1.Effect of tolazoline on persistent hypoxemia in severe hyaline membrane disease.
Kook In PARK ; Ran NAMGUNG ; Chul LEE ; Dong Gwan HAN
Yonsei Medical Journal 1990;31(2):156-162
Ten critically-ill preterm infants with severe hyaline membrane disease received tolazoline because of persistent hypoxemia refractory to the administration of 100% oxygen and mechanical ventilation. Seven infants (70%) responded immediately with an increase in PaO2 greater than or equal to 20 mmHg in the umbilical arterial gas within 60 minutes after bolus infusion (1 to 2 mg/kg) of tolazoline. Twenty-four hours later after the tolazoline infusion, the FiO2 had been decreased from 1.0 to a mean of 0.82 +/- 0.16, and the MAP from 16.5 +/- 1.8 to 15.6 +/- 4.5 cm H2O. Four of 7 infants (57%) who had an immediate response survived, whereas none survived out of 3 infants who failed to respond initially. Three infants experienced relatively severe complications possibly related to tolazoline. There appears to be a place for the use of tolazoline in a severely hypoxemic infant with hyaline membrane disease who is being ventilated, and in whom arterial oxygenation cannot be improved by a further increase in the inspired oxygen concentration or by an alteration of ventilator settings.
Anoxemia/*drug therapy
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Human
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Hyaline Membrane Disease/*complications
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Infant
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Infant, Newborn
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Infusions, Intravenous
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Support, Non-U.S. Gov't
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Tolazoline/administration & dosage/*therapeutic use
2.Nitroglycerin Treatment in Persistent Pulmonary Hypertension of the Newborn.
Ji Sook KIM ; Sung Sook JEON ; Son Sang SEO
Journal of the Korean Pediatric Society 1997;40(11):1529-1536
PURPOSE: Persistent pulmonary hypertension (PPHN) of the newborn has been treated with some vasodilators including tolazoline. But these drugs have many side effects, especially systemic hypotension . To investigate the usefulness of the nitroglycerin as a specific vasodilator with few side effects, this study was done. METHODS: Nitroglycerin was administered within 1st one day after birth in 8 newborn infants who were diagnosed as PPHN by echocardiography. They were born at Il Sin hospital from March 1994 to March 1996. Nitroglycerin was started as 2microgram/kg/min and its maximum dose was 6microgram/kg/min. Muscle relaxants and inotropic drugs were used together in all cases. Arterial blood gas analysis, systemic blood pressure, heart rate, renal function and electrolyte were checked in all patients. Alveolar-arterial oxygen difference (AaDO2) and oxygenation index (OI) were measured. RESULTS: 6 cases (75%) survived but 2 cases expired due to air leak.1) Basal mean AaDO2 was 631.4+/-21.7mmHg. It decreased to 493.9+/-1453.1 mmHg at 10hr after loading infusion and to 373.6+/-217.7mmHg at 48hr (P<0.05). 2) Basal mean OI was 35.1+/-15.7 and it decreased significantly to 12.6+/-14.8 (P<0.05) at 10hr. 3) There was no significant hypotension in systolic, diastolic and mean blood pressure during treatment of nitroglycerin. 4) There was no significant change in renal function, serum electrolyte and heart rate during treatment of nitroglycerin. CONCLUSIONS: Nitroglycerin produced systemic venodilatation and pulmonary arterial dilatation at the dose that produce only minimal systemic arterial dilatation. Nitroglycerin is an effective and safe drug in the treatment of PPHN.
Blood Gas Analysis
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Blood Pressure
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Dilatation
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Echocardiography
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Heart Rate
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Humans
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Hypertension, Pulmonary*
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Hypotension
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Infant, Newborn*
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Nitroglycerin*
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Oxygen
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Parturition
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Tolazoline
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Vasodilator Agents
3.Pathologic Changes of Peripheral Pulmonary Arteries in Ventricular Septal Defect with Pulmonary Hypertension.
Sung Kyu LEE ; Chang Ho HONG ; Jun Hee SUL ; Dong Shik CHIN ; Duk Jin YUN ; Chan Il PARK ; Bum Koo CHO
Korean Circulation Journal 1983;13(2):343-348
Twelve patients with ventricular septal defect with pulmonary hypertension underwent lung biopsy to assess pulmonary obstructive vascular disease at the time of open heart surgery. According to the Heath and Edwards classification in grading of Pulmonary obstructive vasculr disease, there are eleven cases in grade 1 and one case in grade 3. Thickness of media was measured. It was expressed as percentage of medial thickness to outer diameter of artery. The medial thickness was correlated proportionally with elevation of pulmonary arterial pressure and pulmonary vascular resistance to systemic resistance ratio. In tolazoline test performed in 4 cases, one patients who had pulmonary obstructive vascular disease, had no change of pulmonary vascular resistance to systemic vascular resistance after intravenous injection of tolazoline during cardiac catheterization, but Rp/Rs of three cases was decreased significantly.
Arterial Pressure
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Arteries
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Biopsy
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Cardiac Catheterization
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Cardiac Catheters
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Classification
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Heart Septal Defects, Ventricular*
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Humans
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Hypertension, Pulmonary*
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Injections, Intravenous
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Lung
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Pulmonary Artery*
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Thoracic Surgery
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Tolazoline
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Vascular Diseases
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Vascular Resistance
4.Effects of Central Dopaminergic Receptor-Activation on the Cardiovascular System.
Seung Min KIM ; Young Kwan PARK ; Sung Soo LEE ; Chang Mann KO
Journal of the Korean Neurological Association 1992;10(3):308-315
The central dopaminergic receptor is believed to suppress the cardiovascular system So it may be involved in the blood pressure regulation But, it's action is still controversial. Furthermore, the mechanisms involved in the central dopaminergic receptor-induced blood pressure regulation is unclear. So, present study was performed in order to clarify the effects of central dopaminergic receptor and to investigate the mechamisms involved in it. Lisuride a D2-receptor agonist, and clonidine, a alpha2-receptor agonist, were administered into lateral ventricle in rat and the changes of blood pressure were compared The results were as follows; 1. Intracerebroventricular administration of lisuride amd clonidine from 0.3 ug to 10 ug elicited dose related decrease of blood pressure and heart rate. The potencies were similar in both drugs. 2. Centrally administered sulpiride, a D2-antagonist, blocked only the lisuride-induced hypotension while the clonidine induced hypotension was blocked only by centrally adrninistered tolazoline, a alpha2-antagonist. Intravenous administration of both antagonists elicited no or minimal attenuabon of agonists effects. 3. After desipramine pretreatment, which increases the norepinephrine concentration lisuride elicited somewhat further decrease of blood pressure than normal, while clonidine administration caused rather increase in blood pressure. 4. After chemical sympathectomy by 6-hydroxydopamine, lisuride administration still elicited strong suppression of blood pressure. From thses above results, it is concluded that central dopaminergic receptor activation decrease the blood pressure. Suppression of the norepinephrine release at the sympathetic nerve terminal is not related with central dopaminergic receptor induced hypotension.
Administration, Intravenous
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Animals
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Blood Pressure
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Cardiovascular System*
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Clonidine
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Desipramine
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Heart Rate
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Hypotension
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Lateral Ventricles
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Lisuride
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Norepinephrine
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Oxidopamine
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Rats
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Sulpiride
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Sympathectomy, Chemical
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Tolazoline