Ventilatory failure induced by tracheal banding in the hamster

1992 ◽  
Vol 73 (4) ◽  
pp. 1671-1675 ◽  
Author(s):  
W. D. Reid ◽  
J. Noonan ◽  
F. Chung ◽  
C. Tesler-Mabe

Previous animal models of hypercapnic ventilatory failure are limited in that the resistive load has only been applied acutely and often in anesthetized animals. We therefore developed a chronic animal model of hypercapnic ventilatory failure by increasing airway resistance via tracheal banding over several days. To test the efficacy of this model, we compared arterial blood gases, pulmonary function, and internal area of the trachea 6 days after the banding or sham procedure in 20 hamsters. Six days later, banded animals had an increased airway resistance as indicated by a 66% reduction in internal cross-sectional area of the trachea and a 6.5-fold increase in pulmonary resistance compared with control hamsters. The increased airway resistance resulted in a severe respiratory acidosis and hypoxemia in the awake banded hamsters. Banded hamsters were also hyperinflated. This animal model will be useful for investigating the various mechanisms that contribute to hypercapnic ventilatory failure and interventions that may promote recovery.

Author(s):  
Mayra Asas-Jinde ◽  
Fabricio González-Andrade

Abstract Newborns show physiological differences in low- and high-altitude settings of Ecuador; those differences are especially relevant because most important cities in Ecuador are located at high altitude, above 2500 m. This study is an epidemiological, observational, and cross-sectional research performed at San Francisco Hospital in Quito (at 2850 m) and General Hospital in Manta (at 6 m) in the Manabí province. We studied 204 full-term newborns, healthy without any prenatal comorbidities, singleton pregnancy, mestizos, and born of healthy parents born. We found significant differences between the values of red blood cells (RBC), leucocytes, hematocrit, and hemoglobin. There was a difference of 27% more in RBC, 3% at hematocrit, and 0.4 g at hemoglobin in the high-altitude cohort. The leucocyte difference is 1270 cells/µl, which means a difference of 6%. At high-altitude settings, the mean pH was lower than normal values and pO2, pCO2, and HCO3. High-altitude newborns showed RBC of > 4,500,000 cells/µl; leukocytes > 19,000; pO2 ≤ 72 mm Hg; hemoglobin > 17.50 g/dl; and hematocrit > 54%. Both cohorts showed physiological changes of transition to extrauterine life. We observed higher polycythemia, respiratory acidosis, and hypoxemia among high-altitude newborns. High-altitude setting intensifies the physiological changes in hematological and arterial blood gases parameters.


1989 ◽  
Vol 67 (5) ◽  
pp. 1747-1753 ◽  
Author(s):  
A. T. Scardella ◽  
T. V. Santiago ◽  
N. H. Edelman

In a previous study in unanesthetized goats, we demonstrated that cerebrospinal fluid levels of beta-endorphin were significantly elevated after 2.5 h of inspiratory flow-resistive loading. Naloxone (NLX) (0.1 mg/kg) administration partially and transiently reversed the tidal volume depression seen during loading. In the current study, we tested the hypothesis that endogenous opioid elaboration results in depression of respiratory output to the diaphragm. In six studies of five unanesthetized goats, tidal volume (VT), transdiaphragmatic pressure (Pdi), diaphragmatic electromyogram (EMGdi), and arterial blood gases were monitored. A continuous NLX (0.1 mg/kg) or saline (SAL) infusion was begun 5 min before an inspiratory flow-resistive load of 120 cmH2O.l-1.s was imposed. Our data show that the depression of VT induced by the load was prevented by NLX as early as 15 min and persisted for 2 h. At 2 h, Pdi was still 294 +/- 45% of the base-line value compared with 217 +/- 35% during SAL. There was no difference in EMGdi between the groups at any time. However, the augmentation of Pdi was associated with a greater increase in end-expiratory gastric pressure in the NLX group. We conclude that the reduction in VT and Pdi associated with endogenous opioid elaboration is not mediated by a decrease in neural output to the diaphragm, but it appears to be the result of a decrease in respiratory output to the abdominal muscles.


2019 ◽  
Vol 15 (2) ◽  
pp. 79-89 ◽  
Author(s):  
Yamely Mendez ◽  
Francisco E. Ochoa-Martinez ◽  
Tatiana Ambrosii

Chronic obstructive lung disease is a common and preventable disease. One of its pathophysiological consequences is the presence of carbon dioxide retention due to hypoventilation and ventilation/perfusion mismatch, which in consequence will cause a decrease in the acid/base status of the patient. Whenever a patient develops an acute exacerbation, acute respiratory hypercapnic failure will appear and the necessity of a hospital ward is a must. However, current guidelines exist to better identify these patients and make an accurate diagnosis by using clinical skills and laboratory data such as arterial blood gases. Once the patient is identified, rapid treatment will help to diminish the hospital length and the avoidance of intensive care unit. On the other hand, if there is the existence of comorbidities such as cardiac failure, gastroesophageal reflux disease, pulmonary embolism or depression, it is likely that the patient will be admitted to the intensive care unit with the requirement of intubation and mechanical ventilation.


1989 ◽  
Vol 66 (6) ◽  
pp. 2895-2900 ◽  
Author(s):  
T. I. Musch ◽  
B. S. Warfel ◽  
R. L. Moore ◽  
D. R. Larach

We compared the effects of three different anesthetics (halothane, ketamine-xylazine, and diethyl ether) on arterial blood gases, acid-base status, and tissue glycogen concentrations in rats subjected to 20 min of rest or treadmill exercise (10% grade, 28 m/min). Results demonstrated that exercise produced significant increases in arterial lactate concentrations along with reductions in arterial Pco2 (PaCO2) and bicarbonate concentrations in all rats compared with resting values. Furthermore, exercise produced significant reductions in the glycogen concentrations in the liver and soleus and plantaris muscles, whereas the glycogen concentrations found in the diaphragm and white gastrocnemius muscles were similar to those found at rest. Rats that received halothane and ketamine-xylazine anesthesia demonstrated an increase in Paco2 and a respiratory acidosis compared with rats that received either anesthesia. These differences in arterial blood gases and acid-base status did not appear to have any effect on tissue glycogen concentrations, because the glycogen contents found in liver and different skeletal muscles were similar to one another cross all three anesthetic groups. These data suggest that even though halothane and ketamine-xylazine anesthesia will produce a significant amount of ventilatory depression in the rat, both anesthetics may be used in studies where changes in tissue glycogen concentrations are being measured and where adequate general anesthesia is required.


2020 ◽  
Author(s):  
Mostafa Mohammadi ◽  
Hesam Aldin Varpaei ◽  
Majid Amini

Abstract Background: In December 2019, a new pathogen, HCoV, or New Corona Virus 2019 (2019-nCoV), was recognized in Wuhan, China, causing a pandemic. COVID-19 has a wide range of clinical severity. Approximately 3.2% of patients within some periods of the disease require intubation and invasive ventilation. Methods: This study was descriptive-analytical and was conducted in the Imam Khomeini Hospital. Patients with Covid-19 who required endotracheal intubation were identified and their clinical signs and laboratory parameters were recorded. SPSS23 software was used for statistical analysis. Results: 120 patients with coronavirus with different conditions were evaluated. The mean age was 55±14. 30 patients had cardiovascular disease (hypertension) and 20 endocrine disease(diabetes). Respiratory acidosis, decreased oxygen saturation, lymphopenia, and increased CRP were the most common finding before intubation. 31 patients had no comorbidity conditions. However, 27 patients had more than one comorbidity condition, and 23 experienced acute respiratory distress syndrome. The mortality rate was 49.2%. Discussion: Although all laboratory parameters and patients symptoms can affect the treatment outcome, it was found that WBC and absolute lymphocyte count, BUN, SOFA and APACHE scores, inflammatory index ratio CRP / LDH % CRP / ESR% and ESR / LDH%, arterial blood gas indices, pulse rate, and patient temperature before intubation are among the parameters that can affect the patient's 14-day prognosis. Conclusion: Except for the mentioned items, CRP / LDH% ratio seems to be a good indicator for checking the prognosis of discharge or death of patients within 14 days, However, CRP / ESR% and ESR / LDH% are appropriate criteria for determining the prognosis for discharge or stay in the ICU for more than 14 days.


1981 ◽  
Vol 51 (1) ◽  
pp. 78-83 ◽  
Author(s):  
Y. L. Lai ◽  
J. E. Lamm ◽  
J. Hildebrandt

Awake rats, with chronically implanted arterial catheters and abdominal thermistors, were continuously exposed to 5 or 7% CO2 in air in an environmental chamber for up to 3 wk. To obtain measurements, rats were transferred to a body plethysmograph flushed with the same CO2 mixture, and, after stabilization, O2 consumption (Vo2), ventilation (VE), and arterial blood gases (ABG) were determined. After 2-h exposure, VE, tidal volume/inspiratory time (VT/TI), and VO2 were significantly increased. Thereafter, VE and VT/TI fell gradually with time, the largest decrease occurring within the 1st day of exposure. The increase in VO2 was maintained up to 3 days and then declined. ABG revealed extensive metabolic compensation for respiratory acidosis within 3–7 days. delta(VT/TI) correlated well with delta VE and delta [HCO3]a (P less than 0.05). It is likely that the gradual return toward normal pHa reduces ventilatory drive (VT/TI), which in turn lowers VE. Estimated alveolar ventilation did not decrease consistently with time in parallel with VE, suggesting that the early ventilatory overshoot might also be due to an increase in dead space.


1986 ◽  
Vol 122 (1) ◽  
pp. 209-222
Author(s):  
ROBERT G. BOUTILIER ◽  
GRAHAM SHELTON

1. Pre- and post-dive breathing patterns, blood oxygenation and acid-base balance have been examined in voluntarily and forcibly submerged Xenopus laevis. 2. Enforced 30-min dives led to a large acidosis with both respiratory (CO2) and metabolic (lactic acid) components. Complete recovery of the arterial blood variables after such dives took more than 4h. 3. Lung ventilation (measured by a pneumotachograph) following enforced dives was always markedly elevated compared with levels either before or after voluntary dives of the same duration. 4. In undisturbed Xenopus, diving freely for periods of 30 min or more, there was no accumulation of lactic acid and the fall in blood oxygen, increase in CO2 and the associated respiratory acidosis were all corrected within the first few breaths upon surfacing. 5. The evidence presented here leads us to conclude that anaerobiosis is unimportant during voluntary dives, even when these are of considerable duration.


1984 ◽  
Vol 57 (2) ◽  
pp. 396-402 ◽  
Author(s):  
R. F. Fregosi ◽  
J. A. Dempsey

For the first time in the rat, we described the effects of exercise on arterial acid-base status and examined the role of chemical stimuli as determinants of the hyperventilatory response in this species. O2 consumption (VO2), CO2 production (VCO2), arterial blood gases, arterial lactate concentration ([LA-]a), and rectal temperature (Tre) were measured in non-trained male rats at rest and during 10 min of treadmill exercise at various intensities. During mild exercise (2.5-fold increase in VCO2), PaCO2 fell 5.5 +/- 0.6 Torr, and despite a small but significant increase in [LA-]a, respiratory alkalosis prevailed [change in arterial pH (delta pHa) = 0.034 +/- 0.006]. Arterial PO2 (PaO2) increased 4.1 +/- 1.5 Torr and Tre increased 0.6 +/- 0.1 degrees C. A progressive hyperventilation occurred from mild to heavy exercise. This response was not attributable to arterial hypoxemia or acidosis and it was not affected by preventing the exercise-induced increase in body temperature. During maximal exercise, VO2 increased 3.4-fold (72 +/- 1.50 ml X kg-1 X min-1) and VCO2 increased 4.5-fold (74 +/- 1.90 ml X kg-1 X min-1), resulting in a 9-fold increase in [LA-]a and a severe metabolic acidosis (pHa 7.31 +/- 0.02). A marked hyperventilation [arterial PCO2 (PaCO2) 28.5 +/- 1.4 Torr] resulted in partial compensation of pHa, but almost all of this hyperventilation occurred before the onset of metabolic acidosis, [i.e., at less than 65% maximum VO2 (VO2max)], and the increased [H+]a with further elevations in VO2 produced no further hypocapnia.(ABSTRACT TRUNCATED AT 250 WORDS)


1978 ◽  
Vol 44 (3) ◽  
pp. 479-482 ◽  
Author(s):  
A. Wanner ◽  
M. E. Reinhart

Most currently used animal models of allergic airway diseases differ from human asthma in that induced bronchospasm in the former is not accompanied by pulmonary hyperinflation. In the present investigation, we chose unsedated, restrained sheep to determine the effect of cholinergic bronchial provocation on respiratory mechanics, functional residual capacity (FRC), and arterial blood gases. Seven animals had been actively sensitized by intramuscular injections of Ascaris suum extract, and four untreated animals served as controls. After inhalation of nebulized 1% methacholine solution, mean pulmonary resistance increased significantly in the sensitized sheep from a base line of 2.4 +/- 0.7 (SD) cmH2O/(l/s) to a peak value after 5 min of 7.9 +/- 4.0 cmH2O/(l/s). This was accompanied by a significant increase of mean FRC from 0.99 +/- 0.14 liters to 1.31 +/- 0.24 liters. The observed changes were transient, and after 60 min, pulmonary resistance and FRC had returned to base-line values. No significant changes occurred in static lung compliance, PaO2, PaCO2, and pH. In the control animals, methacholine provocation did not produce changes in pulmonary function. These results indicate that, in sensitized conscious sheep, induced bronchospasm is associated with pulmonary hyperinflation.


2019 ◽  
Vol 6 (4) ◽  
pp. 1299
Author(s):  
Poonam Gupta ◽  
Anand Kumar ◽  
Ajeet Kumar Chaurasia ◽  
Arvind Gupta

Background: Microalbuminuria is a sign of glomerular dysfunction in general and sign of tubulointerstitial disease to a lesser extent. Hypoxia induces endothelial cell to release a number of different vasoactive agents including endotheline-1, platelet derived growth factor (PDGF), nitric oxide; that causes endothelial injury and lead to microalbuminuria. This study was aimed to assess the prevalence of microalbuminuria in COPD patients and assess the Relationship of microalbuminuria with the disease severity in the forms of FEV1, PaO2, PaCO2, and BODE INDEX in COPD patients.Methods: Total 130 COPD patients were included in our cross sectional study. Total patients were divided into two groups, 1st group was COPD with microalbuminuria while 2nd group was COPD without microalbuminuria. Lung function test, 6 min walk distance, arterial blood pressure (BP), BODE index, arterial blood gases, fasting and post prandial plasma glucose and kidney function tests were measured. Screening for microalbuminuria was done by measuring urinary microalbumin in a random spot urine collection.Results: The prevalence of microalbuminuria was 29.23% in patients of COPD. As compared with COPD without microalbuminuria group, COPD with microalbuminuria group were more hypoxic (12% vs 74%, P=0.0001 ), more hypercapnic (22% vs 84%, p=0.00001) and most of the patients with grade III (16% vs 34%, p=0.00001) or grade IV (19% vs 47%, p=0.00001) severity (according to GOLD criteria).Conclusions: Patients with severe COPD with hypoxemia or hypercapnia were significantly associated with microalbuminuria.


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