MAGNETIC RESONANCE IMAGING FEATURES OF EMPTY SELLA IN DOGS

In humans, the empty sella is defined as herniation of the subarachnoidal space into the sella turcica with invisible (total empty sella) or reduced (partial empty sella) hypophyseal size. An empty sella can be associated with endocrine disturbances. The purpose of this study was to determine if the empty sella exists in dogs or cats and whether it is associated with endocrinopathy or hydrocephalus. Archived magnetic resonance images of the head of 370 dogs and 77 cats were re-evaluated specifically for the presence or absence of the pituitary gland. Hypophyseal tissue filling more than 50% of the sella was considered normal, between 30% and 50% was defined as partial empty sella and less than 30% was defined as total empty sella. In patients with an empty sella, and in all other imaged dogs of the affected breeds, the ventricle to brain ratio was measured. In patients with an empty sella, the medical record was searched for evidence of endocrinopathy. No cat had an empty sella but 11 dogs (3%) had a small or missing hypophysis. Seven of these dogs had a ventricle to brain ratio greater than 15%. Only small dogs (mean weight of 6.7 kg) were affected. One dog with an empty sella had signs of central hyperadrenocorticism while the other 10 had no sign of endocrinopathy. We conclude that the empty sella exists in dogs but is not generally associated with endocrinopathy.     

Feline hip joint anatomy in magnetic resonance images

The aim of this study was to develop an anatomical model of the feline hip joint for low‐field magnetic resonance imaging (LF‐MRI) based on high‐field magnetic resonance imaging (HF‐MRI). The study was performed on six adult clinically healthy European shorthair cats, aged 1–3 years, with body weight of 2.8–4.4 kg. The animals were examined with the use of the Vet‐MRI Grande Esaote LF (0.25 T) scanner and high‐field Siemens Magnetom TRIO (3 T) MRI scanner. In the LF‐MRI, most satisfactory results in T1‐weighted images were obtained when TE was 26 ms in all three planes and when TR was 350–950 ms in the transverse plane, 950–1150 ms in the sagittal plane and 520–750 ms in the dorsal plane. In T2‐weighted images, TE was 90 ms in the transverse and dorsal plane and 120 ms in the sagittal plane. The results were presented as images acquired with LF‐MRI scanners in three planes. The slice thickness was 3 mm for each plane. In LF‐MRI, muscles in the hip joint region and round ligament were well visualized. Unlike in LF‐MRI, the cross section of the femoral nerve was identified in HF‐MRI scans. In examinations of the feline hip joint, the main limitations of LF‐MRI were a lack of reliable contrast between articular cartilage and synovial fluid as well as longer scan time. Despite the above, LF‐MRI images were characterized by good contrast between bones and the surrounding soft tissues.     

Resting concentrations of cardiac troponin I in fit horses and effect of racing

ObjectivesTo determine normal resting values for cardiac troponin I (cTnI) in healthy Standardbred, Thoroughbred and Warmblood horses and investigate if racing has an influence on cTnI concentrations.BackgroundMeasuring cTnI concentrations in plasma is the gold standard for detecting myocardial injury in humans. Cardiac troponin I is highly conserved between species and has gained interest as a marker for cardiac injury in horses. Increased levels of cTnI have been reported in association with endurance and short-term strenuous exercise on a treadmill in horses. However, the effect of true racing conditions has not yet been reported.Animals, materials and methodsBlood samples for analysis of cTnI concentrations in plasma were collected from 67 Standardbred racehorses, 34 Thoroughbred racehorses and 35 Warmblood dressage horses at rest. Blood samples were also collected prior to and after racing in 22 Standardbred racehorses and 6 Thoroughbred racehorses.ResultsAll horses except one had resting plasma cTnI concentrations <0.022 μg/L. Mild increases in cTnI concentrations were seen in some horses 1–2 h after the race (1/17 Standardbreds and 2/6 Thoroughbreds) as well as 10–14 h after the race (4/21 Standardbreds and 1/6 Thoroughbreds).ConclusionsResting cTnI concentrations in horses are low but mildly elevated cTnI concentrations may be detected in some horses 1–14 h after racing. These findings could be of importance when evaluating horses with suspected cardiac disease that recently have performed hard exercise.     

Azotemia in cats with feline hypertrophic cardiomyopathy: Prevalence and relationships with echocardiographic variables

ObjectivesThe prevalence of renal azotemia in cats with acquired heart disease is not well documented. The aims of this study were therefore (1) to determine the prevalence of azotemia within a hospital population of cats with hypertrophic cardiomyopathy (HCM), and (2) to evaluate the relationship between echocardiographic variables and plasma urea and creatinine.Animals, materials and methods134 client-owned cats were retrospectively studied including 102 cats with HCM and 32 control cats. A complete physical examination, electrocardiography, systolic arterial blood pressure measurement, thoracic radiographs, and echocardiography were performed. Plasma creatinine and urea were determined in all cats. The animal was considered azotemic if plasma creatinine was >1.8 mg/dL and/or urea >65 mg/dL (i.e. BUN> 30 mg/dL).ResultsThe prevalence of azotemia was lower in control cats (25.0%) than in cats with HCM (58.8%) (P = 0.003). No significant differences in plasma urea and creatinine were observed between the HCM and control cats. There was no effect of plasma creatinine and urea on conventional echocardiographic variables in cats with HCM.ConclusionsAzotemia is a frequent finding in cats with HCM but is not dependent on echocardiographic variables.     

Effects of different β-adrenergic receptors on cardiac systolic and diastolic functions in hypoxic stress rats

AIM:To explore the effects of different β-adrenergic receptors (β-AR) on the left and right ventricular systolic and diastolic functions in rats under acute hypoxic stress. METHODS:The healthy male SD rats were randomly divided into 4 groups (n=7):control group, non-selected β-AR blocker propranolol group, selected β₁-AR blocker atenolol group and selected β₂-AR blocker ICI 118,551 group, and then the rats were exposed to normoxia (20.9% O₂, 79.1% N₂) and hypoxia (15.0% O₂, 85.0% N₂) condition respectively at the altitude of 2 260 m (Xining, China). The heart rate (HR), the left ventricular systolic pressure (LVSP), the right ventricular systolic pressure (RVSP), and the maximum raise/decline rate of left and right ventricular pressure (±dp/dt_max) were monitored, and the arterial blood gas in normoxia and hypoxia condition were compared to explore the effect of β-AR on the left and right ventricular systolic and diastolic functions in acute hypoxic stress rats. RESULTS:Under normoxia condition, the LVSP, ±dp/dt_max of left ventricular were decreased in propranolol group, atenolol group and ICI 118,551 group, the RVSP and ±dp/dt_max of right ventricle were decreased in propranolol group and atenolol group (P<0.05). Under hypoxia condition, the PaO₂, LVSP, ±dp/dt_max of left ventricle were decreased in all groups compared with the normoxia group, and the ±dp/dt_max of right ventricle was increased in all groups (P<0.05), also the degree of index change in control group was more obvious than that in propranolol group and atenolol group. CONCLUSION:The activation of β₁-AR is an important compensatory regulation for heart function during hypoxic stress. However, the compensatory enhancement of right heart function under acute hypoxia condition which through tonogenic dilation is more significant for maintaining the normal circulating blood flow.     

Interreader agreement of radiographic left atrial enlargement in dogs and comparison to echocardiographic left atrial assessment

Introduction

Assessing left atrial (LA) size is an integral part of the cardiac evaluation in dogs. Left atrial size is routinely evaluated by thoracic radiographs or echocardiography.

Changes of aryl hydrocarbon receptor in cardiac hypertrophy induced by high glucose in vitro

AIM: To investigate the changes of aryl hydrocarbon receptor (AhR) in the process of cardiomyocyte hypertrophy induced by high glucose, and to explore its potential mechanisms. METHODS: The rat cardiomyocytes (H9c2 cells) were divided into normal glucose group, high glucose group, DMSO group and resveratrol (an AhR antagonist) group. The content and distribution of AhR were observed with immunofluorescence staining. The myocardial cells were stained with rhodamine-labeled phalloidin to visualize cytoskeleton, and the cell surface area were determined after imaging by fluorescence microscopy. The generation of reactive oxygen species (ROS) in the cardiomyocytes was measured using a fluorescent probe DCFH-DA. The mRNA expression of AhR, CYP1A1, atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) were evaluated by real-time quantitative PCR (RT-qPCR). The protein levels of AhR, CYP1A1, ANP and BNP were assessed by Western blot. RESULTS: AhR was constitutively presented in the cytosol under normal-glucose condition and was translocated to the nuclei under high-glucose condition. High glucose induced cardiac hypertrophy, and increased ROS generation. Significant reductions in the cell size and ROS generation were observed after treated with resveratrol. The expression of AhR, CYP1A1, ANP and BNP at mRNA and protein levels in high glucose group was increased as compared with normal glucose group and resveratrol group, and the above-mentioned indexes significantly decreased in resveratrol group as compared with DMSO group. CONCLUSION: High glucose-induced cardiac hypertrophy increases AhR expression, which may be involved in the maintenance of glucose homeostasis in the cardiomyocytes. AhR translocation to the nucleus induced by high glucose results in the increases in CYP1A1 expression and ROS generation, which may be an important mechanism of high glucose-induced cardiomyocyte hypertrophy.