In an effort to better understand the role of vasodilators in the management of pulmonary hypertension associated with chronic heartworm disease (HWD), pulmonary hemodynamic measurements were obtained from 7 experimentally infected, anesthetized dogs before and after hydralazine administration (mean dose, 1.96 mg/kg of body weight). Five dogs were maintained on room air, while 2 were maintained on 100% oxygen during the hydralazine study. The hemodynamic effect of hydralazine in dogs with HWD was evaluated, using heart rate, cardiac index, mean pulmonary artery pressure, mean arterial pressure, total pulmonary resistance, total systemic resistance, total systemic resistance/total pulmonary resistance, left ventricular dP/dt(max), left ventricular end diastolic pressure, and left and right ventricular double products ([mean arterial pressure X heart rate] and [mean pulmonary artery pressure X heart rate], respectively). Responders were defined as those in which total pulmonary resistance decreased greater than or equal to 20% without an increase in mean pulmonary arterial pressure and in which heart rate increase was less than or equal to 10%. Comparison was also made between maximal hemodynamic effect of hydralazine with that after 100% oxygen administration for 15 minutes to previously normoxemic dogs (n = 5). Significance was determined if P < 0.05, using the paired t-test. Hydralazine induced significant reductions in mean pulmonary and systemic arterial pressures and total pulmonary resistance, with no significant change in heart rate, cardiac index, total systemic resistance, left ventricular dP/dt(max), left ventricular end diastolic pressure, or right and left ventricular double products. Four (57%) of the 7 dogs studied were considered responders. Pretreatment cardiac index, mean pulmonary artery pressure, and total pulmonary resistance did not allow differentiation of responders from nonresponders.

Objective: This study was designed to assess the prevalence and the associated risk factors (e.g., sex, age, breed, management system and climate) of Dirofilaria immitis in dogs in Makurdi metropolis in Nigeria. Materials and methods: Prevalence study of canine heartworm disease in dogs was conducted over a period of six months covering five localities of Makurdi metropolis in Benue State, Nigeria. A total of 186 blood samples were collected from apparently healthy and sick dogs, and the samples were examined for the presence of microfilaria between September 2015 and February 2016. Three methods (wet mount, Buffy coat and modified Knott's techniques) were used for the examination of the samples. The Packed Cell Volume (PCV) and complete blood count for each sample were also determined.Results: Out of the 186 dogs, 4 (2.15%) were found to be positive for the presence of microfilaria. Out of the 4 positive cases, 3 (1.61%) were microfilaria and 1 (0.54%) was unidentified motile parasite. A total of 104 females were examined and only 1 (0.96%) was positive, while 3 (3.66%) males out of 82 examined were positive. Out of 141 older dogs examined, 4 (2.84%) were positive. Hematology of the positive dogs revealed mild anemia and moderate thrombocytopenia with Mean+/-SD of 34.8+/-15.30% and 108+/-60.81x109/L, respectively. Conclusion: The study confirms Knott's technique to be the most sensitive in the diagnosis of dirofilariasis in dogs using parasitological techniques. The findings confirm the occurrence of D. immitis in dogs in Makurdi with low prevalence and that the general public are at high risk of spreading infection from the dogs. Infection is more in male and adult dogs. This work can assist in planning appropriate strategies for controlling and prevention of D. immitis infection in Nigeria. [J Adv Vet Anim Res 2016; 3(4.000): 338-344]

In an effort to better understand the role of vasodilators in the management of pulmonary hypertension associated with chronic heartworm disease (HWD), pulmonary hemodynamic measurements were obtained from 7 experimentally infected, anesthetized dogs before and after hydralazine administration (mean dose, 1.96 mg/kg of body weight). Five dogs were maintained on room air, while 2 were maintained on 100% oxygen during the hydralazine study. The hemodynamic effect of hydralazine in dogs with HWD was evaluated, using heart rate, cardiac index, mean pulmonary artery pressure, mean arterial pressure, total pulmonary resistance, total systemic resistance, total systemic resistance/total pulmonary resistance, left ventricular dP/dt(max), left ventricular end diastolic pressure, and left and right ventricular double products ([mean arterial pressure X heart rate] and [mean pulmonary artery pressure X heart rate], respectively). Responders were defined as those in which total pulmonary resistance decreased greater than or equal to 20% without an increase in mean pulmonary arterial pressure and in which heart rate increase was less than or equal to 10%. Comparison was also made between maximal hemodynamic effect of hydralazine with that after 100% oxygen administration for 15 minutes to previously normoxemic dogs (n = 5). Significance was determined if P < 0.05, using the paired t-test. Hydralazine induced significant reductions in mean pulmonary and systemic arterial pressures and total pulmonary resistance, with no significant change in heart rate, cardiac index, total systemic resistance, left ventricular dP/dt(max), left ventricular end diastolic pressure, or right and left ventricular double products. Four (57%) of the 7 dogs studied were considered responders. Pretreatment cardiac index, mean pulmonary artery pressure, and total pulmonary resistance did not allow differentiation of responders from nonresponders. However, pretreatment right ventricular end diastolic pressure was significantly less in responders than in nonresponders. Two dogs sustained hypotension after hydralazine administration, but no dogs had significant tachycardia. In dogs with experimentally induced HWD, treatment with hydralazine had significantly greater effect on cardiac index and mean pulmonary and systemic arterial pressures and resistance than did administration of 100% oxygen. These data indicate that further study of vasodilators for treatment of HWD-induced pulmonary hypertension may be warranted.

Medetomidine, an investigational drug indicated for clinical use as a short-term chemical restraint in dogs, was evaluated for its cardiopulmonary effects, in 10 naturally heartworm-infected (HW+) and 10 noninfected (HW-) Beagles. The drug was randomly administered IV (30 microgram/kg of body weight) and IM (40 microgram/kg) in single injections to all dogs. Heart rate, respiratory rate, ECG, blood gas tensions, blood pH, central venous and arterial pressures were measured at 0, 15, 30, 60, 90, 120, and 180 minutes. Medetomidine induced an immediate significant (P less than or equal to 0.001) increase in mean arterial blood pressure followed by decreased blood pressure that remained below normal throughout the study in both groups, irrespective of route of administration. Medetomidine increased central venous pressure, over time, for both groups and both routes of administration. Heart and respiratory rates were significantly (P less than or equal 0.001) decreased after medetomidine administration and remained reduced for the duration of the study in all dogs. The ECG variables were not significantly different between groups or between routes of administration. The HW+ dogs tended to have higher mean PaO2 than did HW- dogs at several postinjection determination times, particularly when the drug was administered IM. The PaO2 decreased during the first 30 minutes in both groups and tended to increase gradually thereafter. The pH decreased over time for both groups and both routes. A significant (P less than or equal to 0.05) decrease in pH was seen in the HW- dogs, compared with HW+ dogs at each measuring time for both routes. The PaCO2 did not significantly change for groups or routes. In general, bradycardia was the predominant cardiovascular effect seen after medetomidine administration in all dogs, irrespective of route. Lowering of blood pressure and heart rate (after a transient blood pressure increase) was synchronized with sedation in these dogs. The overall clinical response with regard to cardiopulmonary effects in HW+ dogs was similar to that in HW- dogs.

A crude, whole-body extract of female heartworms was administered IV to 10 dogs with and 13 dogs without heartworm (HW) infection. Shock developed in 8 of 10 infected dogs and 11 of 13 non-infected dogs, and blood coagulopathy was observed in 12 of 19 dogs with shock. Prevalence and severity of blood coagulopathy were proportionate to prevalence and severity of shock. Platelet count decreased in all dogs with shock with or without blood coagulopathy; thus, the decrease in platelet count might be related to shock. In 4 dogs, activated partial thromboplastin time (APTT) was prolonged--192.0 seconds at 30 minutes after HW injection--and prothrombin time (PT) was increased--13.8 seconds at initial collapse. In 8 dogs, APTT was increased--200 seconds for 2 hours after HW injection--and PT was increased--200 seconds at 30 minutes after the injection. The APTT prolongation might have been caused mainly by decreases in activities of factors VIII, IX, XI, and XII of the intrinsic blood coagulation pathway. In dogs with severely prolonged PT, plasma fibrinogen concentration and factor II activity decreased slightly. Prolonged PT was corrected in vitro by addition of normal plasma at high concentration (> 80%), but prolonged APTT could not be corrected in vitro by addition of 80% normal plasma. Serum fibrin degradation products concentration was < 10 microgram/ml, and soluble fibrin monomer complex was negative in all dogs. Thrombi were not found in blood vessels of any organ at necropsy and after histologic study. Therefore, it was suggested that blood coagulopathy resulting from inhibition of coagulation factor activities might develop in shock induced by HW extract.

A crude, whole-body extract of female or male heartworms was injected IV into 28 dogs with and 22 dogs without heartworm (HW) infection. The female HW extract caused shock in 22 of 24 dogs with and 12 of 20 dogs without HW infection. The male HW extract induced shock in 4 of 4 dogs with and 1 of 2 dogs without HW infection. Prevalence of shock caused by female HW extract was significantly (P < 0.05) higher in dogs with than without HW infection; shock developed 5 to 30 minutes after HW injection. These signs were observed: marked decrease in blood pressure; collapse (initial collapse); paleness of mucous membranes; weak heart sounds; dyspnea; skin coldness; intestinal hyperperistalsis, and defecation; increases in RBC count, serum total protein concentration, serum osmolality, serum Na and blood glucose concentrations; and decreases in neutrophil, eosinophil, and platelet counts. Alanine transaminase, alkaline phosphatase, and lactate dehydrogenase activities increased substantially from the time of initial collapse to 24 hours after HW injection. Of 39 dogs with shock, 29 recovered from initial collapse, but 5 of the 29 subsequently collapsed again (secondary collapse), with bloody diarrhea followed by death. Of these 39 dogs, 6 died during initial collapse without bloody diarrhea, and 4 were euthanatized during initial collapse. It was confirmed that HW extract had, in fact, induced shock. These clinical, hematologic, and biochemical findings were fundamentally similar to those associated with shock resulting from administration of drugs, such as diethylcarbamazine and milbemycin D, in microfilaremic dogs with HW infection.

Cardiopulmonary function values were determined before and after surgical removal of adult heartworms in 25 dogs with spontaneous and 4 dogs with drug-induced caval syndrome (CS). Fifteen dogs with spontaneous CS (recovery group) and 4 dogs with drug-induced CS (drug-induced CS group) recovered after removal, and 10 dogs with spontaneous cs were euthanatized or died (nonsurviving group). Before heartworm removal, injected radiographic contrast medium was regurgitated from the right ventricle to the right atrium. Mean pulmonary arterial pressure and total pulmonary resistance were not statistically different between the recovery and nonsurviving groups of dogs, but the end-diastolic right ventricular pressure (mean +/- SD, 6.9 +/- 9.1 mm of Hg) and the a (8.7 +/- 9.2 mm of Hg)- and v (6.3 +/- 8.5 mm of Hg)-waves of the right atrial pressure curve in the recovery group were less, respectively, than the end-diastolic right ventricular pressure (17.3 +/- 6.0 mm of Hg) and the a (15.8 +/- 6.1 mm of Hg)- and v (21.4 +/- 6.9 mm of Hg)-waves in dogs of the nonsurviving group. After heartworm removal, contrast medium regurgitation disappeared, and cardiac output of the right ventricle increased in dogs of the recovery (from 2.08 +/- 0.72 to 2.38 +/- 0.68 L/min; P < 0.05) and drug-induced CS (from 1.42 +/- 0.19 to 1.88 +/- 0.26 L/min, P < 0.05) groups. However, regurgitation remained, and cardiac output did not increase in some dogs of the nonsurviving group. Mean pulmonary arterial pressure decreased significantly (from 37.7 +/- 18.3 mm of Hg to 32.0 +/- 16.1 mm of Hg; P < 0.01) at 1 week after heartworm removal in dogs of the recovery group, but not in those of the nonsurviving group. Total pulmonary resistance (from 12,612 +/- 7,670 dynes.sec.cm-5.kg of body weight to 9,776 +/- 6,089 dynes.sec.cm-5.kg; P < 0.01) and right atrial pressure (a-wave: from 8.7 +/- 9.2 mm of Hg to 4.1 +/- 5.6 mm of Hg; v-wave: from 6.3 +/- 8.5 mm of Hg to 2.1 +/- 4.6 mm of Hg) decreased after heartworm removal in dogs of the recovery group. Total pulmonary resistance (from 20,309 +/- 9,682 dynes.sec.cm-5.kg to 15,970 +/- 6,798 dynes.sec.cm.5.kg; P < 0.05) and right atrial pressure (a-wave: from 15.8 +/- 6.1 mm of Hg to 10.1 +/- 6.3 mm of Hg; v-wave: from 21.4 +/- 6.9 mm of Hg to 11.1 +/- 3.7 mm of Hg) also decreased in dogs of the nonsurviving group. However, pressures in the right side of the heart and total pulmonary resistance after heartworm removal were greater in dogs of the nonsurviving group than in dogs of the recovery group. At necropsy pulmonary arterial emboli containing dead heartworms were found in almost all dogs with spontaneous CS, but not in dogs with drug-induced CS. The severity of pulmonary arterial embolism correlated significantly with mean pulmonary arterial pressure before (r = 0.710; P < 0.01) and 1 week after (r = 0.728; P < 0.01) heartworm removal.

Dirofilaria immitis in naturally infected dogs, enzyme-linked immunosorbent assay evaluated for diagnosis of occult infection; collective criteria for diagnosis of occult infection

Hematologic values were determined in blood samples obtained from 203 normal, healthy Jindo dogs of both sexes that ranged in age from 3 months to 10 years. Age-related differences were detected for the total erythrocyte count, hemoglobin content, PCV and the number of eosinophils. The persistent eosinophilia appears to be due to the dirofilariasis and flea-allergy dermatitis