lV) produced significant increases in the heart rate and blood pressure without attenuation with clonidine 4) In the prasosin pretreated group (2 mg/kg~70 kg, PO), ketamine (2 mg/kg, lV) produced increases the in heart rate and blood pressure without attenuation with prasosin. From the above results, it was inferred that the action site of the cardiovascular stimulating effect of ketamine isn't a postsynaptic alpha-1 receptor and is different from the action site of clonidine.
Blood Pressure* ; Brain ; Clonidine* ; Heart Rate* ; Heart* ; Humans ; Ketamine* ; Prazosin*

It is well known that ketamine produces an increase in the heart rate and blood pressure. Lidocaine has a direct myocardial depressant effect with indirect stimulant effects mediated by the autonomic nervous system, and propranolol, beta-adrenergic receptor blockade, has negative chronotropic effects through the beta-adrenergic blockade. In order to investigate the effect of propranolol and lidocaine on the heart rate and blood pressure increased by ketamine, lidocaine, and/or propranolol were administered intravenously in awake patients. The results were as follows. 1) In ketamine(2 mg/kg) receiving group, the heart rate increased 16-19 beats per minute and systolic, diastolic and the mean blood pressure increased significantly. 2) In ketamine(2 mg/kg)-lidocaine(2 mg/kg) receiving group, the heart rate increased l2-14 beats per minute, and the systolic, diastolic and mean blood pressure increased significantly. 3) In ketamine(2 mg/kg)-propranolol(0.02 mg/kg) receiving group, the heart rate increased below 5 beats per minute and systolic, diastolic, and the mean blood pressure increased significantly. 4) In ketamine(2 mg/kg)-propranolol(0.02 mg/kg)-lidocaine(2 mg/kg) receiving group, the heart rate increased only 3-4 beats per minute and systolic, diastolic, and mean pressures increased significantly. From the above results, the chronotropic effect of ketamine was markedly attenuated by propranolol or propranolol-lidocaine but not attenuated by lidocaine, and the pressor effect was not attenuated by lidocaine, or propranolol and propranolol with lidocaine.
Autonomic Nervous System ; Blood Pressure* ; Heart Rate* ; Heart* ; Humans ; Ketamine* ; Lidocaine* ; Propranolol*

BACKGROUND: Lidocaine or verapamil are used as an antiarrhythmic agent or agent blunting the cardiovascular changes induced by intubation or extubation during anesthesia. After recovery from general anesthesia with muscle relaxants, most patients remained in a residual paralytic state, hence it might develop easily recurarization by factors that affect neuromuscular transmission. Lidocaine and verapamil are well known as agents to potentiate the neuromuscular block. We investigated the effects of lidocaine or verapamil on neuromuscular transmission in vitro. METHODS: Square wave, 0.2 ms duration at a frequency of 0.1 Hz supramaximal or train of four stimuli was applied and the twitch height response was recorded mechanomyographically on rat phrenic nerve hemidiaphragm preparations. Dose responses of rocuronium, lidocaine, verapamil, rocuronium pretreated with lidocaine or verapamil, lidocaine pretreated with rocuronium, and verapamil pretreated with rocuronium were observed by cumulative method, and effective doses (Lag dose, ED50 and ED95) between a pretreated and nonpretreated agent were compared statistically. TOF ratios were observed at 80, 70, 40 and 30% of the control twitch height value during the observation of dose responses. RESULTS: Lag dose, ED50 and ED95 of rocuronium were reduced significantly after pretreatment of lidocaine, verapamil or their mixture, and the dose response of lidocaine, verapamil or their mixture were also reduced significantly by rocuronium pretreatment. TOF ratios at the point of each twitch height decreased significantly after pretreatment. CONCLUSIONS: Lidocaine or verapamil itself did not affect the neuromuscular transmission but might have potentiated the neuromuscular blocking effect induced by rocuronium. However, in excessive doses, these agents produced neuromuscular blockade. Consequently, in the residual neuromuscular block induced by rocuronium, lidocaine or verapamil may enhance recurarization.
Anesthesia ; Anesthesia, General ; Animals ; Humans ; Intubation ; Lidocaine* ; Neuromuscular Blockade* ; Phrenic Nerve ; Rats ; Verapamil*

It is well known that small dose of belladonna alkaloid(atropine, scopolarnine) has the effect of decreasing the heart rate in normal conscious subjects, but the mechanism involved in it remains still unanswered. Based on various lines of evidence, the most likely mechanism seems to be the blockade of sympathetic ganglion caused by the alkaloids and it is possible that the effect on the slower heart rate may differ in the depressed state of the sympathetic ganglion when under halothane anesthesia. The present study was undertaken, therefore, on comatose patients and halothane anesthetized patients with and without atropine premedication about 1 hour before anesthesia to observe the effect of a small dose of scopolamine(0.1 mg) which affects the heart rate more significantly than atropine in conscious subjects. The results were as follows: 1) In the comatose patients, scopolamine(0.1 mg) produced a significant decrease in heart rate. 2) During halothane anesthesia without atropine premedication, scopolamine produced a slight decrease in heart rate. 3) During halothane anesthesia with atropine premedication, scopolamine produced a significant increase in the heart rate. These results indicate that scopolamine can further affect the sympathetic ganglion already depressed by halothane, and it is suggested that scopolamine is more effective in blocking the sympathetic ganglion than halothane.
Alkaloids ; Anesthesia ; Atropa belladonna ; Atropine ; Coma ; Ganglia, Sympathetic ; Halothane* ; Heart Rate* ; Heart* ; Humans ; Premedication ; Scopolamine Hydrobromide*

Supplementation of antihypertensive action of sodium nitroprusside (SNP) is almost standard practice and should obviate the need for potentially toxic doses to control blood pressure. Clonidine, an antihypertensive agent known to reduce sympathetic outfiow via alpha2-adrenergic receptor stimulation, has been shown to decrease MAC of halogenated agent, and to reduce the amount of SNP required to reduce the desired hypotension. To determine the effects of clonidine on the hemodynamics and intrapulmonary shunting during SNP infusion, clonidine and/or SNP were administered to 22 patients anesthetized with halothane-N2, O-O2 (FIO2:0.5) In one group of 11 patients, clonidine 1.5ug/kg was injected intravenously. In another group of 11 patients, clonidine 1.5 ug/kg was injected intravenously 30 minutes after starting the SNP infusion (3 ug/kg/min). The results were as follows. 1) Clonidine alone produced a small decrease in MAP (10%) and CI (8%) but other hemodynamic values remained unaltered. 2) Arterial oxygen tension and intrapulmonary shunting was not changed by clonidine. 3) Heart rate (15%) was increased , but MAP (29%), MPAP (24%), PCWP (25%), CVP (32% ), SVR (29%)and PVR(24%) were decreased significantly, and CI, SVI remained unchanged during SNP hypotension. 4) SNP caused a significant increase in intrapulmonary shunt fraction from 8.62% to 10.58% and a decrease in PaO2. 5) In group of clonidine under SNP infusion, conidine did not significantly affect the hemodynamic response to SNP except for 15% decrease in BP. 6) Clonidine caused no significant change on gas exchange effect of SNP. These results indicate that clonidine did not significantly affect the hemodynamics and intrapul-monary shunting during SNP hypotension. Therefore, clonidine could be used as a valuable adjuvant for reducing the amount of SNP and decreasing MAC of halothane.
Anesthesia* ; Blood Pressure ; Clonidine* ; Halothane ; Heart Rate ; Hemodynamics* ; Humans ; Hypotension* ; Nitroprusside* ; Oxygen ; Sodium*

This study investigated the comparison of electromyographic change of neuromuscular blocking effect induced vecuronium between the ulnar, facial and tibial nerve in 24 healthy adult patients anesthetized with thiopental, N2O and enflurane. Neuromuscular monitoring commenced immediately after administration of thiopental. After supramaximal stimulation was achieved, a bolus of vecuronlum 0.08mg/kg was injected intravenously. And then single twitch nerve stimulation(T1) was applied to the nerves using surface electrodes and the electrical response of muscles recorded using the RELAXOGRAPH(Dates Co.). The patients were allocated randomly to 3 groups of 8 patients respectively: the ulnar nerve troup was the control, and the facial nerve group and the tibial nerve group were the studing group. We assessed electromyographic responses from abductor digiti minimi muscle in the ulnar nerve, orbicularis oris muscle in the facial nerve and flexor hallucis brevis muscle in the tibial nerve to single twitch nerve stimulation respectively. And the onset time, the time from injection of vecuronium to 25% and 75% recovery to T1, and recovery index of the ulnar, facial and tibial nerve groups were measured. The obtained results were as follos: 1) The onset time was faster in the facial nerve group compared with the ulnar nerve group. 2) The time from injection of vecuronium to 25% recovery of T1 was more prolonged in the facial nerve group compared with the ulnar nerve group. 3) The time from injection of vecuronium to 75% recovery of T1 and recovery index were more shorter in the tibial nerve group compared with ulnar nerve group.
Adult ; Electrodes ; Enflurane ; Facial Nerve ; Humans ; Muscles ; Neuromuscular Blockade ; Neuromuscular Monitoring ; Thiopental ; Tibial Nerve* ; Ulnar Nerve ; Vecuronium Bromide*

To investigate the effects of ketamine on the hemodynamics decreased by fentanyl-diazepam, twenty-five patients were randomly assigned to three groups. In all patients fentanyl (10 ug/kg) diazepam (0.2 mg/kg) was intravenously administered, and then patients in group 1 recevied saline only, group 2 and group 3 recevied 1 and 2 mg/kg of ketamine, respectively. Hemodynamic parameters were obtained before and 5 minutes after durg in each group. In group 1, fentanyl-diazepam produced a decrease in heart rate (HR:17%), mean arterial pressure (MAP:27%), cardiac index (CI:40%) and sroke volume index (SVI:14%), and a increase in mean pulmonary arterial pressure (MPAP:27%) and pulmonary capillary wedge preasure (PCWP;25%), but no significant change in central venous pressure (CVP) and systemic vascular resistance index (SVRI). Patients in group 2 had decreases in HR(16%), MAP(10%), CI(10%) and SVI(16%), and decrease in MPAP(21%), PAWP(21%), PCWP(26%), CVP(58%) and SVRI(24%), but theae hemodynamic changes were no significant difference compared to those of group 1 except a bit increase in CVP and SVRI. In group 3, HR(11%), MAP(11%), CI(23%), and SVI(13%) were decreased, but MPAP(14%), PCWP(14%), CVP(69%) and SVRI(26%) were increased and these values were no difference compared to those of group 2. These results demonstrated that ketamine did not significantly affect the hemodynamics decreased by fentanyl-diazepam except CVP and SVRI were increased by ketamine. Base on this study, the author suggeeted that the mechanism of cardiovascular depression caused by diazepam-fentanyl might to be the result of myocardial depression, ketamine produced its sympathomimetic actions primarily by direct stimulation of central nervous system, and ketamine might to be unuseful to improve the hemodynamics to patients with cardiovaseulsr depreseion caused by fentanyl-diazepam.
Arterial Pressure ; Capillaries ; Central Nervous System ; Central Venous Pressure ; Depression ; Diazepam ; Fentanyl* ; Heart Rate ; Hemodynamics* ; Humans ; Ketamine* ; Vascular Resistance