Biomedical subjects

J Lavicky

Publications and source records attributed to J Lavicky.

5 recordsLinked to original sources

PubMed1995

Endotoxin administration stimulates cerebral catecholamine release in freely moving rats as assessed by microdialysis.

In vivo microdialysis was used to measure changes in extracellular concentrations of catecholamines and indolamines in freely moving rats in response to administration of endotoxin (lipopolysaccharide, LPS). Dialysis probes were placed stereotaxically in either the medial hypothalamus or the medial prefrontal cortex. We used a repeated-measures design in which each rat received LPS or saline, and each subject was retested with the other treatment one week later. With the dialysis probes in the medial hypothalamus, intraperitoneal (ip) administration of LPS (5 micrograms) increased dialysate concentrations of norepinephrine (NE, 187%), dopamine (DA, 119%), and all their measured catabolites, except normetanephrine. Dialysate concentrations of NE and DA were elevated significantly in the fourth or fifth (20 min) collection period with a peak response at around 2 hr. They returned to baseline by about 4 hr. When the dialysis probes were placed in the medial prefrontal cortex, the same dose of LPS also elevated dialysate concentrations of NE and DA, but the increases were much smaller (ca. 20%). However, a dose of 100 micrograms LPS increased dialysate concentrations of NE and DA from the medial prefrontal cortex to an extent comparable to that of the 5 micrograms dose in the hypothalamus, and the response was more prolonged. Dialysate concentrations of serotonin could not be measured reliably, but those of its catabolite, 5-hydroxyindoleacetic acid (5-HIAA), were also elevated in both regions. The peak of 5-HIAA occurred at around 4 hr. Pretreatment of the rats with indomethacin (10 mg/kg ip) completely prevented the changes due to 100 micrograms LPS in the medial prefrontal cortex.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Changes in cardiac beta-adrenoceptors in human heart diseases: relationship to the degree of heart failure and further evidence for etiology-related regulation of beta 1 and beta 2 subtypes.

Radioligand binding studies were performed to investigate total beta-adrenoceptor density (Bmax) and beta 1 and beta 2 subtype distribution in left ventricular biopsies obtained from 8 prospective transplant donors serving as controls and from 143 patients with different degrees of heart failure (NYHA class II to IV) undergoing aortic or mitral valve surgery due to aortic or mitral stenosis, aortic or mitral regurgitation, as well as combined aortic or mitral valve lesions (stenosis and regurgitation). In 13 other patients, heart failure was due to hypertrophic obstructive cardiomyopathy (N = 6, NYHA III), tetralogy of Fallot (N = 4, NYHA III), or Becker's muscular dystrophy (N = 3, NYHA IV). Bmax was assessed by (-)-(125I)-iodocyanopindolol used as radioligand. Competition experiments with the highly selective beta 1-adrenoceptor antagonist CGP 20712A were performed for determination of beta 1- and beta 2-adrenoceptor subtypes. In biopsies taken from transplant donors, the Bmax was found to be 70.1 +/- 5.8 fmol/mg protein. In all groups investigated the extent of total beta-adrenoceptor downregulation was related to the degree of heart failure. The decrease in Bmax was found to be about 20% (NYHA II), 45% (NYHA III), and 60% (NYHA IV) when compared with controls. There was no significant difference in the reduction of total beta-adrenoceptor density between isolated aortic or mitral valve diseases and combined valve lesions. Independent of the degree of heart failure, selective downregulation of the beta 1 subtype was found in patients with isolated or combined aortic valve diseases, hypertrophic obstructive cardiomyopathy, and Becker's muscular dystrophy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1993

Corticotropin-releasing factor stimulates catecholamine release in hypothalamus and prefrontal cortex in freely moving rats as assessed by microdialysis.

In vivo microdialysis was used to measure changes in extracellular concentrations of catecholamines and indoleamines in freely moving rats in response to administration of corticotropin-releasing factor (CRF). Dialysis probes were placed stereotaxically in either the medial hypothalamus or the medial prefrontal cortex. We used a repeated-measures design in which each rat received artificial CSF or one dose of CRF 3-4 h apart, and each subject was retested with the same treatments in the reverse order 5-7 days later. With the dialysis probe in the hypothalamus, intracerebroventricular administration of CRF (17 or 330 pmol) dose-dependently increased dialysate concentrations of norepinephrine (NE), dopamine (DA), and all their measurable catabolites except normetanephrine. The effects on NE were substantially greater than those on DA. Dialysate concentrations of serotonin could not be measured reliably, but those of its catabolite, 5-hydroxyindoleacetic acid, were also elevated. Concentrations of NE and DA were elevated within the first one or two (20 min) collection periods, with a peak response at approximately 1-2 h. Dialysate concentrations of catecholamines and metabolites normally returned to baseline within 3 h. Similar data were obtained with dialysis probes in the medial prefrontal cortex after intracerebroventricular administration of 17 or 167 pmol of CRF, except that the increases in DA exceeded those of NE in this region. Intraperitoneal administration of CRF (1 nmol) similarly elevated dialysate concentrations of NE, DA, 5-hydroxyindoleacetic acid, and all catecholamine catabolites except normetanephrine in both medial hypothalamus and medial prefrontal cortex. These results support earlier neurochemical data suggesting that CRF administered both centrally and peripherally stimulates the release of both DA and NE in the brain.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1992

Apparent inter-channel interference in dual-electrode electrochemical detection.

During the course of routine high-performance liquid chromatographic analyses of brain catecholamines using dual-electrode electrochemical detection, we encountered an unusual negative peak in the lower-voltage channel. Subsequent investigations suggested that this peak was caused by tyrosine which produced a positive peak in the higher-voltage channel. Our investigations indicate that compounds that generate a peak in one channel appear to be responsible for complex peaks in a second channel set at a lower voltage, close to or below that necessary for oxidation. The complex peaks are biphasic; a sharp negative peak coinciding with the positive peak on the higher-voltage channel, followed by a positive peak. This effect was not specific for tyrosine, but was observed on the lower-voltage channel with all compounds tested that produced signals on the high-voltage channel. The cause of the problem is unknown, but it appears to be an artifact of the electrical coupling of the two electrode channels in a dual-channel system.

Animals↗

PubMed1992

Regional distribution of beta 1- and beta 2-adrenoceptors in the failing and nonfailing human heart.

Total beta-adrenoceptor density and beta 1- and beta 2-subtype distribution in right and left atria and in different ventricular regions from 14 failing and seven nonfailing human hearts have been compared. End-stage heart failure was due to idiopathic dilated cardiomyopathy (n = 8) or ischaemic cardiomyopathy (n = 6). In nonfailing hearts the total beta-adrenoceptor density was similar in the right and left atria and in all the ventricular regions studied (about 70 to 80 fmol/mg protein). The beta 1:beta 2-adrenoceptor ratio in both nonfailing atria was similar (about 70:30%) and was significantly smaller than in the different regions of both ventricles (about 80:20%). The beta 1-subtype density was similar in nonfailing atria and ventricles (about 55 fmol/mg protein). The beta 2-subtype density was significantly higher in the right and left atrium (about 25 fmol/mg protein) than in both ventricles (about 15 fmol/mg protein). In patients with end-stage heart failure due to idiopathic dilated cardiomyopathy or ischaemic cardiomyopathy the total beta-adrenoceptor density was reduced by 50-60% in all regions. On the other hand, the beta 1- and beta 2-subtype distribution differed with the cause of heart failure. In patients with idiopathic dilated cardiomyopathy, the beta 1-adrenoceptor density was not significantly reduced. In patients with ischaemic cardiomyopathy both beta 1- and beta 2-adrenoceptors were reduced in all regions. It is concluded that downregulation of beta-adrenoceptors in patients with end-stage idiopathic dilated cardiomyopathy or ischaemic cardiomyopathy occurs uniformly throughout the heart. The results support the hypothesis that changes in beta-adrenoceptor subtypes may be related to the cause of heart failure.

Adult↗