The catecholamine content was examined in the myocardium of dogs subjected to hemorrhagic hypotension of 40mmHg for a duration of one to hive hours respectively. No marked changes were noticed within two hours after production of homorrhagic hypotension but a significant reduction was found at the end of three hours of hypotension. The reduction of myocardial catecholamines was progressively pronounced with the prolonging the hypotensive period over three hours. Dogs were bled rapidly to an arterial blood pressure of 40mmHg and maintained at this hypotensive level for four hours, followed by reinfusion of the withdrawn blood. Eight out of 11 dogs succumbed within l2 hours, showing a 73 per cent mortality. The myocardial catecholamines in the surviving dogs returned almost to the normal level within 12-15 hours after the blood reinfusion, while those in the dogs which succumbed showed the same low level which was produced during hemorrhagic hypotension. It was also shown that the reduced myocardial catecholamines resulting from the hypotension will not be restored immediately after the reinfusion of the withdrawn blood. When norepinephrine was infused at a rate of five to seven microgram/kg/min for an hour before the reinfusion of the withdrawn blood, five out of six dogs died within 12 hours, showing a 82 per cent mortality. This result appears to indicate that norepinephrine infusion during oligemic hypotension may hasten death or not decrease the mortality of the animals. On the other hand, when norepinephrine was infused at a rate of three microgramkg/min for an hour following reinfusion of the withdrawn blood five out of 15 dogs died, indicating a significant increase of survival rate from hemorrhagic shock. The myocardial catecholamines of surviving dogs and dogs which succumbed following the administration of norepinephrine after blood reinfusion were similar respectively to those of dogs which survived and of dogs which died after blood reinfusion without norepinephrine. When norepinephrine (3 microgramkg/min) was infused for hour following blood reinfusion in the dogs pretreated with either dibenzyline (3mg/kg) or dichloroisoproterenol (1mg/kg), the beneficial effect of norepinephrine on the survival rate from hemorrhagic shock appeared to be absent. The efficacy of norepinephrine on the survival from hemorrhagic shock was discussed on the basis of myocardial catecholamine depletion.
Animals ; Catecholamines/*metabolism ; Dogs ; Epiphyses/*embryology ; Myocardium/*metabolism ; Norepinephrine/*pharmacology ; Shock, Hemorrhagic/*drug therapy

Hypercholesteremia was induced by cholesterol feeding of rabbits for 10 weeks. Gross examination of aorta of these animals showed an evidence of atheromatous lesions. The endogenous catecholamines in heart, adrenal gland, spleen, brain, liver and kidney of these hypercholesteremic rabbits were markedly reduced as compared to those of normal animals, respectively. There may exist some correleration between the serum cholesterol and tissue catecholamines.
Animal ; Arteriosclerosis/etiology* ; Arteriosclerosis/metabolism ; Carbon Isotopes ; Catecholamines/metabolism* ; Cholesterol/blood* ; Female ; Rabbits

The influence of thyroxine upon n the cardiac uptake of catecholamines was investigated in rabbits. A single injection of thyroxine(1.0m/kg) into rabbits did not affect the concentration of myocardial catecholamines. However, this dose of thyroxine greatly increased the cardiac uptake of catecholamine following injection of 2.0mg of norepinephrine as compared to that of untreated normal animals and it remained elevated for several hours. Similarly thyroxine also enhanced the accumulation of myocardial catecholamines following administration of dopa(60-80mg/kg) and epinephrine(1.0-1.5mg/kg).
Animal ; Catecholamines/metabolism* ; Epinephrine/metabolism ; Heart/drug effects* ; Male ; Myocardium/metabolism* ; Norepinephrine/metabolism ; Rabbits ; Thyroxine/pharmacology* ; Tritium

Catecholaminergic polymorphic ventricular tachycardia (CPVT) is a familial cardiac arrhythmia that is related to RYR2 or CASQ2 gene mutation. It occurs in patients with structurally normal heart and causes exercise-emotion-triggered syncope and sudden cardiac death. We experienced a case of CPVT in an 11 year-old female patient who was admitted for sudden cardiovascular collapse. The initial electrocardiogram (ECG) on emergency department revealed ventricular fibrillation. After multiple defibrillations, sinus rhythm was restored. However, recurrent ventricular fibrillation occurred during insertion of nasogastric tube without sedation in coronary care unit. On ECG monitoring, bidirectional ventricular tachycardia occurred with sinus tachycardia and then degenerated into ventricular fibrillation. To our knowledge, there has been no previous case report of CPVT triggered by sinus tachycardia in Korea. Therefore, we report the case as well as a review of the literature.
Catecholamines/*metabolism ; Child ; Electrocardiography ; Female ; Humans ; Tachycardia, Ventricular/*diagnosis/genetics/pathology

Adolescent ; Catecholamines ; secretion ; Female ; Humans ; Lung Neoplasms ; diagnosis ; metabolism ; Paraganglioma, Extra-Adrenal ; diagnosis ; metabolism ; Stomach Neoplasms ; diagnosis ; metabolism

The data obtained from present experiments demonstrated that among several inhalation anesthetics, ether was the most irritable, resulting in marked irregularity of respiratory movement, and halothane depressed respiratory rate more than the other. The pulse rate and blood pressure were decreased marked1y in ether and the halothane anesthesia. the rate of beat of the isolated atria was not greately altered after anesthesia with ether or trichlore-thylene, while it was reduced after chloroform or halothane inhalation. The response of isolated atria to exogeneous norepinephrine was most prominent in the atria isolated from halothane anesthetized rabbits. Myocardial catecholamine contents were reduced uniformly after anesthesia with each anesthetics and most significantly with the halothane inhalation. From the above results, it may be concluded that the increasing cardiac activity with general inhalation anesthetics is closely related to the quantitative changes of the endogenous myocardial catecholamine contents.
Anesthesia, Inhalation/adverse effects ; Anesthetics/*toxicity ; Animals ; Catecholamines/*metabolism ; Heart/*drug effects ; Myocardium/*metabolism ; Norepinephrine/*pharmacology ; Rabbits

We investigated the effect of phenylephrine (PE)- and isoproterenol (ISO)-induced cardiac hypertrophy on subcellular localization and expression of caveolin-3 and STAT3 in H9c2 cardiomyoblast cells. Caveolin-3 localization to plasma membrane was attenuated and localization of caveolin-3 to caveolae in the plasma membrane was 24.3% reduced by the catecholamine-induced hypertrophy. STAT3 and phospho-STAT3 were up-regulated but verapamil and cyclosporin A synergistically decreased the STAT3 and phospho-STAT3 levels in PE- and ISO-induced hypertrophic cells. Both expression and activation of STAT3 were increased in the nucleus by the hypertrophy. Immunofluorescence analysis revealed that the catecholamine-induced hypertrophy promoted nuclear localization of pY705-STAT3. Of interest, phosphorylation of pS727-STAT3 in mitochondria was significantly reduced by catecholamine-induced hypertrophy. In addition, mitochondrial complexes II and III were greatly down-regulated in the hypertrophic cells. Our data suggest that the alterations in nuclear and mitochondrial activation of STAT3 and caveolae localization of caveolin-3 are related to the development of the catecholamine-induced cardiac hypertrophy.
Animals ; Catecholamines/*pharmacology ; Caveolae/*metabolism ; Caveolin 3/*metabolism ; Cell Line ; Hypertrophy/metabolism ; Mitochondria/*metabolism ; Myocardium/cytology/*pathology ; Myocytes, Cardiac/cytology/*drug effects/metabolism ; Rats ; STAT3 Transcription Factor/*metabolism

OBJECTIVETo investigate the effects of catecholamine hormone on the blood and brain of heroin addicts.

METHODSRats were divided into three groups and treated with the glucose (control group), the heroin (im) (heroin group), and the combination of the intramuscular injection of reserpine and heroin (reserpine group). Changes in the levels of the dopamine (DA), cAMP, and cGMP were detected by the radioimmunoassay (RIA) method in the blood and brain tissue.

RESULTSNo significant withdrawal symptoms were observed in the reserpine group. Compared with the control and heroin groups, the blood cAMP levels were increased by 35.36% and 15.53% in the reserpine group, respectively; the cAMP levels in the midbrain ventral tegmental area (VTA), prefrontal cortex (PFC), and hippocampus (Hipp) were increased by 24.08% & 8.53%, 15.66% & 8.13%, and 21.95% & 8.40%, respectively. While compared to the control and heroin groups, the DA levels of the PFC, Hipp, striatum, and nucleus accumbens (NAc) were significantly reduced in the reserpine group, decreasing by 74.09% & 82.86%, 81.06% & 82.23%, 91.62% & 86.55% and 84.35% & 90.63%, respectively. The concentrations of cGMP of the brain tissues in the reserpine group were lower than those in the control group. In addition, the neural electrophysiological testing showed that the electroencephalogram (EEG), electrocardiogram (ECG), and muscle spindle discharge diagram of rats in both the reserpine and heroin groups were apparently changed.

CONCLUSIONCatecholamine hormone plays an important role in heroin addiction.

Animals ; Brain ; drug effects ; metabolism ; Catecholamines ; physiology ; Cyclic AMP ; blood ; metabolism ; Cyclic GMP ; blood ; metabolism ; Dopamine ; blood ; metabolism ; Heroin Dependence ; metabolism ; physiopathology ; Male ; Rats ; Rats, Wistar

Catecholamines ; blood ; cerebrospinal fluid ; metabolism ; Child ; Humans ; Neuropeptides ; blood ; cerebrospinal fluid ; metabolism ; Neurotransmitter Agents ; blood ; cerebrospinal fluid ; metabolism ; Syncope, Vasovagal ; blood ; cerebrospinal fluid ; metabolism ; physiopathology

The present study was designed to examine the possible relationship between the function of the labyrinth and the role of the sympathetic nervous system In experimental motion sickness produced by rotatory movement(8O r.p.m.). The catecholamines in the brain, the heart and the adrenal gland of rats were rapidly reduced to one half of normal values following exposure to rotatory movement. The pretreatment with streptomycin and dramamine completely prevented the depletion by the rotatory movement of the catecholamines in the brain, the heart and the adrenal gland, but scopolamine did not prevent the decrease. Bretylium or chlorpromazine signifcantly inhibited reduction of the catechol-amines in both of the brain and the heart. However they did not influence the decrease in the adrenal gland. The reduction of the tissue catecholamines in rotatory movement is presumed to be caused largely by activation of the sympathetic nervous system mediated through labyrinthine stimulation.
Animals ; Catecholamines/*metabolism ; Labyrinth/*physiopathology ; Male ; Motion Sickness/*etiology ; Rats ; *Rotation ; Sympathetic Nervous System/*physiopathology ; OID - NASA: 70030571