PubMed · 5804347
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1969. An atopic theorem.. https://pubmed.ncbi.nlm.nih.gov/5804347/
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We demonstrate sensitive spatially resolved detection of physiological chromophores that emit in the ultraviolet (<330 nm). An atypical laser source (a visible wavelength femtosecond optical parametric oscillator), and an unconventional collection geometry (a lensless detector that detects the forward-emitted fluorescence) enable this detection. We report the excitation spectra of the catecholamines dopamine and norepinephrine, together with near-UV emitters serotonin and tryptophan, in the range of 550-595 nm. We estimate the molecular two-photon action cross section of dopamine, norepinephrine, and serotonin to be 1.2 mGM (1 GM, or Goppert Mayor, is equal to 10(-58) m4 s(-1) photon(-1)), 2 mGM, and 43 mGM, respectively, at 560 nm. The sensitivity achieved by this method holds promise for the microscopic imaging of vesicular catecholamines in live cells.
OBJECTIVE: The objective of the study was to perform a descriptive approach of the current use of catecholamines by French physicians. DESIGN: A questionnaire of 12 questions with 4 items established by a group of French intensivists. POPULATION: French physicians from 433 departments working in the following practicing areas: intensive care unit (ICU), emergency department, and pre-hospital setting. MEASUREMENTS: Responding physicians were asked about the catecholamine that they would select in various clinical settings. RESULTS: The response rate was 82%. Of the responding physicians, 277 (78%) worked in an ICU, 28 (8%) in an emergency department, and 21 (6%) in a pre-hospital setting. Dobutamine was chosen for patients with cardiogenic shock by 90% of the respondents. Norepinephrine was the first choice agent as vasopressor in patients with septic shock in 52% of the cases. Dopamine was selected in a clinical setting requiring an optimization of regional blood flow, as in the concept of high-risk surgical patients. Dopexamine was used as a second or third choice agent to improve regional blood flow and cardiac output. The indications of epinephrine for anaphylactic shock and cardio-circulatory arrest were obvious for more than 90% of responding physicians. CONCLUSION: A lack of standardization appears in the use of catecholamines by French physicians, particularly for improvement of regional circulation and management of high-risk surgical patients. Guidelines that define the place of each catecholamine in these settings are required to improve the quality of prescription.
Activation of human peripheral blood mononuclear cells (PBMC) triggers endogenous production of catecholamines (CA) through protein kinase (PK) C-dependent induction of tyrosine hydroxylase (TH; EC 1.14.16.2), the first and rate-limiting enzyme in the synthesis of CA. Since CA themselves are major mediators of the neural input to the immune system, we have examined their ability to affect PKC-induced TH mRNA expression and CA production in human isolated PBMC. In T- and B-lymphocytes (but not in monocytes) the PKC activator 12-O-tetradecanoylphorbol-13-acetate (TPA) (but not its inactive analogue 4alpha-phorbol-12,13-didecanoate) induced TH mRNA expression which was followed by an increase in the amount of intracellular CA. Coincubation of human PBMC with dopamine (DA) (but not with norepinephrine or epinephrine) inhibited TPA-induced TH mRNA expression. The effect of DA was concentration-dependent and was mimicked by the dopaminergic D1-like receptor agonist SKF-38393 but not by the D2-like receptor agonist bromocriptine. The D1-like antagonist SCH-23390 shifted to the right the concentration-response curves of both DA and SKF-38393, while neither the D2-like antagonist domperidone, nor the alpha1-adrenoceptor antagonist prazosin, the alpha2-adrenoceptor antagonist yohimbine, or the beta-adrenoceptor antagonist propranolol affected to any significant extent the inhibitory effect of DA. SKF-38393 also significantly reduced TPA-induced increase of intracellular CA, an effect which was antagonized by SCH-23390. It is thus suggested that in human T- and B-lymphocytes PKC activation leads to TH mRNA expression and subsequent increase of intracellular CA, which can be inhibited by D1-like receptor activation. Inhibition of intracellular CA production in human PBMC promotes cell survival through reduction of activation-induced apoptosis, and dopaminergic modulation of TH expression and intracellular CA content may thus represent a novel mechanism in the cross-talk between the nervous and the immune system as well as among immune system cells.