Tracheal smooth muscle responses to substance P and neurokinin A in the piglet

1992 ◽  
Vol 72 (3) ◽  
pp. 1090-1095 ◽  
Author(s):  
B. Haxhiu-Poskurica ◽  
M. A. Haxhiu ◽  
G. K. Kumar ◽  
M. J. Miller ◽  
R. J. Martin
Keyword(s):  
Smooth Muscle ◽  
Substance P ◽  
Muscle Contraction ◽  
Muscle Tension ◽  
Age Groups ◽  
Smooth Muscle Contraction ◽  
Tracheal Smooth Muscle ◽  
Neurokinin A ◽  
Dose Dependent Increase ◽  
Dose Dependent

The tachykinins substance P (SP) and neurokinin A (NKA) have been shown to induce airway smooth muscle contraction in mature animals, and the enzyme neutral endopeptidase (NEP) modulates this effect. We evaluated maturation of SP- and NKA-induced tracheal smooth muscle contraction and modulation of their effects by NEP in anesthetized, paralyzed, and artificially ventilated piglets less than 4 days, 2–3 wk, and 10 wk of age. Tracheal smooth muscle tension was measured in vivo from an open tracheal segment by use of a force transducer. Intravenous SP caused a dose-dependent increase in tracheal tension in all three age groups; however, the response in less than 4-day-old piglets was significantly weaker than in 2- to 3- and 10-wk-old piglets. NKA caused a dose-dependent increase in tracheal tension only in 2- to 3- and 10-wk-old piglets. The response of tracheal tension to NKA was weaker than the response to SP in all age groups. Atropine (2 mg/kg) significantly diminished the responses of tracheal tension to SP and NKA, indicating a cholinergic contribution to these responses at all ages. Intravenous thiorphan, a known NEP inhibitor, potentiated the effects of SP only in 2- to 3- and 10-wk-old piglets and did not affect the response of tracheal tension to NKA at any age. Biochemical analyses demonstrated a significant increase in tracheal NEP activity in comparably aged piglets over the first 10 wk of life.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of antigen on tracheal circulation and smooth muscle in sheep of different ages

1989 ◽  
Vol 67 (3) ◽  
pp. 1256-1264 ◽  
Author(s):  
S. E. Webber ◽  
R. O. Salonen ◽  
M. E. Deffebach ◽  
J. G. Widdicombe
Keyword(s):  
Smooth Muscle ◽  
Muscle Contraction ◽  
Perfusion Pressure ◽  
Muscle Tone ◽  
Smooth Muscle Contraction ◽  
Tracheal Smooth Muscle ◽  
External Diameter ◽  
Smooth Muscle Tone ◽  
Residual Response ◽  
Dose Dependent

The effects of Ascaris suum antigen on tracheal circulation and tracheal smooth muscle tone were compared in two groups of sheep: the first group was 1 yr old (14 sheep) and the second 5 yr old (8 sheep). Cranial tracheal arteries of anesthetized and paralyzed sheep were perfused at constant flow with monitoring of perfusion pressure. Tracheal smooth muscle tone was assessed by measuring changes in the external diameter of the cranial trachea. Close-arterial injection of antigen (1–20 micrograms) in young sheep produced dose-dependent vasodilation (6.1–15.5% fall in perfusion pressure) and smooth muscle contraction (0.06–0.28 mm reduction in tracheal diam). In old sheep, antigen (1–20 micrograms) produced vasoconstriction (4.1–16.8%) but no smooth muscle response. The smooth muscle contraction in young sheep was blocked by mepyramine (2 mg/kg iv) suggesting mediation by release of histamine. The vasodilation in young sheep and the vasoconstriction in old sheep were reduced by indomethacin (5 mg/kg iv), and the residual response was further reduced by FPL 55712 (2 mg/kg iv), suggesting mediation by both cyclooxygenase products and leukotrienes. Thus antigen given in the tracheal vasculature releases a mixture of inflammatory mediators. This mixture of mediators or their actions on the tracheal vasculature and smooth muscle may depend on the age of the sheep.

Reflex tracheal smooth muscle contraction and bronchial vasodilation evoked by airway cooling in dogs

1997 ◽  
Vol 82 (5) ◽  
pp. 1566-1572 ◽  
Author(s):  
Thomas E. Pisarri ◽  
Gordon G. Giesbrecht
Keyword(s):  
Smooth Muscle ◽  
Muscle Contraction ◽  
Airway Obstruction ◽  
Pulmonary Circulation ◽  
Muscle Tension ◽  
Smooth Muscle Contraction ◽  
Arterial Flow ◽  
Tracheal Smooth Muscle ◽  
Cervical Vagotomy ◽  
The Right

Pisarri, Thomas E., and Gordon G. Giesbrecht. Reflex tracheal smooth muscle contraction and bronchial vasodilation evoked by airway cooling in dogs. J. Appl. Physiol. 82(5): 1566–1572, 1997.—Cooling intrathoracic airways by filling the pulmonary circulation with cold blood alters pulmonary mechanoreceptor discharge. To determine whether this initiates reflex changes that could contribute to airway obstruction, we measured changes in tracheal smooth muscle tension and bronchial arterial flow evoked by cooling. In nine chloralose-anesthetized open-chest dogs, the right pulmonary artery was cannulated and perfused; the left lung, ventilated separately, provided gas exchange. With the right lung phasically ventilated, filling the right pulmonary circulation with 5°C blood increased smooth muscle tension in an innervated upper tracheal segment by 23 ± 6 (SE) g from a baseline of 75 g. Contraction began within 10 s of injection and was maximal at ∼30s. The response was abolished by cervical vagotomy. Bronchial arterial flow increased from 8 ± 1 to 13 ± 2 ml/min, with little effect on arterial blood pressure. The time course was similar to that of the tracheal response. This response was greatly attenuated after cervical vagotomy. Blood at 20°C also increased tracheal smooth muscle tension and bronchial flow, whereas 37°C blood had little effect. The results suggest that alteration of airway mechanoreceptor discharge by cooling can initiate reflexes that contribute to airway obstruction.

Measurement of cytoplasmic free Ca2+ concentration in bovine tracheal smooth muscle using aequorin

1987 ◽  
Vol 253 (6) ◽  
pp. C817-C827 ◽  
Author(s):  
Y. Takuwa ◽  
N. Takuwa ◽  
H. Rasmussen
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Contraction ◽  
Isometric Tension ◽  
Tracheal Smooth Muscle ◽  
Base Line ◽  
Gradual Decline ◽  
High K ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Plateau Level

The cytoplasmic free Ca2+ concentration in bovine tracheal smooth muscle strips was measured using aequorin. Carbachol induces a rapid rise in aequorin luminescence, which reaches a peak within 1-2 min and then falls to a plateau level in 5-6 min. This plateau gradually declines but remains significantly above the base-line value after 2 h. The initial Ca2+ transient is due to Ca2+ mobilization from an intracellular caffeine-sensitive pool. The plateau appears to be due to Ca2+ influx. Histamine or 5-hydroxytryptamine (serotonin) also induce a Ca2+ transient followed by a plateau phase which is lower than that induced by carbachol. The isometric tension generated by either of these two agonists shows a gradual decline in contrast to the sustained plateau seen in the carbachol-induced contraction. Extracellular high K+ induces a dose-dependent increase in aequorin luminescence that is totally due to Ca2+ influx across the plasma membrane and is greatly inhibited by a Ca2+-channel antagonist, nimodipine. These results suggest that two temporally and spatially different Ca2+-dependent mechanisms are involved in carbachol-induced tracheal smooth muscle contraction.

A Minority of Muscarinic Receptors Mediate Rabbit Tracheal Smooth Muscle Contraction

1992 ◽  
Vol 6 (3) ◽  
pp. 279-286 ◽  
Author(s):  
Vinit K. Mahesh ◽  
Linda M. Nunan ◽  
Marilyn Halonen ◽  
Henry I. Yamamura ◽  
John D. Palmer ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Muscle Contraction ◽  
Muscarinic Receptors ◽  
Smooth Muscle Contraction ◽  
Tracheal Smooth Muscle

Role of platelets in contraction of canine tracheal muscle elicited by PAF in vitro

1988 ◽  
Vol 65 (2) ◽  
pp. 914-920 ◽  
Author(s):  
K. J. Popovich ◽  
G. Sheldon ◽  
M. Mack ◽  
N. M. Munoz ◽  
P. Denberg ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Muscle Contraction ◽  
Airway Smooth Muscle ◽  
Airway Epithelium ◽  
Platelet Activating Factor ◽  
Smooth Muscle Contraction ◽  
Tracheal Smooth Muscle ◽  
Serotonin Antagonist

To elucidate mechanisms of platelet-activating factor (PAF)-induced contraction, we studied the effect of PAF on 203 canine tracheal smooth muscle (TSM) strips from 45 dogs in vitro in the presence and absence of platelets. PAF (10(-11) to 10(-7) M) alone caused no contraction of TSM even in the presence of airway epithelium. In the presence of 2 x 10(5) platelets/microliter, PAF was an extremely potent contractile agonist (threshold 10(-11) M). This response was inhibited by the PAF antagonist, CV-3988 (10(-6) M), and reversed by the serotonin antagonist, methysergide (EC50 = 3.7 +/- 0.79 x 10(-9) M). Neither atropine nor chlorpheniramine (10(-9) to 10(-6) M) attenuated the response to PAF + platelets. In the presence of platelets, 10(-7) M PAF caused an increase in perfusate concentration of serotonin from 0.93 +/- 0.037 x 10(-8) to 1.7 +/- 0.046 x 10(-8) M (P less than 0.001). Tachyphylaxis, previously demonstrated to be irreversible, was shown to be a platelet-dependent phenomenon; contraction could be repeated in the same TSM after addition of fresh platelets. We demonstrate that PAF-induced contraction of canine TSM is caused by the release of cellular intermediates such as serotonin from platelets. We also demonstrate the site of PAF-induced tachyphylaxis in airway smooth muscle contraction.

The influence of neuraminidase treatment on tracheal smooth muscle contraction

1992 ◽  
Vol 220 (2-3) ◽  
pp. 181-185 ◽  
Author(s):  
Kai Hirofumi ◽  
Makise Kiyomi ◽  
Matsumoto Sachiko ◽  
Ishii Takayuki ◽  
Takahama Kazuo ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Muscle Contraction ◽  
Smooth Muscle Contraction ◽  
Tracheal Smooth Muscle ◽  
Neuraminidase Treatment
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