RESUMEN
Respiratory diseases (especially pneumonia) are very common disorders in pet rats. The suspected diagnosis is mostly based on the clinical signs, thoracic auscultation, and thoracic radiography. However, auscultation is insensitive in determining the severity of the disease, and radiographs are often unremarkable. Non-cardiac thoracic ultrasonography is increasingly used in veterinary medicine; however, it has not been described in detail in rats. Thoracic ultrasonic examination was conducted on 400 client-owned conscious pet rats. The rats were examined in the period from June 2023 to August 2023 in two veterinary clinics. Due to the small size of the animal, different anatomical considerations, and different evaluation protocols, as well as to meet the optimal outcome of detailed thoracic ultrasound, a standard methodological protocol was developed, and the name RATTUS (Rat Thoracic Ultrasound) was proposed. Typical signs of normal RATTUS were described (bat sign, lung sliding, A-lines, abdominal curtain sign, ski jump sign, lung pulse, seashore sign in M-mode, and bamboo sign). The new evaluation of lung inflation symmetry by substernal access was also described. The methodical approach presented and the normal findings description are proposed to be used for a standard/routine thoracic ultrasound examination in pet rats.
RESUMEN
A 1,5-year-old male Maltipoo was presented to the emergency service for dyspnea, weakness, and cough. An echocardiographic examination showed evidence of pulmonary hypertension with a McConnell sign. Lung ultrasound, including color Doppler, was performed and identified two distinct populations of lung consolidation. Color Doppler analysis of the first type of consolidation showed the absence of blood flow within regions of the consolidation and flow amputation. These findings were consistent with the "vascular sign" reported in human medicine and prompted consideration of pulmonary thromboembolism as a differential diagnosis. In the second type of consolidation, color Doppler identified blood flow within the pulmonary vessels of the consolidated lung, forming a "branching tree-like" pattern that followed the anatomical course of the pulmonary vasculature. These findings suggested that blood flow was preserved within the pulmonary vasculature of the consolidated lung and prompted consideration of inflammatory causes of pulmonary pathology. On recheck 6 days later, recanalization of the first type of consolidation was identified with color Doppler. The case was followed serially once a month for 5 months with LUS, which showed continued improvement. Based on a positive fecal Baermann test, a final diagnosis of Angiostrongylus vasorum was made. New or Unique information Provided-this is the first report of color Doppler LUS being used to characterize and help differentiate the cause of lung consolidation in dogs.
RESUMEN
Trimethylamine (TMA) is a gut bacteria product oxidized by the liver to trimethylamine-N-oxide (TMAO). Clinical evidence suggests that cardiovascular disease is associated with increased plasma TMAO. However, little headway has been made in understanding this relationship on a mechanistic and molecular level. We investigated the mechanisms affecting plasma levels of TMAO in Spontaneously Hypertensive Heart Failure (SHHF) rats. Healthy Wistar Kyoto (WKY) and SHHF rats underwent metabolic, hemodynamic, histopathological and biochemical measurements, including tight junction proteins analysis. Stool, plasma and urine samples were evaluated for TMA and TMAO using ultra performance liquid chromatography-mass spectrometry. SHHF presented disturbances of the gut-blood barrier including reduced intestinal blood flow, decreased thickness of the colonic mucosa and alterations in tight junctions, such as claudin 1 and 3, and zonula occludens-1. This was associated with significantly higher plasma levels of TMA and TMAO and increased gut-to-blood penetration of TMA in SHHF compared to WKY. There was no difference in kidney function or liver oxidation of TMA to TMAO between WKY and SHHF. In conclusion, increased plasma TMAO in heart failure rats results from a perturbed gut-blood barrier and increased gut-to-blood passage of TMAO precursor, i.e., TMA. Increased gut-to-blood penetration of bacterial metabolites may be a marker and a mediator of cardiovascular pathology.
Asunto(s)
Bacterias/química , Insuficiencia Cardíaca/microbiología , Metilaminas/sangre , Animales , Cromatografía Líquida de Alta Presión , Heces/química , Heces/microbiología , Microbioma Gastrointestinal , Insuficiencia Cardíaca/sangre , Insuficiencia Cardíaca/etiología , Insuficiencia Cardíaca/orina , Masculino , Espectrometría de Masas , Metilaminas/orina , Ratas , Ratas Endogámicas SHR , Ratas Endogámicas WKYRESUMEN
Trimethylamine-oxide (TMAO) is present in seafood which is considered to be beneficial for health. Deep-water animals accumulate TMAO to protect proteins, such as lactate dehydrogenase (LDH), against hydrostatic pressure stress (HPS). We hypothesized that TMAO exerts beneficial effects on the circulatory system and protects cardiac LDH exposed to HPS produced by the contracting heart. Male, Sprague-Dawley and Spontaneously-Hypertensive-Heart-Failure (SHHF) rats were treated orally with either water (control) or TMAO. In vitro, LDH with or without TMAO was exposed to HPS and was evaluated using fluorescence correlation spectroscopy. TMAO-treated rats showed higher diuresis and natriuresis, lower arterial pressure and plasma NT-proBNP. Survival in SHHF-control was 66% vs 100% in SHHF-TMAO. In vitro, exposure of LDH to HPS with or without TMAO did not affect protein structure. In conclusion, TMAO reduced mortality in SHHF, which was associated with diuretic, natriuretic and hypotensive effects. HPS and TMAO did not affect LDH protein structure.
Heart failure is a common cause of death in industrialized countries with aging populations. Japan, however, has lower rates of heart failure and fewer deaths linked to this disease than the United States or Europe, despite having the highest proportion of elderly people in the world. Dietary differences between these regions may explain the lower rate of heart failure in Japan. The Japanese diet is rich in seafood, which contains nutrients that promote heart health, such as omega-3 fatty acids. Seafood also contains other compounds, including trimethylamine oxide (TMAO). Fish that live in deep waters undergo high pressures, which can damage their proteins, but TMAO seems to protect the proteins from harm. In humans, eating seafood increases TMAO levels in the blood and urine, but it is unclear what effects this has on heart health. Increased levels of TMAO in the blood are associated with cardiovascular diseases, but scientists are not sure whether TMAO itself harms the heart. A toxic byproduct of gut bacteria called TMA is converted in TMAO in the body, so it is possible that TMA rather than TMAO is to blame. To assess the effects of dietary TMAO on heart failure, Gawrys-Kopczynska et al. fed the compound to healthy rats and rats with heart failure for one year. TMAO had no effects on the healthy rats. Of the rats with heart failure that were fed TMAO, all of them survived the year, while one third of rats with heart failure that were not fed TMAO died. TMAO-treated rats with heart failure had lower blood pressure and urinated more than untreated rats with the condition. The experiments suggest that dietary TMAO may mimic the effects of heart failure treatments, which remove excess water and salt and lower pressure on the heart. More studies are needed to confirm whether TMAO has this same effect on humans.