bradycardia/tyrosine

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Loss of Hand2 in a population of Periostin lineage cells results in pronounced bradycardia and neonatal death.

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The Periostin Cre (Postn-Cre) lineage includes endocardial and neural crest derived mesenchymal cells of the cardiac cushions, neural crest-derived components of the sympathetic and enteric nervous systems, and cardiac fibroblasts. In this study, we use the Postn-Cre transgenic allele to

Mechanism of the acute pressor effect and bradycardia elicited by diaspirin crosslinked hemoglobin in anesthetized rats.

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Diaspirin crosslinked hemoglobin (DCLHb) is a chemically stabilized hemoglobin (Hb) that induces an increase in blood pressure and a decrease of heart rate when injected intravenously in some animals. The mechanism by which DCLHb elicits these hemodynamic effects was studied in

Vasopressin-induced bradycardia in fetal and adult sheep is not dependent on an increase in blood pressure.

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Other investigators have reported that intravenous infusion of synthetic arginine vasopressin into fetal lambs increases mean arterial pressure and decreases heart rate. To determine if the bradycardia produced by arginine vasopressin is a reflex response to the increase in blood pressure, we

Targeted disruption of the tyrosine hydroxylase locus results in severe catecholamine depletion and perinatal lethality in mice.

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Tyrosine 3-hydroxylase (TH, EC 1.14.16.2) catalyzes the first and rate-limiting step of the catecholamine biosynthetic pathway in the nervous and endocrine systems. The TH locus was disrupted in mouse embryonic stem cells by homologous recombination. Mice heterozygous for the TH mutation were

Cardiovascular effects of L-tyrosine: influence of blockade of tyrosine metabolism.

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Tyrosine is the precursor of catecholamines. Small doses of tyrosine produce tachycardia and hypertension while higher doses produce bradycardia and hypotension in anaesthetised rats. The mechanism of these effects has not been established. An increased synthesis and release of catecholamines has

When crizotinib-induced bradycardia becomes symptomatic: role of concomitant drugs.

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Crizotinib is an orally active multi-target tyrosine kinase inhibitor which is the standard of care in patients with anaplastic lymphoma kinase translocated non-small-cell lung cancer. Common adverse events in clinical trials with crizotinib included visual disorders, nausea-vomiting, diarrhea and

Atrial fibrillation was changed into sinus bradycardia in a ROS1-positive advanced lung adenocarcinoma patient who achieved durable response to Crizotinib: A case report and literature review.

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BACKGROUND The c-ros oncogene 1 receptor tyrosine kinase (ROS1)-rearrangements represent a new and rare genetic subtype of non-small-cell lung cancer. In recent years, the use of crizotinib in ROS1-rearranged lung cancer exhibits significant clinical efficacy. Crizotinib is generally well tolerated

Whole brain tyrosine hydroxylase activity during the development of deoxycorticosterone acetate-1% sodium chloride-induced hypertension in rats.

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Water was chosen as the optimal medium for the extraction of tyrosine hydroxylase (TH) from rat brain. Determination of TH activity in crude homogenates failed to exhibit a linear relationship between enzyme concentration and measured activity, however, when a supernatant was used, a linear

Do endogenous opioids contribute to the bradycardia of rats with obstructive cholestasis?

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Endogenous opioids have nitric oxide (NO)-dependent cardiovascular actions. In the light of biological evidence of accumulation of endogenous opioids in cholestasis and also existence of NO-dependent bradycardia in cholestatic subjects, this study was carried out to evaluate the role of endogenous

Further studies on the mechanism of the cardiovascular effects of L-tyrosine.

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Tyrosine is the precursor amino acid of catecholamines. Low doses of tyrosine produce tachycardia and hypertension, while higher doses induce bradycardia and hypotension in anaesthetised rats. The mechanism and site of action of L-tyrosine are not fully understood. Eight groups of Wistar rats

Depressant effects of L-tyrosine on isolated perfused rat and rabbit hearts.

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Tyrosine exerts potent cardiovascular effects: smaller doses induce tachycardia and hypertension while higher doses induce bradycardia and hypotension. However, the direct cardiac effects of this amino acid have not been characterised. In the present study increasing doses of L-tyrosine were

Tyrosine hydroxylase is expressed during early heart development and is required for cardiac chamber formation.

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OBJECTIVE Tyrosine hydroxylase (TH) is the first and rate-limiting enzyme in catecholamine biosynthesis. Whereas the neuroendocrine roles of cathecolamines postnatally are well known, the presence and function of TH in organogenesis is unclear. The aim of this study was to define the expression of

The cardiac sympathetic co-transmitter galanin reduces acetylcholine release and vagal bradycardia: implications for neural control of cardiac excitability.

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The autonomic phenotype of congestive cardiac failure is characterised by high sympathetic drive and impaired vagal tone, which are independent predictors of mortality. We hypothesize that impaired bradycardia to peripheral vagal stimulation following high-level sympathetic drive is due to

Factors associated with sinus bradycardia during crizotinib treatment: a retrospective analysis of two large-scale multinational trials (PROFILE 1005 and 1007).

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Decreases in heart rate (HR) have been described in patients receiving crizotinib. We performed a large retrospective analysis of HR changes during crizotinib therapy. HRs from vital-sign data for patients with anaplastic lymphoma kinase (ALK)-positive nonsmall cell lung cancer enrolled in PROFILE

The HCN4 channel mutation D553N associated with bradycardia has a C-linker mediated gating defect.

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OBJECTIVE The D553N mutation located in the C-linker of the cardiac pacemaker channel HCN4 is thought to cause sino-atrial dysfunction via a pronounced dominant-negative trafficking defect. Since HCN4 mutations usually have a minor defect in channel gating, it was our aim to further characterize the

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