Dilation In Dogs Research Articles

Sub-Tenon’s anaesthesia in canine eyes: computed tomography analysis of contrast distribution in cadavers

Sub-Tenon’s anaesthesia is a safe technique to achieve extraocular muscle akinesia and pupil dilation in dogs (Ahn et al. 2013, Bayley & Read 2018). However, there are no studies describing the anatomical distribution of the injectate in the canine sub-Tenon’s space.

Echocardiographic features of pre- and postcapillary pulmonary hypertension with a focus on the right ventricle in dogs

ABSTRACT: Pulmonary hypertension (PH) in dogs is a syndrome that can occur secondary to several causes, including left heart disease (postcapillary) and chronic respiratory disease (precapillary). This study evaluates morphological and functional consequences in the right ventricle (RV) of dogs with pre- and postcapillary PH through echocardiography, and also considers the severity of PH (mild, moderate or severe). Echocardiography was performed on 66 dogs of various breeds and weights (age >3 years old) which were assigned to three groups: postcapillary PH, which included mitral valve disease/endocardiosis, precapillary PH, which included chronic respiratory diseases (bronchitis, collapse of the trachea and primary lung cancer or metastasis), and finally, a healthy group of controls. The parameters for RV morphology were RV1, RV2, and RV3 for systole and diastole. The following measurements were used to assess RV systolic function: tricuspid annular plane systolic excursion (TAPSE), TAPSE:Ao (aorta), maximum velocity of the tricuspid systolic wave obtained by tissue Doppler (S’), S’:Ao, right ventricle end-diastolic area (RVEDA); RVEDA:BSA (body surface area); flow velocity integral (FVI) and FVI:Ao. The variables were assessed using ANOVA. The results showed that RV3d, RV1s, S’:Ao, S’, and FVI were able to distinguish cases of pre- and postcapillary PH in this study. Remodeling of the RV of dogs with PH was observed, which can be influenced by the pre- or postcapillary origin of the PH, with dilation in dogs with postcapillary PH and severe PH. The results for RV systolic function were similar, with FVI and FVI:Ao showing that RV ejection function is reduced in dogs with postcapillary PH and with severe PH.

Outcomes following balloon dilation for management of urethral obstruction secondary to urothelial carcinoma in dogs: 12 cases (2010-2015).

To describe outcomes for dogs that underwent balloon dilation for palliative treatment of urethral obstruction caused by urothelial carcinoma. 12 client-owned dogs. Medical records were searched to identify dogs with urothelial (bladder, urethra, or prostate) carcinoma that underwent balloon dilation for treatment of urethral obstruction between April 2010 and December 2015. Information regarding history, signalment, clinical signs, diagnostic imaging findings, balloon dilation technique, clinical outcomes, complications, and additional treatments was obtained by review of medical records. Improvement in clinical signs of urethral obstruction was observed after the initial dilation procedure for 9 of 12 dogs. Urethral obstruction was known to recur in 5 dogs 48 to 296 days after the initial procedure. Three of these dogs underwent a second dilation procedure, with clinical improvement in all 3 dogs for 41 to 70 days. One of 2 dogs that had a third procedure after the second reobstruction had clinical improvement in urinary tract signs until subsequent death from metastatic disease 22 days later. Complications included hematuria, urinary incontinence, and dysuria; these resolved within a few days after treatment. Urethral balloon dilation was a minimally invasive procedure that provided relief of urethral obstruction from urothelial carcinoma in most dogs of the study population. Prospective studies are needed to identify optimal techniques for balloon dilation in dogs with neoplastic urethral obstructions and to identify patients that are likely to benefit most from the treatment.

Serum and fecal canine α1-proteinase inhibitor concentrations reflect the severity of intestinal crypt abscesses and/or lacteal dilation in dogs

Gastrointestinal (GI) protein loss, due to lymphangiectasia or chronic inflammation, can be challenging to diagnose. This study evaluated the diagnostic accuracy of serum and fecal canine α1-proteinase inhibitor (cα1PI) concentrations to detect crypt abscesses and/or lacteal dilation in dogs. Serum and fecal cα1PI concentrations were measured in 120 dogs undergoing GI tissue biopsies, and were compared between dogs with and without crypt abscesses/lacteal dilation. Sensitivity and specificity were calculated for dichotomous outcomes. Serial serum cα1PI concentrations were also evaluated in 12 healthy corticosteroid-treated dogs.Serum cα1PI and albumin concentrations were significantly lower in dogs with crypt abscesses and/or lacteal dilation than in those without (both P < 0.001), and more severe lesions were associated with lower serum cα1PI concentrations, higher 3 days-mean fecal cα1PI concentrations, and lower serum/fecal cα1PI ratios. Serum and fecal cα1PI, and their ratios, distinguished dogs with moderate or severe GI crypt abscesses/lacteal dilation from dogs with only mild or none such lesions with moderate sensitivity (56–92%) and specificity (67–81%). Serum cα1PI concentrations increased during corticosteroid administration. We conclude that serum and fecal α1PI concentrations reflect the severity of intestinal crypt abscesses/lacteal dilation in dogs. Due to its specificity for the GI tract, measurement of fecal cα1PI appears to be superior to serum cα1PI for diagnosing GI protein loss in dogs. In addition, the serum/fecal cα1PI ratio has an improved accuracy in hypoalbuminemic dogs, but serum cα1PI concentrations should be carefully interpreted in corticosteroid-treated dogs.

Low frequency therapeutic ultrasound causes vasodilation and enhanced tissue perfusion

It has been found that ultrasound has a unique effect on arterial and venous dilation as well as tissue perfusion. Our group found that low frequency ultrasound (20 kHz, 0.1 w/cm2) results in coronary arterial and coronary venous dilation in dogs. The magnitude of vasodilation is similar to that seen with nitroglycerine (NTG) administration but unlike NTG, USD does not lower blood pressure. Our human studies show that USD induces brachial arterial dilation after 1 min with the vasodilatory effect lasting 20 min. In animals we ligated coronary arteries, stopping epicardial coronary flow, resulting in a drop in myocardial tissue perfusion to 70% of normal; myocardial tissue pH fell from 7.43 to 7.05. After 60 min of USD, tissue perfusion improved by 20% and pH normalized in spite of persistent coronary artery occlusion. The enhanced perfusion effect of ultrasound was eliminated if an inhibitor of nitric oxide synthase was given prior to ultrasound exposure. Conclusions: low frequency ultrasound causes vasodilation and improves tissue perfusion. These effects appear to be mediated at least in part by the USD enhancing tissue release of nitric oxide.

Long-term Therapy with the Acorn Cardiac Support Device Normalizes Gene Expression of Growth Factors and Gelatinases in Dogs with Heart Failure

Passive mechanical containment of the failing left ventricle with the Acorn Cardiac Support Device (CSD) was shown to prevent progressive left ventricular dilation in dogs with heart failure and increase left ventricular ejection fraction. To examine possible mechanisms for improved cardiac function with a CSD, we examined the effect of CSD therapy on the mRNA gene expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), matrix metalloproteinases (MMP) 2 and 9, and tissue inhibitors of metalloproteinases (TIMP) 1 and 2. Heart failure was produced in 12 dogs by multiple sequential intracoronary microembolizations. Six dogs were implanted with the CSD and 6 served as concurrent controls. Left ventricular tissue from 6 normal dogs was used for comparison. Compared with normal dogs, dogs with untreated heart failure showed downregulation of mRNA expression for VEGF and bFGF, whereas upregulation of mRNA expression for MMP-2 and MMP-9 was observed. Normalization of mRNA expression for all these genes was seen after treatment with the CSD. This study shows that preventing left ventricular dilation and myocardial stretch with the CSD promotes normalization of growth factor and MMP gene expression. These results suggest that modulation of gene activity may, in part, contribute to the improvement of left ventricular function observed with CSD therapy.

Reversal of chronic molecular and cellular abnormalities due to heart failure by passive mechanical ventricular containment.

Passive mechanical containment of failing left ventricle (LV) with the Acorn Cardiac Support Device (CSD) was shown to prevent progressive LV dilation in dogs with heart failure (HF) and increase ejection fraction. To examine possible mechanisms for improved LV function with the CSD, we examined the effect of CSD therapy on the expression of cardiac stretch response proteins, myocyte hypertrophy, sarcoplasmic reticulum Ca2+-ATPase activity and uptake, and mRNA gene expression for myosin heavy chain (MHC) isoforms. HF was produced in 12 dogs by intracoronary microembolization. Six dogs were implanted with the CSD and 6 served as concurrent controls. LV tissue from 6 normal dogs was used for comparison. Compared with normal dogs, untreated HF dogs showed reduced cardiomyocyte contraction and relaxation, upregulation of stretch response proteins (p21ras, c-fos, and p38 alpha/beta mitogen-activated protein kinase), increased myocyte hypertrophy, reduced SERCA2a activity with unchanged affinity for calcium, reduced proportion of mRNA gene expression for alpha-MHC, and increased proportion of beta-MHC. Therapy with the CSD was associated with improved cardiomyocyte contraction and relaxation, downregulation of stretch response proteins, attenuation of cardiomyocyte hypertrophy, increased affinity of the pump for calcium, and restoration of alpha- and beta-MHC isoforms ratio. The results suggest that preventing LV dilation and stretch with the CSD promotes downregulation of stretch response proteins, attenuates myocyte hypertrophy and improves SR calcium cycling. These data offer possible mechanisms for improvement of LV function after CSD therapy.

Acute ventricular reduction with the acorn cardiac support device: effect on progressive left ventricular dysfunction and dilation in dogs with chronic heart failure.

Surgical resection of myocardium that acutely reduces left ventricular (LV) volume in patients with advanced heart failure (HF), the so-called "Batista Operation," remains controversial. We examined the effects of acute LV reduction with the Acorn Cardiac Support Device (CSD) in dogs with HF (LV ejection fraction < 30%). HF was produced in 15 dogs by intracoronary microembolization. In nine dogs, intravenous dobutamine was administered to reduce LV end-diastolic dimension (LVEDD) by 10%-25%. While on dobutamine infusion, the CSD, a preformed knitted polyester device, was surgically placed around the ventricles, anchored to the arteriovenous (AV) groove, and tailored anteriorly to fit snugly over the ventricles. Dogs were then weaned off dobutamine. On average, the procedure reduced LVEDD by 7 +/- 1 mm (range 5-12 mm). Of the nine dogs, two died before completion of the study and seven survived for the entire period. Six dogs did not undergo device placement and served as controls. All were followed for 3 months prior to sacrifice. In controls, LV end-diastolic volume increased after 3 months (66 +/- 5 mL vs 77 +/- 6 mL; p = 0.007), while in CSD-treated dogs (n = 7), it decreased (80 +/- 5 mL vs 60 +/- 3 mL; p = 0.002). In controls, LV ejection fraction (EF) decreased after 3 months (27 +/- 1% vs 23 +/- 1%; p = 0.001) but was unchanged in CSD-treated dogs (25 +/- 1% vs 26 +/- 1%; p = 0.66). Compared to controls, CSD-treated dogs showed improved LV diastolic dysfunction and chamber sphericity, decreased wall stress, and no functional mitral regurgitation (MR). In dogs with advanced HF, acute LV reduction with the Acorn CSD prevents progressive global LV dilatation and ameliorates functional MR.

Effects of long‐term therapy with ecadotril on the progression of left ventricular dysfunction and dilation in dogs with moderate heart failure

Effects of long‐term therapy with ecadotril on the progression of left ventricular dysfunction and dilation in dogs with moderate heart failure

Effects of long-term monotherapy with enalapril, metoprolol, and digoxin on the progression of left ventricular dysfunction and dilation in dogs with reduced ejection fraction.

Recent clinical trials have suggested that therapy with angiotensin-converting enzyme inhibitors in asymptomatic patients with reduced left ventricular (LV) function can significantly reduce the incidence of congestive heart failure compared with patients receiving placebo. In the present study, we examined the effects of long-term monotherapy with enalapril, metoprolol, and digoxin on the progression of LV systolic dysfunction and LV chamber enlargement in dogs with reduced LV ejection fraction (EF). LV dysfunction was produced in 28 dogs by multiple sequential intracoronary microembolizations. Embolizations were discontinued when LVEF was 30% to 40%. Three weeks after the last embolization, dogs were randomized to 3 months of oral therapy with enalapril (10 mg twice daily, n = 7), metoprolol (25 mg twice daily, n = 7), digoxin (0.25 mg once daily, n = 7), or no treatment (control, n = 7). As expected, in untreated dogs, LVEF decreased (36 +/- 1% versus 26 +/- 1%, P < .001) and LV end-systolic volume (ESV) and end-diastolic volume (EDV) increased during the 3-month follow-up period (39 +/- 4 versus 57 +/- 6 mL, P < .001, and 61 +/- 6 versus 78 +/- 8 mL, P < .002, respectively). In dogs treated with enalapril or metoprolol, LVEF remained unchanged or increased after therapy compared with before therapy (35 +/- 1% versus 38 +/- 3% and 35 +/- 1% versus 40 +/- 3%, respectively, P < .05), whereas ESV and EDV remained essentially unchanged. In dogs treated with digoxin, EF remained unchanged but ESV and EDV increased significantly. In dogs with reduced LVEF, long-term therapy with enalapril or metoprolol prevents the progression of LV systolic dysfunction and LV chamber dilation. Therapy with digoxin maintains LV systolic function but does not prevent progressive LV enlargement.

The Efficacy and Safety of Milrinone for Treating Heart Failure in Dogs

Milrinone has been studied in a variety of situations. In experimental dogs it has been documented to increase contractility to a similar degree as beta-receptor agonists and to produce mild arteriolar dilation in dogs. In canine patients with heart failure, milrinone produces demonstrable improvement in echocardiographic ventricular function and hemodynamic variables. In addition, it improves clinical signs in these patients, improving their quality of life. Milrinone is superior to digoxin as evidenced by the improvement in clinical signs noted in dogs that were unresponsive or no longer responding to digoxin administration. There is no doubt that milrinone improves short-term prognosis and in so doing prolongs life. Many of the patients that the author has observed would not have gone home without the benefits of milrinone. Milrinone's effects on long-term survival cannot be assessed, but its effects on survival time are certainly not dramatic enough to be evident without a comparison population. Therefore, milrinone administration should be considered palliative, as is administration of all other cardiovascular medications for heart failure. In addition to its beneficial effects, milrinone also appears to be relatively safe when compared with the alternative of digoxin administration. Fatal events attributable to milrinone administration are rare, and those directly attributable to enhanced ventricular arrhythmia can generally be avoided by monitoring an electrocardiogram after initial milrinone administration commences. Milrinone does not increase the incidence of sudden death in Doberman Pinschers. It is possible that a small number of dogs with mitral regurgitation may develop mitral chordal rupture. For this reason and possibly others, milrinone probably will not be indicated in early heart failure due to mitral regurgitation when heart failure is readily responsive to diuretic administration. The risk-to-benefit ratio turns markedly in the favor of milrinone administration in the dog with mitral regurgitation that is partially or completely refractory to other cardiovascular drugs. Milrinone appears to be a more effective and safer positive inotrope for long-term treatment of dogs with congestive heart failure than drugs currently available. The author and all the investigators involved in the milrinone clinical trials hope that it will soon be available for use by the veterinary community.

Altered endothelial cell-mediated arterial dilation in dogs with D. immitis infection.

Vascular endothelial cells regulate arterial diameter in vivo and in vitro. Stimulation of endothelial cell muscarinic receptors by acetylcholine results in the production and release of a nonprostaglandin metabolite of arachidonic acid that causes vascular smooth muscle relaxation. We examined femoral artery endothelium-dependent vasodilator responses in normal dogs and dogs with heartworm (Dirofilaria immitis) infection. Endothelium-dependent vascular reactivity was attenuated in dogs with D. immitis infection studied in the spring but not in the fall. The dilator response was inversely related to the number of female worms but not related to the presence of circulating microfilariae. Indomethacin markedly depressed responses to acetylcholine in dogs with D. immitis but did not alter acetylcholine-induced dilation in normal dogs. These data suggest that D. immitis releases substances that alter distal arterial endothelial cell arachidonic acid metabolism. The seasonal pattern may reflect the onset of maximal reproductive activity in the spring and its decline as the vector season ends in the fall.

Prostatic urethra: experimental dilation in dogs.

An animal study was undertaken to develop a balloon dilation technique that could be used in humans to treat the common ailment of benign prostatic hypertrophy. Dogs were used as a model because of the similarities in the prostate between the two species and the ready availability of the canines. A retrograde transurethral approach was used for dilation. Balloon catheters, 8-20 mm in diameter, were used. Significant, long-lasting dilatation of the prostatic urethra was not accomplished until 20-mm balloons (or two 10-mm ones) inflated for 10 minutes were used. The animals were followed for up to 14 months. No deleterious histologic effects of dilation were identified within the urethra or prostate that could lead to stenosis of the prostatic urethra in later stages.

Gastric dilation in dogs.

Gastric dilation in dogs.

Pericardial adaptations during chronic cardiac dilation in dogs.

The manner in which the pericardium adapts to chronic cardiac dilation is not known. Recent work from our laboratory indirectly suggested that the size of the pericardium and/or its pressure-volume relation was altered by chronic cardiac enlargement. To examine this question further, we compared pericardial pressure-volume and stress-strain relations, surface area, mass, and average thickness in seven normal dogs and seven with chronic volume overload hypertrophy due to a systemic arteriovenous fistula. Dogs with significant cardiac hypertrophy had an increased pericardial volume at any pressure and a proportionality constant for the slope of the entire curve as determined by nonlinear regression analysis. This was associated with parallel increases in pericardial surface area and mass such that average thickness was unchanged. Stress-strain analysis of the data revealed that the mechanical properties of the pericardium were not significantly different in dogs with chronic cardiac dilation. These results indicate that during chronic cardiac dilation the pericardium enlarges in size and mass. The pericardial chamber is more compliant, although the intrinsic stiffness of the pericardium appears to be unchanged. Further, since pericardial mass is increased, the response to chronic dilation appears to also involve the addition of new pericardial tissue.