Monthly, daily, and circadian variations of measurements of pulmonary mechanics in horses with chronic obstructive pulmonary disease

OBJECTIVES: To determine temporal variations of pulmonary function in horses without respiratory tract disease (controls) and horses with chronic obstructive pulmonary disease (COPD) and determine whether reversibility of airway obstruction after environmental control can be predicted by response to atropine administration. ANIMALS: 7 COPD-affected and 5 control horses. PROCEDURES: Pulmonary function testing was performed monthly during 3 consecutive months, daily for 5 consecutive days, and at 6-hour intervals for 24 hours before and after administration of atropine (0.02 mg/kg of body weight, i.v.) and after 5 consecutive months at pasture. Respiratory rate, tidal volume (VT), minute ventilation (VE), maximal change in transpulmonary pressure (deltaP(L)), pulmonary resistance (R(L)), and pulmonary elastance (E(L)) were calculated. RESULTS: COPD-affected horses had a significantly higher expiratory to inspiratory time ratio (T(E)/T(I)) and deltaP(L), E(L), and R(L) than horses without respiratory tract diseases during all periods and higher V(E) during monthly and daily evaluations. Daily variation in VT and monthly and circadian variation in E(L) were significant in COPD-affected horses. In control horses, significant changes were apparent only in T(E)/T(I) during daily recordings. In COPD-affected horses, reduction in deltaP(L), R(L), and E(L) was significant after atropine administration and after maintenance on pasture. CONCLUSIONS AND CLINICAL RELEVANCE: Despite variations in measurements of respiratory mechanics in both groups of horses, values remained significantly different between groups over time. Despite individual variation, measurements were repeatable during short and long periods. Response to administration of atropine to COPD-affected horses underestimated improvement in respiratory tract function that resulted from maintenance on pasture.     

Oxymorphone: cardiovascular, pulmonary, and behavioral effects in dogs

Cardiovascular, pulmonary, and behavioral effects of multiple doses of oxymorphone in 10 nonanesthetized, spontaneously breathing, healthy dogs were studied. Oxymorphone (0.4 mg/kg of body weight) was administered IV, and at 20, 40, and 60 minutes after the first injection was given, 0.2 mg of oxymorphone/kg was administered. Cardiovascular and pulmonary variables were measured before (base line) and at 5, 15, 35, 55, 75, 100, 120, 150, 180, 210, 240, 270, and 300 minutes after the first oxymorphone injection. Degree of sedation and behavioral effects also were recorded. Naloxone (0.04 mg/kg, IV) was administered 4.5 hours after the 4th oxymorphone injection, and behavioral changes were recorded. Oxymorphone induced mild respiratory depression. After transient apnea developed, respiratory rate increased to a pant, tidal volume decreased, and minute ventilation increased, but these values were not significantly (P = 0.05) different from base line. The PaCO2, physiologic dead space, and base deficit increased; alveolar tidal volume decreased; and alveolar minute ventilation did not change. The PaO2 decreased, hemoglobin and arterial O2 content increased, and O2 transport did not change. Venous admixture transiently increased. Oxymorphone induced minimal cardiovascular depression. Mean arterial blood pressure, stroke volume, central venous pressure, pulmonary artery pressure, and pulmonary wedge pressure increased. Heart rate decreased, systemic vascular resistance transiently increased, and cardiac output transiently decreased. Because the dogs moved spontaneously, responded to sound with sudden, vigorous movements, and breathed with excessive effort, oxymorphone alone was considered inadequate as a general anesthetic.     

Calcium antagonists,diltiazem and nifedipine,protect broilers against low temperature‐induced pulmonary hypertension and pulmonary vascular remodeling

This study was designed to determine whether calcium antagonists, diltiazem and nifedipine, can depress low temperature‐induced pulmonary hypertension (PH) in broilers (also known as ascites) and to characterize their efficacy on hemodynamics and pulmonary artery function. Chicks were randomly allocated into six experimental groups and orally administered with vehicle, 5.0 mg/kg body weight (BW)/12 h nifedipine or 15.0 mg/kg BW/12 h diltiazem from 16 to 43 days of age under low temperature. The mean pulmonary arterial pressure (mPAP), the ascites heart index (AHI), the erythrocyte packed cell volume (PCV) and the relative percentage of medial pulmonary artery thickness were examined on days 29, 36 and 43. The data showed that administration of diltiazem protected broilers from low temperature‐induced pulmonary hypertension and vascular remodeling. Although nifedipine prevented mPAP from increasing during the early stage, it did not suppress the development of PH during the late stage and did not keep heart rate (HR), PCV, AHI and the thickness of pulmonary small artery smooth muscle layer at the normal levels. Taken together, our results showed that diltiazem can effectively prevent low temperature‐induced pulmonary hypertension in broilers with fewer side‐effects and may be a potential compound for the prevention of this disease in poultry industry.     

Subcutaneous emphysema, pneumomediastinum, and pulmonary emphysema in a young schipperke

A 4-month-old, intact female schipperke was presented for evaluation and treatment of subcutaneous (SC) emphysema. Radiographs revealed pneumomediastinum and SC emphysema. Sequential radiographs confirmed a worsening of the SC emphysema. Extensive, nonsurgical evaluation failed to reveal the source of the air within the mediastinum. Exploratory thoracotomy revealed an emphysematous right middle lung lobe. Lobectomy of the right middle lung lobe resolved both the pneumomediastinum and SC emphysema. Histopathological evaluation confirmed pulmonary emphysema. A variation of congenital pulmonary emphysema was considered in this case.     

Abscess disease, caseous lymphadenitis, and pulmonary adenomatosis in imported sheep

The occurrence of abscess disease, caseous lymphadenitis, and pulmonary adenomatosis in sheep in Denmark is reported for the first time. Subcutaneous abscesses were observed in imported 4- to 5-month-old lambs of the Lacaune breed 10 days after arrival in Denmark. Abscesses were mostly located in the head, neck and shoulder regions close to the regional lymph nodes. Bacteriological examinations revealed growth of Staphylococcus aureus ssp. anaerobius in all animals with subcutaneously located abscesses containing a viscous white-yellow odourless mass. In addition, Corynebacterium pseudotuberculosis was isolated from abscesses in one animal and lesions consistent with pulmonary adenomatosis were found in four animals.     

Effect of L-NAME on pulmonary arterial pressure,plasma nitric oxide and pulmonary hypertension syndrome morbidity in broilers

1. Experiments were conducted to evaluate the effect of a synthetic inhibitor of nitric oxide (NO) synthase (L-NAME) on pulmonary arterial pressure (PAP) and pulmonary hypertension syndrome (PHS) morbidity in broilers. 2. In Experiment 1, broilers were infused intravenously with L-NAME, and the mean pulmonary arterial pressure (mean PAP) and plasma NO were measured at 0, 1, 2 and 4 h after the start of infusion. The mean PAP increased and plasma NO was reduced at 1 to 2 h in broilers treated with L-NAME. 3. In Experiment 2, 180 Arbor Acres broilers were evenly divided into three groups: a control group (group C), and two groups exposed to low environmental temperatures and fed a 3, 3, 5-triiodothyronine (T3) supplemented diet alone (group A) or also including 100 ppm L-NAME (group B). 4. The PHS morbidity of group A was higher than for group C but lower than for group B. Plasma endothelin-1 was higher in broilers in groups A and B than in group C. Plasma NO was not significantly lower in broilers of group B when compared with those in group A. 5. The right/total ventricular weight ratio (RV/TV) and mean PAP were higher in groups A and B than in group C, and the RV/TV ratio increased one week earlier in group B than in group A. 6. These results suggest that L-NAME increases broiler PAP by inhibiting the endogenous synthesis of NO, leading to pulmonary hypertension, right ventricular hypertrophy and the increased morbidity of PHS in broilers.     

Correlation of clinical score, intrapleural pressure, cytologic findings of bronchoalveolar fluid, and histopathologic lesions of pulmonary tissue in horses with summer pasture-associated obstructive pulmonary disease

OBJECTIVE: To correlate clinical score, intrapleural pressure, cytologic findings of bronchoalveolar lavage fluid (BALF), and histologic lesions of pulmonary tissue in horses affected with summer pasture-associated obstructive pulmonary disease (SPAOPD). ANIMALS: 8 adult horses affected with SPAOPD and 6 adult horses without evidence of respiratory tract disease. PROCEDURE: Clinical score, change in intrapleural pressure (deltaPpl) during tidal breathing, results of cytologic examination and bacteriologic culture of BALF, and results of histologic examination of pulmonary parenchyma were evaluated. RESULTS: Clinical scores for SPAOPD-affected horses (median, 5.75; range, 4.0 to 7.5) were significantly greater, compared with clinically normal horses (median, 2.0; range, 2.0 to 3.0). Cytologic examination of BALF from SPAOPD-affected horses revealed predominantly nondegenerate neutrophils. Histologic lesions were identified throughout pulmonary tissue and included severe accumulation of mucus and neutrophils within the small airways, metaplasia of bronchiolar goblet cells, and mild peribronchial infiltrate. Histologic examination of specimens collected via percutaneous biopsy was predictive of disease and corresponded to findings at postmortem examination. Clinical score and deltaPpl were highly correlated with mucus accumulation in the airways of affected horses. Peribronchial inflammatory infiltrate correlated with percentage of neutrophils in BALF of affected horses. CONCLUSIONS AND CLINICAL RELEVANCE: Clinical scoring and deltaPpl provided valid estimates of disease severity. Findings from cytologic examination of BALF of SPAOPD-affected horses varied, although, in most instances, it was diagnostically useful. Severe mucus accumulation in the airways was the most remarkable histopathologic finding in SPAOPD-affected horses. Examination of biopsy specimens collected from pulmonary parenchyma was consistently useful in diagnosing SPAOPD.     

Plasma pharmacokinetics, pulmonary distribution, and in vitro activity of gamithromycin in foals

The objectives of this study were to determine the plasma and pulmonary disposition of gamithromycin in foals and to investigate the in vitro activity of the drug against Streptococcus equi subsp. zooepidemicus (S. zooepidemicus) and Rhodococcus equi. A single dose of gamithromycin (6 mg/kg of body weight) was administered intramuscularly. Concentrations of gamithromycin in plasma, pulmonary epithelial lining fluid (PELF), bronchoalveolar lavage (BAL) cells, and blood neutrophils were determined using HPLC with tandem mass spectrometry detection. The minimum inhibitory concentration of gamithromycin required for growth inhibition of 90% of R. equi and S. zooepidemicus isolates (MIC(90)) was determined. Additionally, the activity of gamithromycin against intracellular R. equi was measured. Mean peak gamithromycin concentrations were significantly higher in blood neutrophils (8.35±1.77 μg/mL) and BAL cells (8.91±1.65 μg/mL) compared with PELF (2.15±2.78 μg/mL) and plasma (0.33±0.12 μg/mL). Mean terminal half-lives in neutrophils (78.6 h), BAL cells (70.3 h), and PELF (63.6 h) were significantly longer than those in plasma (39.1 h). The MIC(90) for S. zooepidemicus isolates was 0.125 μg/mL. The MIC of gamithromycin for macrolide-resistant R. equi isolates (MIC(90)=128 μg/mL) was significantly higher than that for macrolide-susceptible isolates (1.0 μg/mL). The activity of gamithromycin against intracellular R. equi was similar to that of azithromycin and erythromycin. Intramuscular administration of gamithromycin at a dosage of 6 mg/kg would maintain PELF concentrations above the MIC(90) for S. zooepidemicus and phagocytic cell concentrations above the MIC(90) for R. equi for approximately 7 days.     

A case of acute pulmonary edema, splenomegaly, and ascites in guinea fowl

Acute pulmonary edema, splenomegaly, and ascites were observed in a disease outbreak in adult white and pearl guinea fowl. The clinical history and gross and microscopic lesions resembled those described for marble spleen disease of pheasants and avian adenovirus group II splenomegaly of chickens. A small number of intranuclear inclusion bodies were found in liver, spleen, and lung sections of affected guinea fowl. Attempts to isolate virus and serological tests to detect the presence of viral antigens were unsuccessful. Adult female pearl guinea fowl experimentally exposed to pheasant and turkey isolates of type II avian adenoviruses developed gross and microscopic lesions similar to those seen in the field outbreak. The pheasant isolate was the more virulent. Intranuclear inclusion bodies were observed in liver, spleen, and lung sections of pearl guinea fowl inoculated with either of the virus isolates, and direct immunofluorescent examination revealed viral antigen in the spleen and lung.     

Pneumopericardium,pneumomediastinum, pneumothorax and pneumoretroperitoneum complicating pulmonary metastatic carcinoma in a cat

This report describes a case of severe spontaneous tension pneumopericardium with concurrent pneumomediastinum, pneumothorax and retropneumoperitoneum in a cat presenting with dyspnoea and signs of cardiac tamponade secondary to metastatic pulmonary carcinoma. Spontaneous pneumopericardium is an extremely uncommon condition consisting of pericardial gas in the absence of iatrogenic/traumatic causes. In humans, it has been described secondary to pneumonia or lung abscess and very rarely secondary to pulmonary neoplasia.     

Clinicopathologic features,comorbid diseases,and prevalence of pulmonary hypertension in dogs with bronchomalacia

BackgroundReports of clinicopathologic features of bronchomalacia (BM) differ because of inconsistent definitions and frequent prevalence of comorbid cardiopulmonary disease. Pulmonary hypertension (PH) secondary to BM is poorly described.ObjectivesDogs with BM will be older but of any somatotype, and increased expiratory effort, ≥1 comorbid disease, and PH will be more common than in dogs without BM.AnimalsClient‐owned dogs (n = 210) evaluated for respiratory signs.MethodsMedical records of dogs with paired inspiratory: expiratory‐breath‐hold computed tomography, tracheobronchoscopy, or both between January 2016 and December 2019 were retrospectively reviewed. Comparisons between dogs with and without BM using Mann‐Whitney rank sum or χ ² tests (P < .05 significant were made). Because of high numbers of variables, criteria with high prevalence (>25%) were identified (n = 10) for univariate analysis (P < .005 significant). Significant variables were submitted for multivariate analysis.ResultsBronchomalacia was identified in 41% of dogs of all sizes/somatotypes; 38% were >10 kg. All dogs with BM had ≥1 comorbid cardiopulmonary disorder. Dogs with BM were significantly older (P < .001), smaller (P < .001), and were more likely diagnosed with tracheal or mainstem bronchial collapse (P < .001) or bronchiectasis (P < .001). Multivariate analysis confirmed associations with age, tracheal or mainstem bronchial collapse, and bronchiectasis. In dogs with BM, PH was more prevalent.Conclusions and Clinical ImportanceAlthough significantly more common in older, smaller dogs, BM occurs in dogs of all sizes and in all instances with comorbidities. Echocardiography should be considered in dogs with BM to identify PH.     

Relationship between pulmonary arterial pressure and lesions in the pulmonary arteries and parenchyma, and cardiac valves in canine dirofilariasis.

The relationship between pulmonary hypertension and lesions was examined in 41 dogs infested naturally with heartworms, which consisted of 28 cases with pulmonary heartworm disease and 13 cases with caval syndrome. Pulmonary arterial pressure (PAP) was measured before and 1 or 7 days after heartworm removal with a flexible alligator forceps. In these dogs, lesions were examined after the last measurement of PAP. The mean PAP was 28.2 +/- 16.0 mmHg (10.9 to 81.4 mmHg in range) at post-removal phase. Pulmonary arterial intimal lesions, pulmonary thromboemboli, pneumonic lesions, tricuspid valvular lesions and mitral valvular lesions were macroscopically recognized in 95, 59, 39, 54 and 56% of cases, respectively. These lesions were classified by severity and the relationship with PAP was examined by the multiple correlation analysis. The multiple coefficient correlation was found the highest between PAP and thromboemboli, followed by mitral valvular lesion, tricuspid valvular lesion, and pneumonic lesion. There was no significant correlation between PAP and intimal lesions. The coefficient of determination showed the highest value in thromboemboli when one variable was used, and increased only very slightly when a variable of thromboemboli was added to those of other lesions. The cases with high PAP had fresh thromboemboli in large pulmonary arteries. From these evidences, it was concluded that thromboemboli following natural death of heartworm was the most important factor causing an increase in PAP and developing clinical signs in canine heartworm disease.     

Clinical, radiographic, endoscopic, bronchoalveolar lavage and lung biopsy findings in horses with exercise-induced pulmonary hemorrhage

A clinical study was performed to determine whether clinical, endoscopic, radiographic, bronchoalveolar lavage (BAL) cytological, and pulmonary biopsy findings could be correlated in horses with exercise-induced pulmonary hemorrhage (EIPH) compared with controls. Racing standardbred horses were selected as either EIPH (n = 10) or control (n = 10), based on repeated postexertional endoscopy of the lower airways. Complete physical and respiratory examinations were performed and blood samples were submitted for arterial blood gas analysis, hematologic study, and fibrinogen determination. Bilateral chest radiographs were taken with the horse standing, and a BAL sample was obtained for cytological examination. Lung was biopsied transcutaneously. Weighted scores were calculated for clinical, radiographic, and pulmonary biopsy findings. The conclusion was that only routine physical examination may help the clinician when EIPH is suspected in horses, especially when there are abnormal findings on percussion of the caudodorsal areas of the chest.     

NT-proBNP, NT-proANP and cTnI concentrations in dogs with pre-capillary pulmonary hypertension

Objectives

To compare [NT-proBNP], [NT-proANP] and [cTnI] between control dogs with respiratory disease without pulmonary hypertension (PH) and dogs with pre-capillary PH, and to assess the accuracy of [NT-proBNP], [NT-proANP], [cTnI] to predict Doppler-derived peak tricuspid regurgitation (TR) gradient.

Animals

20 dogs. 8 control dogs with respiratory disease with no PH and 12 with pre-capillary PH.

Methods

[NT-proBNP], [NT-proANP] and [cTnI] were compared between the 2 groups and simple linear regression analysis was used to predict peak TR gradients from various blood biomarkers.

Results

Median [NT-proBNP] was higher in the dogs with PH (2011 pmol/L, 274–7713 pmol/L) compared to control dogs (744 pmol/L; 531–2710 pmol/L) (p = 0.0339). [NT-proBNP] was associated with peak TR gradient (R² = 0.7851, p = 0.0001). Median [NT-proANP] did not differ between dogs with PH (1747 fmol/L; 894–2884 fmol/L) and control dogs (1209 fmol/L; 976–1389 fmol/L (p = 0.058). [NT-proANP] was not associated with peak TR gradient (R² = 0.2780, p = 0.0781). Median [cTnI] did not differ between dogs with PH (0.2850 ng/mL; 0.19–1.13 ng/mL) and control dogs (0.2 ng/mL; 0.19–0.82 ng/mL, p = 0.3051). Median [TnI] was not associated with peak TR gradient (R² = 0.024, p = 0.6307).

Conclusions

[NT-proBNP] concentration is significantly higher in dogs with pre-capillary PH when compared to dogs with respiratory disease without PH, and [NT-proBNP] may be useful to predict the severity of estimated PH. Elevations in [NT-proBNP] due to pre-capillary PH may complicate the interpretation of [NT-proBNP] elevations in patients presenting with cardiorespiratory abnormalities. [NT-proANP] and [cTnI] were not elevated in dogs with pre-capillary PH.     

Effects of ketanserin on pulmonary hemodynamics, lung mechanics, and gas exchange in endotoxemic pigs

The effects of ketanserin on pulmonary hemodynamics, lung mechanics, and gas exchange were determined in anesthetized 10- to 14-week-old pigs after they were endotoxemic for 1 or 4.5 hours. Saline solution was given to controls (group 1). Escherichia coli endotoxin (055-B5) was infused IV at a dosage of 5 micrograms/kg for 1 hour (group 2). In group 3, endotoxin was infused at 5 micrograms/kg the first hour plus a continuous infusion of endotoxin at 2 micrograms/kg/hr. Ketanserin, a specific serotonin receptor antagonist, was infused IV (300 micrograms/kg) after pigs were endotoxemic for 1 or 4.5 hours (groups 2 and 3, respectively). At 1 hour of endotoxemia, mean pulmonary artery pressure and pulmonary vascular resistance were increased, and cardiac index was decreased. Ketanserin caused a small attenuation of the increases in mean pulmonary artery pressure and pulmonary vascular resistance, indicating that serotonin may have a small role in the endotoxin response at 1 hour. At 4.5 hours of endotoxemia, mean pulmonary artery pressure, pulmonary vascular resistance, alveolar dead space ventilation, and alveolar-arterial oxygen gradient were increased, and cardiac index and lung dynamic compliance were decreased; ketanserin significantly attenuated the endotoxin-induced changes in cardiac index, mean pulmonary artery pressure, pulmonary vascular resistance, and lung dynamic compliance. Ketanserin also decreased the blood temperature after pigs were endotoxemic for 4.5 hours. However, the endotoxin-induced increases (at 4.5 hours) in alveolar-arterial oxygen gradient and alveolar dead space ventilation were not acutely reversed by ketanserin.(ABSTRACT TRUNCATED AT 250 WORDS)     

ACVIM consensus statement guidelines for the diagnosis,classification, treatment,and monitoring of pulmonary hypertension in dogs

Pulmonary hypertension (PH), defined by increased pressure within the pulmonary vasculature, is a hemodynamic and pathophysiologic state present in a wide variety of cardiovascular, respiratory, and systemic diseases. The purpose of this consensus statement is to provide a multidisciplinary approach to guidelines for the diagnosis, classification, treatment, and monitoring of PH in dogs. Comprehensive evaluation including consideration of signalment, clinical signs, echocardiographic parameters, and results of other diagnostic tests supports the diagnosis of PH and allows identification of associated underlying conditions. Dogs with PH can be classified into the following 6 groups: group 1, pulmonary arterial hypertension; group 2, left heart disease; group 3, respiratory disease/hypoxia; group 4, pulmonary emboli/pulmonary thrombi/pulmonary thromboemboli; group 5, parasitic disease (Dirofilaria and Angiostrongylus); and group 6, disorders that are multifactorial or with unclear mechanisms. The approach to treatment of PH focuses on strategies to decrease the risk of progression, complications, or both, recommendations to target underlying diseases or factors contributing to PH, and PH-specific treatments. Dogs with PH should be monitored for improvement, static condition, or progression, and any identified underlying disorder should be addressed and monitored simultaneously.