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At least 253 records · Page 14Linked to original sources
PubMed1976

Failure of histamine antagonists to prevent hypoxic pulmonary vasoconstriction in dogs.

The role of histamine as a mediator of hypoxic pulmonary vasoconstriction was examined in intact anesthetized dogs. Antagonism of histamine vasoconstrictor (H1) receptors with a classic antihistaminic drug (chlorpheniramine) failed to prevent or modify the pulmonary vascular responses to hypoxia (10% O2). Blockade of histamine vasodilator (H2) receptors with a newly synthesized blocking agent (metiamide) potentiated the vasoconstriction induced by hypoxia and prevented the normal increase in heart rate. Combined H1- and H2-receptor blockade also did not prevent or reduce the hypoxic pulmonary pressor response, although it did effectively abolish the cardiovascular actions of infused histamine. In other dogs, histamine infused (3.6 mug/kg per min) during hypoxia attenuated the pulmonary vasoconstriction induced by hypoxia. The results imply that, in the dog, histamine does not mediate hypoxic pulmonary vasoconstriction. However, histamine does appear to be released during hypoxia, and it may play a role in modulating the pulmonary vascular responses to hypoxia by opposing the hypoxia induced vasoconstriction. The results also imply that histamine may be responsible for the increase in heart rate during hypoxia.

Animals↗
PubMed2005

Endocrine effects of tamoxifen plus exemestane in postmenopausal women with breast cancer.

PURPOSE: In some specific circumstances, combined hormonal therapies for breast cancer seem to be more effective than single maneuvers. In two laboratory mammary cancer models, the combination of the aromatase inactivator exemestane plus tamoxifen gives a higher response rate than is found with either agent alone. To evaluate the endocrine effects of the combination of exemestane and tamoxifen, we studied 33 postmenopausal women disease-free following primary treatments for breast cancer who were taking tamoxifen for at least 3 months. DESIGN: After observation for symptoms on tamoxifen for 4 weeks, blood samples were taken and patients were begun additionally on exemestane 25 mg p.o. qd. Eight weeks later, blood samples were again taken, and exemestane was discontinued. RESULTS: A decrease in alkaline phosphatase was found with exemestane treatment (P = 0.06), whereas no change in osteocalcin level was observed. A decrease in high-density lipoprotein cholesterol level was found (P = 0.0025), whereas total cholesterol, low-density lipoprotein cholesterol and triglyceride levels showed no changes with exemestane treatment. Estradiol, estrone, and estrone sulfate levels decreased to immeasurable or very low levels with exemestane treatment (all P < 0.001). No significant changes in frequencies of common drug-associated side effects, such as vasomotor symptoms or weight change, were found. CONCLUSIONS: Based on the absence of adverse endocrine effects with the addition of exemestane to tamoxifen therapy observed in this study, further clinical evaluation of the efficacy of this combination is warranted.

Adult↗
PubMed1984

Dynamic mechanisms in human coronary stenosis.

At the clinical level, coronary stenoses frequently behave as though the obstruction to flow were variable and not as rigidly fixed as previously imagined. Pressure (energy) lost in flow through a stenosis is the primary determinant of its hemodynamic impact. Ischemic episodes occur when pressure distal to the stenosis falls below that needed to perfuse the subendocardium. Three important properties of the stenosis contribute to variation in its pressure loss. First, loss is proportional to the square of stenosis flow. Thus proper distribution of perfusion is doubly vulnerable to conditions such as exercise, anemia, or pharmacologic vasodilation, which ordinarily increase myocardial blood flow. Second, pressure loss is proportional to the inverse fourth power of minimum lumen diameter. As a result, seemingly small changes in diameter are amplified to large changes in stenosis resistance. Third, a compliant arc of normal arterial wall borders part of the lumen in the majority of coronary lesions. This extremely important morphologic feature of stenoses permits transient variation in stenosis lumen diameter in response to drugs or to variation in endogenous vasomotor activity or intraluminal pressure. Although our understanding is incomplete, many of the clinical features of coronary disease and its pharmacologic responses are explained in terms of these stenosis properties and their interaction.

Arteriosclerosis↗
PubMed1991

Effects of cocaine on canines' coronary arteries.

Nine canines were anesthetized with pentobarbital and studied by both selective and semiselective coronary artery angiography following intravenous bolus doses of 1,3,5,8, or 10 mg/kg of cocaine. Catheterization was accomplished with a 5 Fr catheter over a 0.035 inch guidewire under fluoroscopic control, and angiograms were obtained by injection of a diatrizoate solution. Digital subtraction angiography (DSA) was performed prior to cocaine administration and at minutes 0.5, 1, 1.5, 3, 5, and, in some cases, minutes 10 and 15 after cocaine administration. The 1 and 3 mg/kg doses of cocaine had no effect on the coronary arteries. The 5 mg/kg dose significantly dilated the coronary arteries. The 8 mg/kg dose produced significant dilation at 30 seconds after cocaine but nonsignificant dilation of the coronary arteries at all other times. The 10 mg/kg dose produced significant dilation at 30 seconds, nonsignificant dilation at 60 seconds followed by significant constriction at 90 seconds after cocaine, which led to immediate death in most animals. The coronary dilation and constriction produced by 10 mg/kg of cocaine could be prevented by either preadministration or postadministration of naloxone, but this did not prevent subsequent death.

Angiography, Digital Subtraction↗
PubMed1975

The significance of histamine H1 and H2 receptors on the carotid vascular bed in the dog.

Intra-arterial histamine produced a dose-dependent increase in common carotid blood flow due to an active vasodilation. A supramaximal dose of mepyramine (H1-blocker) only partially suppressed the effects of lower doses of histamine without influencing those of its higher amounts. Both metiamide and burimamide (H2-blockers) effectively antagonized the mepyramine-resistant carotid vasodilator responses to histamine. The results permit us to conclude that two distinctly different types of histaminergic receptors (H1 and H2) are present in the carotid vascular bed and both of these receptor types are equally important in subserving histamine vasodilation. This fact may explain why, despite incriminating evidence for a pathophysiologic role of histamine, the usual antihistaminic agents are rather ineffective in migrainous headaches. It is suggested that the use of both types of antihistaminic agents concurrently may provide a new approach to the treatment of migrainous headaches, particularly cluster-type headaches.

Animals↗
PubMed1985

Copper salicylate complex: thermoregulatory and biochemical effects.

The antipyretic properties of copper (II) salicylate and its effect on plasma copper, iron, zinc and ceruloplasmin concentrations was investigated in adult rabbits at an ambient temperature of 21.5 +/- 0.5 degrees C. The experiments indicated that copper salicylate (200 mg/kg/h i.v.) was a more potent antipyretic than sodium salicylate given in the same manner and doses. This pharmacological activity was found on a model of experimental fever induced by i.v. injection of lipopolysaccharide Escherichia coli at a dose of 1 microgram/kg. Furthermore, unlike sodium salicylate, this copper complex caused a decrease in core temperature in normothermic rabbits. At the same time copper salicylate activated heat dissipation much more efficiently than the parent drug, as manifested by decreases in vasomotor tone and reversal of postpyrogen inhibition of RF. As was expected, treatment with copper salicylate increased plasma copper and ceruloplasmin levels in both normothermic and febrile rabbits. These increases did not lead to any disturbances in iron and zinc concentrations. Neither salicylate affected postpyrogen falls in plasma iron concentrations. They both, however, delayed the appearance of zinc decreases in febrile rabbits. The results of this study suggest that copper modifies the thermoregulatory effects of salicylate. Moreover, the increased amounts of this metal do not seem to disturb seriously the ionic status of the blood.

Animals↗
PubMed1982

[Non-ventilatory functions of the cells of the respiratory system].

The physiology of the respiratory system was limited until recently to study of the structures subjected to simple physical laws and involved in gas exchanges only. Today, the airways and lung itself are conceived as complex living structures adapted to defence against exogenous, microbiological, organic and inorganic substances which reach the respiratory epithelium, contained in the 10 to 12 m3 of air entering and leaving the lungs daily. In addition, the considerable surface area represented by the endothelium of the pulmonary circulation is a site of synthesis and elimination, the implications of which are increasingly important in the area of the metabolism of endogenous substances: prostaglandins, vasomotor substances and the bioconversion of drugs and toxic agents. This is an increasingly large area of research and investigation, the clinical applications of which appear to be more and more frequent and important.

Arachidonic Acids↗
PubMed1991

[The mechanism of cholinergic effects on lowering intraocular pressure].

The relationship between vasomotoric activity and blood vessel permeability was studied in the course of discovering the ocular hypotonising mechanism of cholinergic drug activity (pilocarpin and carbamylcholin). The authors found, in experimental conditions, that the vasomotoric activity (vasodilatation) of the two cholinergic drugs is expressed in the increased permeability of the blood-aqueour barrier. In the presence of an elevated extracirculatory pressure (IOP), as in glaucoma, vasodilatation under the influence of cholinergic drugs, is converted to passive vasoconstriction which leads to reduced aqueous humor production. Carbamilcholin reduces aqueous humor production in a greater extent than pilocarpin.

Animals↗
PubMed2003

The influence of vasopressin on tonic activity of cardiovascular neurones in the ventrolateral medulla of the hypertensive rat.

In normotensive Wistar rats, vasopressin may act as an excitatory neurotransmitter at synapses of paraventricular neurones on rostral ventrolateral medullary vasomotor neurones. We studied the influence of this neurotransmitter in spontaneously hypertensive rats to determine if it contributed to the increases in sympathetic nerve traffic in these rats.A five-barrel micropipette assembly was used for extracellular recording of neuronal activity and for microiontophoresis of drugs into the vicinity of identified medullary vasomotor neurones. Excitatory effects of iontophoretically applied vasopressin were blocked by simultaneous iontophoretic application of V(1a) antagonist. Similar application of the vasopressin receptor antagonist did not block an excitatory effect of iontophoretically applied glutamate. Excitatory effects produced by activating paraventricular neurones were also blocked by the V(1a) antagonist. However, the vasopressin antagonist did not alter the ongoing activity of medullary vasomotor neurones. Therefore, in these anaesthetised hypertensive rats, we concluded that vasopressin neurones do not exert a significant tonic drive to rostral ventrolateral medullary-spinal vasomotor neurones.

Animals↗
PubMed1992

[Drug induced orthostatic hypotension].

Therapeutic drugs are the main cause of postural hypotension, notably in elderly people. This syndrome is harmful as it reduces patients' compliance with treatment and is responsible for severe accidents. Drugs which lower cardiac output by acting on heart rate and cardiac muscle contractility, and drugs which decrease blood volume may produce postural hypotension; diuretics are often responsible for hypovolemia and hypokalaemia. The principal mechanisms involved are interferences of drugs with vegetative blood pressure regulation. They include vasomotor centre depressors (morphine-like compounds, antihypertensive agents, neurosedatives, neuroleptics, antiparkinsonians); ganglioplegics; inhibitors of noradrenaline production (methyldopa, disulfiram) or re-uptake (antidepressants); catecholamine depressors (guanethidine); drugs acting on chromaffin granules (monoamine oxidase inhibitors) and those which inhibit post-synaptic receptors (alpha- and beta-blockers). Drugs which act on vascular smooth muscle tone (nitrites, calcium channel antagonists, angiotensin-converting enzyme inhibitors) occasionally cause postural hypotension. To the actions of these drugs must be added endogenous and exogenous factors and notably physiological ageing of the baroceptor reflex; these factors must be taken into account whenever therapeutic drugs are prescribed.

Adolescent↗
PubMed2004

Dobutamine inhibits phorbol-myristate-acetate-induced activation of nuclear factor-kappaB in human T lymphocytes in vitro.

Adrenergic drugs are often used for hemodynamic support of cardiac output and vasomotor tone in critically ill patients. Recent evidence shows that the administration of these vasoactive drugs may affect cytokine release and could influence the inflammatory response. However, the mechanism of this immunomodulatory effect remains unknown. The nuclear transcription factor-kappaB (NF-kappaB) regulates the expression of many cytokines and plays a central role in the immune response. Therefore, we examined the effects of various adrenergic drugs (dobutamine, xamoterol, clenbuterol, epinephrine, norepinephrine, and phenylephrine) on the activation of NF-kappaB, on the NF-kappaB-driven reporter gene activity, and on the expression of the NF-kappaB target gene interleukin (IL)-8. In addition, we quantified the amount of the NF-kappaB inhibitors IkappaBalpha and IL-10. Here we report that dobutamine inhibited the activation of NF-kappaB in primary human CD3(+) T lymphocytes. Suppression of NF-kappaB involved the stabilization of its inhibitor, IkappaBalpha. The effect appears to be beta(2)-receptor specific, because beta(1)-adrenergic and alpha-adrenergic substances (i.e., xamoterol, epinephrine, norepinephrine, and phenylephrine) did not affect NF-kappaB activation and because dobutamine-mediated inhibition of NF-kappaB could be prevented by a specific beta(2)-antagonist. Our results demonstrate that dobutamine is a potent and specific inhibitor of NF-kappaB, and they thus provide a possible molecular mechanism for the immunomodulation associated with beta-adrenergic therapy.

Adrenergic Agents↗