Aortic to caudal vena cava ratio measurements using abdominal ultrasound are increased in dogs with confirmed systemic hypertension

Chronically sustained systemic hypertension in dogs can damage the kidneys, eye, brain, heart, and vessels. In human medicine, systemic hypertension has been implicated as the most common risk factor for aorta dilation, which can progress to an aneurysm. Abdominal ultrasound has been commonly used to monitor the size of the abdominal aorta in people with systemic hypertension. In this retrospective cross‐sectional abdominal ultrasound study, evaluation of the size of the abdominal aorta relative to the caudal vena cava was performed in 18 control dogs and 128 dogs with confirmed systemic hypertension. Preexisting conditions contributing to systemic hypertension in these dogs were renal disease, hyperadrenocorticism, diabetes mellitus, adrenal tumors, and previous administration of phenylpropanolamine or palladia. The abdominal aorta and caudal vena cava were assessed from longitudinal images cranial to the trifurcation with measurements made from outer border to outer border of the walls, being careful not to compress the caudal vena cava that would alter its size. Our hypothesis was the ratio of the diameter of the abdominal aorta to caudal vena cava would be higher in dogs with systemic hypertension compared to dogs with normal blood pressure. The mean abdominal aorta‐caudal vena cava ratio was 1.028 in control dogs with a normal blood pressure and 1.515 in dogs with systemic hypertension. In dogs with confirmed systemic hypertension, the abdominal aorta was dilated compared to the caudal vena cava in the caudal abdomen. An increase in the abdominal aorta‐caudal vena cava ratio in a dog should raise suspicion for the presence of systemic hypertension and prompt evaluation of blood pressure.     

Immobilization of African buffaloes (Syncerus caffer) using etorphine–midazolam compared with etorphine–azaperone

ObjectiveTo compare induction times and physiological effects of etorphine–azaperone with etorphine–midazolam immobilization in African buffaloes.Study designRandomized crossover study.AnimalsA group of 10 adult buffalo bulls (mean body weight 353 kg).MethodsEtorphine–azaperone (treatment EA; 0.015 and 0.15 mg kg^–1, respectively) and etorphine–midazolam (treatment EM; 0.015 and 0.15 mg kg^–1, respectively) were administered once to buffaloes, 1 week apart. Once in sternal recumbency, buffaloes were instrumented and physiological variables recorded at 5 minute intervals, from 5 minutes to 20 minutes. Naltrexone (20 mg mg^–1 etorphine dose) was administered intravenously at 40 minutes. Induction (dart placement to recumbency) and recovery (naltrexone administration to standing) times were recorded. Arterial blood samples were analysed at 5 and 20 minutes. Physiological data were compared between treatments using a general linear mixed model and reported as mean ± standard deviation. Time data were compared using Mann-Whitney U test and reported as median (interquartile range) with p ≤ 0.05.ResultsActual drug doses administered for etorphine, azaperone and midazolam were 0.015 ± 0.001, 0.15 ± 0.01 and 0.16 ± 0.02 mg kg^–1, respectively. Induction time for treatment EA was 3.3 (3.6) minutes and not different from 3.2 (3.2) minutes for treatment EM. The overall mean arterial blood pressure was significantly lower for treatment EA (102 ± 25 mmHg) than that for treatment EM (163 ± 18 mmHg) (p < 0.001). The PaO₂ for treatment EA (37 ± 12 mmHg; 5.0 ± 1.6 kPa) was not different from that for treatment EM (43 ± 8 mmHg; 5.8 ± 1.1 kPa). Recovery time was 0.8 (0.6) minutes for treatment EA and did not differ from 1.1 (0.6) minutes for treatment EM.Conclusions and clinical relevanceTreatment EA was as effective as treatment EM for immobilization in this study. However, systemic arterial hypertension was a concern with treatment EM, and both combinations produced clinically relevant hypoxaemia. Supplemental oxygen administration is recommended with both drug combinations.     

A Syndrome Resembling Idiopathic Noncirrhotic Portal Hypertension in 4 Young Doberman Pinschers

We describe 4 young male Doberman Pinschers (3 littermates and 1 unrelated dog) with a syndrome resembling idiopathic or noncirrhotic portal hypertension of humans. Each dog was evaluated for a hepatopathy resulting in portal hypertension, development of portosystemic collateral vessels, and hepatic encephalopathy. These dogs differ from previous reports of young dogs with hepatic insufficiency associated with portal hypertension and acquired portal systemic shunting by their lack of intrahepatic arteriovenous fistulae, portal vein atresia, or intrahepatic fibrosis. Clinicopathologic features included erythrocyte microcytosis, normal to mildly increased liver enzyme activities, increased concentrations of serum bile acids, reduced plasma indocyanine green clearance, and normal total bilirubin concentration. Abdominal ultrasonography disclosed a small liver and portosystemic collateral vessels. Radiographic imaging studies confirmed hepatofugal portal circulation and discounted hepatic arteriovenous fistulae. Histopathologic features in liver tissue from each dog were similar and consistent in all sections examined. Common findings included increased cross-sectional views of hepatic arterioles; hepatic lobular atrophy; scanty increase in connective tissue around some large portal triads; and absence of inflammation, disturbed lobular architecture, bile duct proliferation, or intrahepatic cholestasis.     

The suitability of some blood gas and biochemical parameters as diagnostic tools or early indicators of ascites syndrome in broiler sire lines

In recent few years, there have been some attempts to find a reliable indicator trait as a selection criterion against susceptibility to ascites syndrome (AS). Blood parameters were of great interest as they could be measured in live animals without implementing an ascites‐inducing challenge (AIC). In this work, the suitability of some blood parameters was evaluated for diagnosing AS‐susceptible chicks in later steps of the disease in trial 1 as well as their early predictive ability in trial 2. In the first trial, one hundred 1‐day‐old chicks from two pure broiler lines namely S₁ and S₂ and, in the second trial, 226 1‐day‐old chicks from line S₂ were subjected to AIC. Saline drinking water (1200 mg/l) and lower‐than‐standard ambient temperatures were the implemented AICs in trials 1 and 2 respectively. The blood parameters including pH, partial pressure of O₂ (pO₂), partial pressure of CO₂ (pCO₂), bicarbonate ion concentration (BIC), percentage of haematocrit (HCT) and saturated haemoglobin (SaO₂) were measured twice per each bird at days 28 and 35 in trial 1 and once in trial 2 at day 21. The results of the first trial revealed that in line S₂ some of the blood parameters differed significantly between the ascitic and non‐ascitic groups following exposure to AIC. In this line, the incidence of AS was accompanied by a lower pO₂, SaO₂ and BIC, while with higher pCO₂ and HCT values. In the second trial, however, although almost all of the parameters showed meaningful differences between the ascitic and non‐ascitic broilers, only mean difference of BIC parameter was statistically significant. The general conclusion of this study is that the blood parameters can somewhat have diagnostic ability in the condition in which the AIC is already present, whereas the results did not approve their usefulness as early predictors of AS.     

Evaluation of the white-coat effect in cats

The diagnosis and management of systemic hypertension in cats requires a reliable method for measurement of systemic arterial blood pressure (BP) in clinical patients. Unfortunately, the setting of a clinical practice and the act of measuring BP might raise BP and heart rate (HR), an effect referred to as the white-coat effect in human patients. The purpose of the present study was to determine if a white-coat effect was experienced by cats. Radiotelemetric implants were used to measure BP and HR in 13 conscious cats in a research colony while undisturbed in their cages and while subjected to simulated visits to a veterinarian's office. The white-coat effect was taken to be the difference between the overall 24-hour average value for parameters of BP and HR and the corresponding value during the simulated office visit. A white-coat effect was observed in cats. In healthy cats, the systolic BP measured during the examination period of the simulated office visit exceeded the 24-hour average systolic BP by 17.6+/-1.5 mm Hg. However, marked heterogeneity occurred in the pattern and magnitude of the increase in systolic BP above the 24-hour baseline and the increase varied between 75.3 and -27.2 mm Hg for the healthy cats. Variation in response to the simulated office visit was observed among cats and among visits by the same cat. During an office visit, the magnitude of the white-coat effect tended to decrease, but not disappear, over time. The magnitude of the white-coat effect varied when cats were subjected to 5 repeat office visits, but did not diminish in the group as a whole. The mean increase in systolic BP during the examination (22.3+/-0.9 mm Hg) was greater (P < .05) in cats with renal insufficiency. Although the heterogeneity of response expected from companion animals might be greater than that observed in these colony cats, these results indicate that veterinarians should carefully consider the white-coat effect in evaluation of BP in cats. A quiet, undisturbed environment and adequate time for acclimation should be included in the standard protocol for measurements of BP. Because of day-to-day variation in the white-coat effect in individual cats, multiple serial measurements following a standard protocol should provide the best estimate of BP in cats.     

Intraocular pressure development after cataract surgery: a prospective study in 50 dogs (1998-2000)

Objective To study the course of intraocular pressure (IOP) after cataract surgery in 50 dogs. Design Prospective study. Animals Fifty dogs without preoperative ocular hypertension were selected for cataract surgery. Methods All dogs underwent cataract surgery: 25 by manual extracapsular extraction and 25 by phacoemulsification. For each dog, intraocular pressure was measured before surgery, and 1, 3, 5, 18 h, 1 week and 1 month post surgery. Results No significant difference of mean intraocular pressure between the two surgical methods was observed for each time measurement. Nine dogs had postoperative hypertension (IOP > 25 mmHg) during the first 5 hours post surgery. Incidence of postoperative hypertension was not significantly different with manual extracapsular extraction (16%) vs. phacoemulsification (20%). A decrease of mean IOP was observed 1 h after surgery (8.49 mmHg vs. 10.91 mmHg), then an increase 3 and 5 h post surgery (12.3 and 13.32 mmHg, respectively). At 18 h, 1 week and 1 month post surgery, mean IOP decreased. Mean IOP was 10.38, 10.38 and 8.84 mmHg, respectively. Conclusion In this study incidence of POH is not high. However, a follow‐up of IOP in the first hours after cataract surgery is required to avoid complications of the retina and optic nerve and to administer hypotensive treatment if necessary.     

Malignant pheochromocytoma presenting as a bradyarrhythmia in a dog

Objective: To describe a case of atrioventricular block and syncope secondary to systemic hypertension in a dog with malignant pheochromocytoma. Case Summary: A 13‐year‐old spayed female mixed‐breed dog presented following an acute onset of collapse. The dog was hypertensive and had paradoxical high‐grade second‐degree atrioventricular block with concurrent syncope. Initial emergent therapy included a nitroprusside infusion for the systemic hypertension and vagolytic therapy for the bradyarrhythmia. A left adrenal mass was seen on abdominal ultrasound and was further characterized by MRI. Following medical stabilization with phenoxybenzamine and propantheline, a left adrenalectomy was performed. Histological diagnosis was consistent with a malignant pheochromocytoma. Following tumor removal there has been no further hypertension, atrioventricular block or syncope. Unique information provided: This is the first documented case of a malignant pheochromocytoma presenting as syncope secondary to hypertension induced atrioventricular block.     

Acute onset of pulmonary necrotising arteritis in a dog with a left-to-right patent ductus arteriosus

A 12-week-old, clinically normal Chihuahua was referred for investigation for a continuous heart murmur. Cardiac evaluation revealed an anatomically and haemodynamically typical left-to-right shunting patent ductus arteriosus. The continuous wave Doppler measurement of peak ductal jet velocity of 5.6 m/s was suggestive of a normal pulmonary to systemic arterial pressure ratio. The dog returned 16 days later with right heart failure and severe pulmonary hypertension. Marked reduction in left-to-right shunting was demonstrated and the ductal jet velocity had decreased to 2.5 m/s. Immediate ductus ligation, oxygen therapy before and after the operation, and administration of hydralazine failed to reduce pulmonary hypertension, and the dog was euthanased. Histopathological examination of the lung showed pulmonary necrotising arteritis with acute and chronic arterial lesions. Chronic pulmonary vascular changes related to high flow have been associated with altered nitric oxide and endothelin responses. These changes may be responsible for the acute onset of pulmonary hypertension due to relatively minor vascular insults in some human and veterinary patients with left-to-right shunts. The potential for acute progression supports the recommendations for early ductus ligation and the prognostic importance of detecting pulmonary hypertension presurgically in patent ductus arteriosus patients.     

Effect of hypercapnia on lysyl oxidase-dependent collagen cross-linking and hypoxia-induced pulmonary hypertension in rat

AIM: To investigate the effect of hypercapnia on hypoxia-induced pulmonary hypertension and the changes of lysyl oxidase (LOX) and extracellular matrix collagen cross-links in the rat. METHODS: Sprague-Dawley rats were randomly divided into 4 groups:normoxia group, hypoxia group, hypercapnia group and hypoxia+hypercapnia group. LOX activity was detected by fluorescence spectrophotometry. LOX protein expression was detected by immunohistochemistry and Western blot. The mRNA expression of LOX in the pulmonary artery was detected by real-time PCR. RESULTS: The levels of mean pulmonary artery pressure (mPAP), RV/(LV+S) and WA/TA in hypoxia group were significantly higher than those in normoxia group (P<0.01). Moreover, the levels of mPAP and RV/(LV+S) in hypoxia+hypercapnia group were significantly lower than those in hypoxia group (P<0.01). However, no significant difference of mPAP and RV/(LV+S) between hypercapnia group and normoxia group was observed. In hypoxia group, the collagen cross-links in the lung tissue was significantly higher than that in normoxia group and hypercapnia group (P<0.01). Importantly, collagen cross-links in the lung tissue of hypoxia+hypercapnia group was significantly lower than that in hypoxia group (P<0.01). There was no significant difference in collagen cross-links between hypercapnia group and normoxia group. The expression of LOX at mRNA and protein levels and its activity in the pulmonary arteries of hypoxia group were significantly increased as compared with normoxia group (P<0.01). Furthermore, the expression of LOX at mRNA and protein levels and its activity in the pulmonary arteries in hypoxia+hypercapnia group were lower than those in hypoxia group (P<0.01). CONCLUSION: Hypoxia not only up-regulates LOX but also promotes collagen cross-linking in the rat lung, which contributes to the development of pulmonary hypertension. Hypercapnia inhibits hypoxia-induced LOX expression and collagen cross-linking, therefore impairing the progress in hypoxia-induced pulmonary hypertension.     

Impact of hydrogen sulfide donor on endothelin-1 and connective tissue growth factor expression in rats with pulmonary hypertension induced by high pulmonary blood flow

AIM: To explore the possible impact of hydrogen sulfide (H2S) donor-sodium hydrosulfide (NaHS) on endothelin-1 (ET-1) and connective tissue growth factor (CTGF) expressions in rats with pulmonary hypertension induced by high pulmonary blood flow. METHODS: Thirty-two male SD rats were randomly divided into 4 groups: shunt group, shunt+NaHS group, sham group and sham+NaHS group. Rats in shunt group and shunt+NaHS group were subjected to an abdominal aorta-inferior vena cava shunt to create an animal model of high pulmonary flow. After 11 weeks of experiment, rat systolic pulmonary artery pressure (SPAP), lung tissue H2S, plasma ET-1 concentration and lung tissue ET-1mRNA expression, as well as pulmonary artery CTGF protein expression were detected.RESULTS: After 11 weeks of experiment, SPAP, lung tissue ET-1mRNA, plasma ET-1 as well as pulmonary artery CTGF expressions were increased markedly, respectively, whereas H2S in lung tissue decreased significantly in rats of shunt group as compared with that in sham group (all P<0.05). After administration of NaHS for 11 weeks, H2S in lung tissue increased significantly, whereas SPAP, plasma ET-1 and lung tissue ET-1 mRNA expression as well as pulmonary artery CTGF protein expression decreased significantly, respectively, in rats of shunt+NaHS group as compared with that in shunt group (all P<0.05).CONCLUSION: NaHS might be involved in the development of pulmonary hypertension induced by high pulmonary blood flow by down-regulating vasoactive peptides ET-1 and CTGF expressions in lung tissues of rats.