Massive postmortem bronchoconstriction in guinea pig lungs

1984 ◽  
Vol 56 (2) ◽  
pp. 308-314 ◽  
Author(s):  
Y. L. Lai ◽  
W. J. Lamm ◽  
D. L. Luchtel ◽  
J. Hildebrandt
Keyword(s):  
Guinea Pig ◽  
Airway Obstruction ◽  
Latent Period ◽  
Lung Tissue ◽  
Inflation Pressure ◽  
Lung Inflation ◽  
High Inflation ◽  
Trapped Gas ◽  
Gas Volume

A special phenomenon (difficult to inflate and deflate) occurring in the postmortem guinea pig lungs was studied in 40 animals. Thirty minutes after excision of the lungs or exsanguination, less than 50% of the lungs could be inflated even at high inflation pressure (34 cmH2O), and most gas was trapped during deflation. The amount of trapped gas volume at 30 min was related to the degree of lung inflation maintained during the 5- to 30-min period after exsanguination. Since stiffness of the lung tissue was unlikely to explain the phenomenon, we speculated airway obstruction as the major factor. No foam or bubbles were found in larger airways and we thus hypothesized that the obstruction was due to bronchoconstriction. This was confirmed histologically in that the lumina of both bronchi and bronchioles were constricted. The latent period to the onset of this constriction was short (approximately 5 min). It was not associated with O2 availability but was delayed an additional 15 min by a thromboxane inhibitor (dazoxiben). Neither maintaining lung temperature at 37 degrees C nor vagotomy and/or cervical transection prevented the constriction. Without exsanguination, onset of bronchoconstriction was delayed by about 1 h. We conclude that postmortem bronchoconstriction may be caused by release of an endogenous constrictor agent.

scholarly journals ANTIBODIES INVOLVED IN ANTIGEN-INDUCED RELEASE OF SLOW REACTING SUBSTANCE OF ANAPHYLAXIS (SRS-A) IN THE GUINEA PIG AND RAT

1967 ◽  
Vol 125 (1) ◽  
pp. 127-147 ◽  
Author(s):  
Daniel J. Stechschulte ◽  
K. Frank Austen ◽  
Kurt J. Bloch
Keyword(s):  
Mast Cells ◽  
Guinea Pig ◽  
Latent Period ◽  
Lung Tissue ◽  
Lysosomal Enzymes ◽  
Time Interval ◽  
Pharmacological Agents ◽  
Peritoneal Tissue ◽  
Definite Time ◽  
Hyperimmune Rabbit

The antigen-induced release of SRS-A and histamine was studied in the guinea pig and rat using whole and fractionated antiserum preparations. Guinea pig 7Sγ1-antibody sensitized sliced guinea pig lung tissue for antigen-induced release of both SRS-A and histamine; neither substance was released from lung tissue prepared with 7Sγ1-antibody. Rats injected intraperitoneally with hyperimmune rabbit or rat antiserum released only SRS-A in significant amounts when challenged with antigen by the same route. A definite time interval between the injection of antiserum and challenge with antigen was required for optimal release of SRS-A. Fractionation of rat antiserum demonstrated that the immunoglobulin responsible for most of the SRS-A release from rat peritoneal tissue was a γG-antibody or fraction thereof. Acting in this capacity, the γG-antibody or its subfraction may be considered a second type of homocytotropic antibody. Fractions of rat antisera containing the first type of homocytotropic antibody, i.e. antibody mediating release of histamine and serotonin, prepared peritoneal tissues for the release of large amounts of these pharmacological agents and only small amounts of SRS-A. Two different mechanisms for the production of PCA lesions in the rat were considered. One of these involves the antigen-induced release of histamine and serotonin from mast cells sensitized by homocytotropic antibody. This reaction has an optimal latent period of 24–72 hr. The second mechanism involves the local combination of antigen with "hyperimmune" heterologous or homologous antisera. This reaction can be elicited after a latent period of 4 but not 24 hr; host complement and leukocyte lysosomal enzymes, as well as SRS-A, may be involved.

PROBLEMS OF COMBINING TUBERCULOSIS OF THE RESPIRATORY ORGANS WITH CYSTIC FIBROSIS

2021 ◽  
pp. 28-31
Author(s):  
А.Г. ИСАЕВА ◽  
Л.Ш. КАСЕНОВА ◽  
Л.Д. БЕКЖАНОВА ◽  
А.М. АБДУКАЛЫКОВ ◽  
З.М. АТАШОВА ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Airway Obstruction ◽  
Lung Tissue ◽  
Clinical Symptoms ◽  
Lesion Area ◽  
Standard Mode ◽  
Chronic Pneumonia

Клиническая симптоматика туберкулеза в сочетании с муковисцидозом была обусловлена суммацией проявлений сочетанной патологии и протекала, как тяжелая хроническая пневмония, непрерывно рецидивирующая, с выраженным синдромом обструкции дыхательных путей. Туберкулезное воспаление характеризовалось большей площадью поражения, деструкцией легочной ткани и обнаружением микобактерий туберкулеза в мокроте. Независимо от наличия сопутствующей патологии применялась химиотерапия в стандартном режиме.Цель исследования: оценить течение заболевания и эффективность лечения туберкулезом органов дыхания с учетом наличия сопутствующих заболеваний. Clinical symptoms of tuberculosis in association with cystic fibrosis was determined by summation of the manifestations of comorbidity and proceeded as severe chronic pneumonia, recurrent continuously, with marked airway obstruction syndrome. Tuberculous inflammation was characterized by a larger lesion area, destruction of the lung tissue and the detection of MBT in sputum. Regardless of the presence of concomitant pathology, chemotherapy was used in standard mode.

The release of slow-reacting substance of anaphylaxis from guinea pig lung: effects of calcium antagonists

1985 ◽  
Vol 63 (1) ◽  
pp. 23-29 ◽  
Author(s):  
Melissa A. Damiano ◽  
Edward J. Barbieri
Keyword(s):  
Guinea Pig ◽  
Intracellular Calcium ◽  
Lung Tissue ◽  
Calcium Antagonists ◽  
Lung Parenchyma ◽  
Free Medium ◽  
Bicarbonate Buffer ◽  
Normal Medium ◽  
Voltage Dependent ◽  
High Concentrations

The effects of three calcium antagonists, verapamil, lanthanum, and 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate (TMB-8) were studied on the release of slow-reacting substance of anaphylaxis (SRS-A) from ovalbumin-sensitized chopped guinea pig lung parenchyma in calcium-containing and calcium-free media. The SRS-A levels (mean ± SEM) obtained from tissues incubated in normal and calcium-free Krebs–bicarbonate buffer were 51 ± 8 (N = 19) and 21 ± 4 (N = 14) U/mL, respectively. TMB-8 (0.1–10 μM) a reported intracellular calcium antagonist, reduced antigen-stimulated SRS-A release from lung tissue incubated in calcium-containing, but not calcium-free, medium; A23187-induced SRS-A release from normal guinea pig lung was not significantly altered by TMB-8 at concentrations up to 10 μM. Verapamil and lanthanum consistently reduced SRS-A release only at high concentrations (100 μM and 1 mM, respectively). The quantities of SRS-A released from lung tissue incubated in the presence of verapamil in normal medium were similar to those obtained in calcium-free medium. Tissues incubated in the presence of potassium chloride (60 and 100 mM) did not release significant quantities of SRS-A, and release which did occur was not blocked by verapamil, suggesting that antigen-induced SRS-A release is not dependent on membrane depolarization and that verapamil was not exerting inhibition via blockade of voltage-dependent calcium channels. These data suggest that although intracellular calcium is important for the regulation of SRS-A secretion from guinea pig lung tissue, extracellular calcium is necessary for optimal release of SRS-A.

A comparison of the effect of inhaled diuretics on airway reflexes in humans and guinea pigs

1992 ◽  
Vol 72 (2) ◽  
pp. 434-438 ◽  
Author(s):  
J. A. Karlsson ◽  
N. B. Choudry ◽  
C. Zackrisson ◽  
R. W. Fuller
Keyword(s):  
Citric Acid ◽  
Guinea Pig ◽  
Airway Obstruction ◽  
Guinea Pigs ◽  
Airway Resistance ◽  
Loop Diuretic ◽  
Airflow Obstruction ◽  
Respiratory Resistance ◽  
Airway Mucosa ◽  
Maximum Inhibition

The effects of nebulized diuretics on citric acid-induced cough and airway obstruction in guinea pigs and capsaicin-induced cough and increase in airway resistance in humans have been studied. Half-maximum inhibition of cough in the guinea pig was produced by 1.3 mM furosemide and 0.25 mM hydrochlorothiazide. Cough was inhibited by 78 +/- 9% by 3 mM furosemide (P less than 0.05) and 89 +/- 11% by 3 mM hydrochlorothiazide (P less than 0.01). At the same time, airway obstruction was inhibited by 50 +/- 9% (P less than 0.001) and 42 +/- 15% (P less than 0.05), respectively. Nebulized furosemide (3 mM) was without effect on the airway obstruction produced by inhaled histamine or acetylcholine in the guinea pigs. Intravenously administered furosemide (270 nmol/kg) did not affect citric acid-induced responses. In humans, aerosolized furosemide (9 mM) and hydrochlorothiazide (3.4 mM) reduced the percent increase in respiratory resistance from 22.1 +/- 3.7 and 15.6 +/- 3.4 to 10.5 +/- 4.9 and 9.4 +/- 3.3%, respectively (P less than 0.05), but were without effect on cough due to capsaicin. Thus both furosemide and hydrochlorothiazide inhibited airway obstruction in the guinea pig and reduced the capsaicin-induced increase in airway resistance in humans. However, whereas coughing was inhibited in the guinea pig, neither drug affected cough in humans. This difference in the action of the loop diuretic and thiazide, which interact differently with Na(+)-K(+)-Cl-transport within the airway mucosa, on the cough and airflow obstruction in guinea pig and humans supports the view that different sensory limbs are involved in these reflexes.(ABSTRACT TRUNCATED AT 250 WORDS)

Power spectra of inspiratory nerve activity with lung inflations in cats

1988 ◽  
Vol 64 (4) ◽  
pp. 1709-1720 ◽  
Author(s):  
C. A. Richardson
Keyword(s):  
High Frequency ◽  
Power Spectra ◽  
High Peak ◽  
Spectral Peak ◽  
Respiratory Pattern ◽  
Inflation Pressure ◽  
High Frequency Peak ◽  
Lung Inflation ◽  
Consistent Manner ◽  
Inspiratory Activity

To investigate the effect of lung inflations on the high-frequency synchrony (70-122 Hz) observed in the inspiratory activity of respiratory motor nerves of decerebrate cats, I applied a step increase in lung inflation pressure at fixed delays into the inspiratory phase and computed power spectra of phrenic neurograms before and during inflation. In 25 decerebrate paralyzed cats the frequency of the high spectral peak was 92.3 +/- 11.1 Hz before and 105.3 +/- 12.1 Hz during the step in inflation pressure, shifting upward by 13.0 +/- 6.0 Hz. For 8 of the 25 cats, the recurrent laryngeal and phrenic neurograms were recorded simultaneously. The high spectral peak was present during inspiration in the recurrent laryngeal power spectra and coherent with the high peak in the phrenic power spectra. In response to lung inflation, the high peak disappeared from the power spectra of the recurrent laryngeal nerve as the inspiratory activity was inhibited; a shift upward in frequency was not detectable. Comparing inspiratory times (TI, based on the phrenic neurograms) for breaths with no lung inflations to those for breaths with lung inflations, I found that lung inflations early in inspiration caused a decrease in TI, lung inflations at intermediates times had no effect on TI, and lung inflations late in inspiration caused an increase in TI. Despite lung inflation decreasing, not affecting, or increasing inspiratory duration and amplitude of the phrenic neurogram, lung inflation always caused a shift upward in the high-frequency peak of the phrenic power density. The fact that lung inflation, a powerful respiratory stimulus, affected the frequency of the high peak in a consistent manner suggests that the high-frequency synchrony is an important and robust feature of the central respiratory pattern generator.

Pulmonary mechanics during induced pulmonary edema in anesthetized dogs

1959 ◽  
Vol 14 (2) ◽  
pp. 177-186 ◽  
Author(s):  
C. D. Cook ◽  
J. Mead ◽  
G. L. Schreiner ◽  
N. R. Frank ◽  
J. M. Craig
Keyword(s):  
Pulmonary Edema ◽  
Lung Compliance ◽  
Tidal Range ◽  
Pulmonary Mechanics ◽  
Vascular Congestion ◽  
Anesthetized Dogs ◽  
Trapped Gas ◽  
Aortic Obstruction ◽  
Gas Volume ◽  
Normal Lungs

In order to study the mechanisms underlying the changes in the mechanical properties of the lungs during pulmonary edema, pulmonary vascular congestion was produced in spontaneously breathing, anesthetized dogs by partial aortic obstruction and intravenous infusion. Brief periods of congestion were associated with small changes in the lung compliance compared with the progressive and striking compliance reduction (-78%) noted with more prolonged congestion. Lung volume at end-expiration showed little change if edema fluid and trapped gas as well as the ventilated gas volume were taken into account. When edematous lungs were forcibly inflated beyond the tidal range, it was found that the overall compliance at a distending pressure of 30 cm H2O was not much less (-6%) than that of normal lungs. Furthermore, edematous lungs manifested marked ‘static’ hysteresis during such maneuvers. These findings suggested that surface phenomena were responsible for the mechanical behavior of edematous lungs rather than vascular congestion, per se, or intrinsic tissue changes. This was borne out by experiments on excised lungs which showed that the elastic properties of edematous lungs were not significantly different from normal lungs when surface forces were minimized. Submitted on August 25, 1958

scholarly journals Lung mechanical and vascular changes during positive- and negative-pressure lung inflations: importance of reference pressures in the pulmonary vasculature

2009 ◽  
Vol 106 (3) ◽  
pp. 935-942 ◽  
Author(s):  
Ferenc Peták ◽  
Gergely Albu ◽  
Enikö Lele ◽  
Zoltán Hantos ◽  
Denis R. Morel ◽  
...  
Keyword(s):  
Negative Pressure ◽  
Time Windows ◽  
Low Frequency ◽  
Lung Mechanics ◽  
Pulmonary Vasculature ◽  
Positive Pressure ◽  
Vascular Changes ◽  
Inflation Pressure ◽  
Lung Inflation ◽  
Impedance Data

The continuous changes in lung mechanics were related to those in pulmonary vascular resistance (Rv) during lung inflations to clarify the mechanical changes in the bronchoalveolar system and the pulmonary vasculature. Rv and low-frequency lung impedance data (Zl) were measured continuously in isolated, perfused rat lungs during 2-min inflation-deflation maneuvers between transpulmonary pressures of 2.5 and 22 cmH2O, both by applying positive pressure at the trachea and by generating negative pressure around the lungs in a closed box. Zl was averaged and evaluated for 2-s time windows; airway resistance (Raw), parenchymal damping and elastance (H) were determined in each window. Lung inflation with positive and negative pressures led to very similar changes in lung mechanics, with maximum decreases in Raw [−68 ± 4 (SE) vs. −64 ± 18%] and maximum increases in H (379 ± 36 vs. 348 ± 37%). Rv, however, increased with positive inflation pressure (15 ± 1%), whereas it exhibited mild decreases during negative-pressure expansions (−3 ± 0.3%). These results demonstrate that pulmonary mechanical changes are not affected by the opposing modes of lung inflations and confirm the importance of relating the pulmonary vascular pressures in interpreting changes in Rv.

Factors affecting trapped gas volume in perfused dog lungs.

1970 ◽  
Vol 29 (3) ◽  
pp. 332-339 ◽  
Author(s):  
J M Hughes ◽  
D Y Rosenzweig
Keyword(s):  
Factors Affecting ◽  
Trapped Gas ◽  
Gas Volume

scholarly journals OCCURRENCE OF DELAYED HYPERSENSITIVITY DURING THE DEVELOPMENT OF ARTHUS TYPE HYPERSENSITIVITY

1958 ◽  
Vol 107 (1) ◽  
pp. 109-124 ◽  
Author(s):  
S. B. Salvin ◽  
Keyword(s):  
Lymph Node ◽  
Guinea Pig ◽  
Latent Period ◽  
Guinea Pigs ◽  
Specific Antigen ◽  
Egg Albumin ◽  
Lymph Node Cells ◽  
Type Inclusion ◽  
Antibody Determination ◽  
Circulating Antibody

Guinea pigs were injected in the footpads with either purified diphtheria toxoid or recrystallized egg albumin in Freund adjuvant without mycobacteria. Each guinea pig was then skin-tested only once with the specific antigen and bled for antibody determination. After injection of the sensitizing antigen, a latent period occurred during which neither sensitivity nor circulating antibody could be detected. A period of delayed sensitivity followed wherein circulating antibody could not be discerned and which could be transferred by lymph node cells. Ultimately, the Arthus type sensitivity developed, accompanied by circulating antibody. The duration and severity of reactions to homologous antigens during the last 2 phases varied with the antigen and with the dose. An increase in the sensitizing dose decreased the duration of the delayed type of allergy, a decrease in the dose prolonged the delayed type. Inclusion of mycobacterium in the sensitizing inoculum tended to introduce delayed sensitivity earlier and delay the onset of Arthus type sensitivity. When specific precipitate in antibody excess was included with the toxoid in the sensitizing dose, the onset of the Arthus phase was hastened. When lymph nodes from a large number of sensitized donors were removed during the latter part of the latent period, recipients of the cells showed a delayed type sensitivity.

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