Histamine H1- and H2-receptors in pulmonary and systemic vasculature of the dog

Tucker, Adam; Weir, E. K.; Reeves, J. T.; Rf, Grover

doi:10.1152/ajplegacy.1975.229.4.1008

Cited by 92 publications

(38 citation statements)

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“…Smaller doses of histamine may cause modest and only transient increases in cardiac output (Delaunois et al, 1959;Tucker et al, 1975). In our experiments there was no evidence that histamine infusions, covering a dose range from 1 x 10-8 to 3.3 x 10-7 mol kg-' min-' had any significant effect on cardiac output.…”

Section: Discussioncontrasting

confidence: 48%

Tissue Blood Flow and Distribution of Cardiac Output in Cats: Changes Caused by Intravenous Infusions of Histamine and Histamine Receptor Agonists

Johnston¹,

Owen²

1977

British J Pharmacology

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The effects of infusions of histamine on blood pressure, cardiac output, heart rate, total peripheral resistance, stroke volume and tissue blood flow have been determined in anaesthetized cats using radio‐active microspheres to measure cardiac output and tissue blood flow. Histamine caused dose‐dependent falls in blood pressure and total peripheral resistance over the dose‐range 1 × 10−8 to 3.3 × 10−7 mol kg−1 min−1. Histamine had no effect on cardiac output, heart rate or stroke volume. Histamine caused vasodilatation in the heart and stomach, with increased blood flow through these organs, and in the small and large intestine where blood flow was maintained despite the falls in arterial blood pressure. Blood flow to the brain, kidneys, liver, adrenal glands, skeletal muscle, spleen and skin was reduced when arterial blood pressure fell. Vascular resistance increased in the skin and spleen, presumably due to reflex vasoconstriction when blood pressure fell. The selective H1‐receptor agonist 2‐(2‐aminoethyl)pyridine lowered blood pressure and decreased total peripheral resistance but did not change cardiac output, heart rate or stroke volume. 2‐(2‐Aminoethyl)pyridine caused vasodilatation in the heart, small and large intestine and kidneys. Vascular resistance was increased in the spleen and skin. The selective H2‐receptor agonist 4‐methylhistamine also lowered blood pressure and decreased total peripheral resistance but did not change cardiac output, heart rate or stroke volume. 4‐Methylhistamine caused vasodilatation in the heart, stomach, small and large intestines and skeletal muscle. Vascular resistance was increased in the skin.

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Section: Discussioncontrasting

confidence: 48%

Tissue Blood Flow and Distribution of Cardiac Output in Cats: Changes Caused by Intravenous Infusions of Histamine and Histamine Receptor Agonists

Johnston¹,

Owen²

1977

British J Pharmacology

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“…This is consistent with the notion that the sensory nerves responsible for the regulation of respiratory rate are independent of those that regulate bronchomotor tone, although both C fibers and rapidly adapting sensory nerves may play a role in both responses (9). The observations that the immediate marked decreases in BP were not due to commensurate decreases in heart rate, that these decreases were progressively larger when similar masses of histamine were administered predominantly to the bronchi, alveoli, and iv, and that these decreases were only slightly attenuated by transection of the vagosympathetic trunks indicate that the major portion of these histamine-induced decreases in BP were likely due to pulmonary vasoconstriction and systemic vasodilation, as previously reported in dogs (24); both effects were markedly ameliorated by combined H 1 and H 2 blockade.…”

Section: Discussionsupporting

confidence: 72%

Bronchial, alveolar, and vascular-induced anaphylaxis and irritant-induced cardiovascular and pulmonary responses.

Yeates

Mussatto

Hameister

et al. 2001

Environ Health Perspect

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Inhaled irritants and allergens initiate a pulmonary chemoreflex that can result in responses both in the lung and heart as well as in the systemic and the peripheral vasculatures. These responses are due to both neural reflexes and the activation of humoral receptors by circulating mediators (1). Histamine, a major mediator released by IgE activation, participates in many of the immediate cardiopulmonary physiologic consequences of inhaled antigen in both humans (2) and dogs (3). Histamine is released from mast cells and basophils in the alveolar interstitium and in bronchial mucosa. The number of mast cells in the alveoli (350/mm 2 ) (4) markedly exceeds that in the bronchial mucosa, 226/mm 2 (5) when the relative surface areas of each are considered. Histamine can activate pulmonary C fibers (6), bronchial C fibers (7), and bronchial irritant fibers (6,8). The stimulation of select subsets of each of these fibers has been shown to increase bronchopulmonary smooth muscle tone (9) and elicit the pulmonary chemoreflex typified by rapid shallow breathing, bradycardia, and hypotension. Histamine (10) and inhaled allergens (11) stimulate mucociliary transport. As the functions of the respiratory central pattern generator, bronchial and vascular smooth muscle, and the mucosa are quite distinct, the relative responses of and pathways through which each of these responds to histamine and allergens must each be evaluated.To determine the relative cardiovascular, respiratory, and epithelial responses elicited by histamine administered to the alveolar, bronchial, and vascular compartments and the role of neural pathways in mediating these events, we conducted a series of experiments in beagle dogs. In addition we evaluated cardiovascular, respiratory, and epithelial responses elicited by ragweed allergen administered to the alveolar and bronchial compartments in a cohort of ragweed-sensitized dogs and nonsensitized siblings. Activation of the pulmonary chemoreflex was demonstrated by the measurements of respiratory rate, heart rate, and arterial blood pressure. Efferent responses of the mucosa were assayed in terms of mucociliary clearance, whereas responses of smooth muscles were indicated by either pulmonary resistance or transpulmonary pressure and compliance. Indication of histamine or allergen-induced impairment of gas exchange was determined from the measurement of minute ventilation and arterial blood gases. In these experiments, equivalent total masses of histamine (approximately 185 µg) deposited in the lungs were partitioned such that in one set of experiments 71% was deposited in the bronchi; in the other set 91% was deposited in the alveoli. Responses from the predominantly alveolar deposition due to the 9% deposited in the bronchi were assessed separately by depositing 16 µg in the bronchi. The contribution of vagal transmission was ascertained following bilateral sectioning of the vagosympathetic trunks. To evaluate the extent to which histamine-induced responses due to its translocation from the airways to...

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“…Some explanations may be raised: firstly this could be related to improved and more effective ventilation due to a better wall compliance and a fully synchronize infant's breathing (decreased struggling) but our patient was comfortable under a fentanyl continuous perfusion and on HFO. The neuromuscular blocker could trigger a release of histamine, which in two studies [9,10], has been recognised as a pulmonary vasodilator acting on H2-receptors in pulmonary vasculature in dogs and rats; however our patient did not present any signs of systemic vasodilatation, and pancuronium is known to usually have an overall hypertensive effect. Respiratory paralysis may reduce oxygen consumption by eliminating the work of breathing and may also reduce peak transthoracic pressure decreasing risk of barotrauma, but our patient was ventilated on HFO and was already apneic prior to curare.…”

Section: Discussionmentioning

confidence: 52%

Refractory Persistent Pulmonary Hypertension of the Newborn Responsive Only to Neuromuscular Blockade

Delco

2013

J Med Cases

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We discuss the case of a premature newborn boy presenting with severe persistent pulmonary hypertension (PPHN) at 48 hours of life in the context of Staphylococcus aureus sepsis. PPHN was refractory to classical treatment (oxygen, control of acid basic balance, sedation, high frequency oscillation ventilation, inhaled nitric oxide and antibiotics). We observed an improvement only after administration of a curare. Despite much progress in the management of this entity, a clear and well defined therapy is still missing and especially when PPHN is refractory to classical treatment. The use of neuromuscular blockers in the treatment of this kind of PPHN has been described and some physiological explanations are likely. Neuromuscular blocking agents are rarely useful to treat PPHN since the introduction of iNO, nevertheless, it might still be a useful rescue therapy in some selected newborns with PPHN refractory to classical treatments.

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Histamine H1- and H2-receptors in pulmonary and systemic vasculature of the dog

Cited by 92 publications

References 0 publications

Tissue Blood Flow and Distribution of Cardiac Output in Cats: Changes Caused by Intravenous Infusions of Histamine and Histamine Receptor Agonists

Tissue Blood Flow and Distribution of Cardiac Output in Cats: Changes Caused by Intravenous Infusions of Histamine and Histamine Receptor Agonists

Bronchial, alveolar, and vascular-induced anaphylaxis and irritant-induced cardiovascular and pulmonary responses.

Refractory Persistent Pulmonary Hypertension of the Newborn Responsive Only to Neuromuscular Blockade

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