Differences in responses of guinea-pig and rabbit airway smooth muscle to adrenaline and adrenergic nerve stimulation

1980 ◽  
Vol 65 (1) ◽  
pp. 53-58 ◽  
Author(s):  
Judith M. Doidge ◽  
D.G. Satchell
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Airway Smooth Muscle ◽  
Nerve Stimulation ◽  
Adrenergic Nerve

IL-1 beta and IL-6 induce hyperplasia and hypertrophy of cultured guinea pig airway smooth muscle cells

1995 ◽  
Vol 78 (4) ◽  
pp. 1555-1563 ◽  
Author(s):  
S. De ◽  
E. T. Zelazny ◽  
J. F. Souhrada ◽  
M. Souhrada
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Protein Content ◽  
Airway Smooth Muscle ◽  
Dna Content ◽  
Thymidine Incorporation ◽  
Interleukin 1 ◽  
Total Protein Content ◽  
Leucine Incorporation ◽  
Airway Smooth Muscle Cells

Guinea pig airway smooth muscle (ASM) cells were maintained in a primary tissue culture (passages 1–3). Cells were exposed to human recombinant interleukin-1 beta (IL-1 beta; 20–100 pg/ml) or interleukin-6 (IL-6; 1–4 ng/ml) in the presence of indomethacin (1 microgram/ml) for up to 5 days. Proliferation of ASM cells was assessed with two techniques, direct counting of cells with a hemacytometer and [3H]thymidine incorporation corrected for total protein content. Hypertrophy of ASM cells was assessed by [3H]leucine incorporation (evaluation of protein synthesis), determination of total DNA content, DNA content per cell, and protein content per cell. We observed that the exposure of ASM cells to human recombinant IL-1 beta or IL-6, in all studied concentrations, significantly increased the number of cells as well as [3H]thymidine incorporation into ASM cells. We also found that exposure of ASM to these two cytokines increased [3H]leucine incorporation into the ASM cells and increased protein content and DNA content per single cell. These changes were also concentration dependent. We conclude that the two proinflammatory cytokines, IL-1 beta and IL-6, which are present in asthmatic lungs, increased the proliferation of ASM cells (hyperplasia) as well as their overall size and size of their nuclei, as measured by biochemical markers. These findings are compatible with the presence of ASM hypertrophy.

Effects of mucosal removal on guinea-pig airway smooth muscle responsiveness

1986 ◽  
Vol 70 (6) ◽  
pp. 571-575 ◽  
Author(s):  
Christopher Murlas
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Airway Smooth Muscle ◽  
Contractile Response ◽  
Electrical Field Stimulation ◽  
Physiological Salt Solution ◽  
Induced Responses ◽  
Field Stimulation ◽  
Electrical Field ◽  
Airway Mucosa

1. The contractile response to histamine, acetylcholine (ACh), KCl or electrical field stimulation (EFS) was examined in paired tracheal rings (one of each being denuded by mucosal rubbing), which were mounted in muscle chambers filled with a continuously aerated physiological salt solution at 37°C. 2. Removal of the respiratory mucosa increased the sensitivity of airway muscle to ACh, histamine and EFS, but not to KCl. The hypersensitivity of denuded rings to histamine and EFS was greater than to ACh. Atropine reduced the histamine hypersensitivity observed. 3. Pretreating intact preparations with indomethacin augmented their responsiveness to EFS, histamine and ACh. 4. Indomethacin augmentation of histamine- and EFS-induced responses was greater in preparations without epithelium. 5. We conclude that the airway mucosa may be associated with a factor that reduces airway smooth muscle responsiveness to stimulation.

scholarly journals Ovalbumin sensitization of guinea pig at birth prevents the ontogenetic decrease in airway smooth muscle responsiveness

2014 ◽  
Vol 2 (12) ◽  
pp. e12241
Author(s):  
Pasquale Chitano ◽  
Lu Wang ◽  
Simone Degan ◽  
Charles L. Worthington ◽  
Valeria Pozzato ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Airway Smooth Muscle

Prostacylin modulates the responses to leukotrienes C4 and D4 of guinea-pig airway smooth muscle

1984 ◽  
Vol 104 (1-2) ◽  
pp. 1-7 ◽  
Author(s):  
Kenneth G. Mugridge ◽  
Gerald A. Higgs ◽  
Salvador Moncada
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Airway Smooth Muscle

Characterization of P2Y receptors mediating ATP induced relaxation in guinea pig airway smooth muscle: involvement of prostaglandins and K+ channels

2011 ◽  
Vol 462 (4) ◽  
pp. 573-585 ◽  
Author(s):  
Luis M. Montaño ◽  
José E. Cruz-Valderrama ◽  
Alejandra Figueroa ◽  
Edgar Flores-Soto ◽  
Luz M. García-Hernández ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Airway Smooth Muscle ◽  
P2y Receptors ◽  
Muscle Involvement ◽  
K Channels

Mechanisms of Bronchoprotection by Anesthetic Induction Agents 

1999 ◽  
Vol 90 (3) ◽  
pp. 822-828 ◽  
Author(s):  
Robert H. Brown ◽  
Elizabeth M. Wagner
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Nerve Stimulation ◽  
Airway Resistance ◽  
Bronchial Artery ◽  
Random Order ◽  
Systemic Blood Pressure ◽  
Vagal Nerve ◽  
Vagal Nerve Stimulation ◽  
High Concentrations

Background Propofol and ketamine have been purported to decrease bronchoconstriction during induction of anesthesia and intubation. Whether they act on airway smooth muscle or through neural reflexes has not been determined. We compared propofol and ketamine to attenuate the direct activation of airway smooth muscle by methacholine and limit neurally mediated bronchoconstriction (vagal nerve stimulation). Methods After approval from the institutional review board, eight sheep were anesthetized with pentobarbital, paralyzed, and ventilated. After left thoracotomy, the bronchial artery was cannulated and perfused. In random order, 5 mg/ml concentrations of propofol, ketamine, and thiopental were infused into the bronchial artery at rates of 0.06, 0.20, and 0.60 ml/min. After 10 min, airway resistance was measured before and after vagal nerve stimulation and methacholine given via the bronchial artery. Data were expressed as a percent of baseline response before infusion of drug and analyzed by analysis of variance with significance set at P< or =0.05. Results Systemic blood pressure was not affected by any of the drugs (P>0.46). Baseline airway resistance was not different among the three agents (P = 0.56) or by dose (P = 0.96). Infusion of propofol and ketamine into the bronchial artery caused a dose-dependent attenuation of the vagal nerve stimulation-induced bronchoconstriction to 26+/-11% and 8+/-2% of maximum, respectively (P<0.0001). In addition, propofol caused a significant decrease in the methacholine-induced bronchoconstriction to 43+/-27% of maximum at the highest concentration (P = 0.05) Conclusions The local bronchoprotective effects of ketamine and propofol on airways is through neurally mediated mechanisms. Although the direct effects on airway smooth muscle occur at high concentrations, these are unlikely to be of primary clinical relevance.

Reduced spontaneous relaxation in immature guinea pig airway smooth muscle is associated with increased prostanoid release

2008 ◽  
Vol 294 (5) ◽  
pp. L964-L973 ◽  
Author(s):  
Lu Wang ◽  
Valeria Pozzato ◽  
Graziella Turato ◽  
Aasakiran Madamanchi ◽  
Thomas M. Murphy ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Electrical Stimulation ◽  
Guinea Pig ◽  
Airway Smooth Muscle ◽  
Cysteinyl Leukotriene ◽  
Spontaneous Relaxation ◽  
Leukotriene Receptor ◽  
Cox 2 ◽  
Cysteinyl Leukotriene Receptor ◽  
Cox 1

Airway smooth muscle (ASM) from infant guinea pigs has less spontaneous relaxation during stimulation than ASM from adults. Inhibition of cyclooxygenase (COX), which catalyzes the production of prostanoids, increases this relaxation in infant ASM and abolishes age differences, thus suggesting that prostanoids reduce relaxation in infant ASM. In this study, we investigated whether leukotrienes are also involved in reducing spontaneous relaxation; whether the two COX isoforms, COX-1 and COX-2, differentially regulate spontaneous relaxation; and whether prostanoid release is developmentally regulated in guinea pig ASM. In different age groups, we measured relaxation during and after electrical stimulation in tracheal strips as well as prostanoid release from tracheal segments. Relaxation was studied in the absence and in the presence of a lipoxygenase inhibitor, a cysteinyl leukotriene receptor-1 antagonist, a COX-1 inhibitor, or a COX-2 inhibitor. We found that inhibition of lipoxygenase or cysteinyl leukotriene receptor-1 antagonism did not increase spontaneous relaxation at any age, thus excluding a role for leukotrienes in this phenomenon. Inhibition of COX-2, but not COX-1, promoted spontaneous relaxation. The basal release of prostanoids was more abundant in tissue from infant animals and decreased significantly with age. Thromboxane B2 was the most abundant metabolite released at all ages. Electrical stimulation and epithelium removal did not affect the age difference in prostanoid release. We conclude that increased basal prostanoid release contributes to the reduced spontaneous relaxation in immature guinea pig ASM compared with older animals. By regulating ASM relaxation, prostanoids may play a role in the airway hyperresponsiveness at a young age.

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