Effects of sodium nitroprusside after load reduction and/or atropine pre-treatment prior to dexmedetomidine administration on cardiovascular variables in dogs

The purpose of this study was to determine the cardiovascular effects of sodium nitroprusside (SNP)‐induced after load reduction in dogs administered dexmedetomidine (DEX). Using a randomized crossover design and allowing at least 2 weeks between treatments 12 adult hound dogs of either sex weighing 22 ± 1.7 SD kg were anesthetized by face mask administration of 2.9% ET sevoflurane to facilitate instrumentation prior to administration of treatment drugs. Dogs were intubated and instrumented to enable measurement of heart rate (HR), systolic (SAP), mean (MAP) and diastolic (DAP) arterial pressures, mean pulmonary arterial pressure (PAP), pulmonary capillary wedge pressure (PCWP), central venous pressure (CVP), pulmonary arterial temperature (TEMP), and cardiac output (CO). Systemic (SVR) and pulmonary vascular resistances were calculated. Following completion of instrumentation dogs were allowed to recover for 40 minutes. After collection of baseline data, dogs were administered one of four treatments at T–10 minutes prior to injection of DEX (500? g M^–2 IM): 1) saline (SAL); 2) atropine (ATR, 0.02 [n = 6] or 0.04 [n = 6] mg kg^–1 IM); 3) SAL + SNP (infused at 1–10 ?g kg^–1 minute^–1, IV as needed to maintain MAP between 90–110 mm Hg; or 4) ATR + SNP. Cardiovascular data were collected at T‐20 minutes prior to administration of DEX, T‐5 and at 5, 10, 20, 30, 40, and 60 minutes following DEX. Data were analyzed using anova for repeated measures with post hoc differences between means identified using Bonferroni's method (p < 0.05). Differences in ATR dose were not found to be significant and thus results for ATR dose groups were pooled. Administration of SAL (dexmedetomidine alone) was associated with decreases in HR and CO and increases in SAP, MAP, DAP, CVP, and SVR. Administration of ATR was associated with an increase in HR and CO compared with SAL. Administration of SNP was associated with an increase in HR and CO and a decrease in SVR, MAP and CVP compared with SAL. Administration of SNP + ATR was associated with effects similar to that of SNP or ATR alone and resulted in an additive increase in CO. We conclude that SNP‐induced afterload reduction with or without atropine is effective in mitigating DEX‐induced impairment of cardiovascular function.     

Recovery from neuromuscular block in dogs: restoration of spontaneous ventilation does not exclude residual blockade

ObjectiveTo evaluate if return of spontaneous ventilation to pre-relaxation values indicates complete recovery from neuromuscular blockade.Study designProspective, with each individual acting as its own control.AnimalsTen healthy adult female Beagle dogs weighing 6.2–9.4 kg.MethodsDogs were anesthetized with propofol, dexemedetomidine and isoflurane. Spontaneous ventilation was assessed by measuring end-tidal CO₂, expired tidal volume, peak inspiratory flow, respiratory rate and minute ventilation. Vecuronium 25 μg kg^?1 IV was administered and neuromuscular block was evaluated by measuring the train-of-four (TOF) ratio with acceleromyography in the hind limb. During spontaneous recovery from neuromuscular block, the TOF ratio when each ventilatory variable returned to baseline was recorded.ResultsThis dose of vecuronium produced moderate neuromuscular block in all dogs, with TOF ratio values of 0–18% at maximal block. Expired tidal volume, peak inspiratory flow and minute ventilation returned to pre-relaxation values when the median TOF ratio was ≤ 20%. The median TOF ratio was 42% when the end-tidal CO₂ returned to pre-relaxation values.Conclusions and clinical relevanceSignificant residual neuromuscular block could be measured at the hind limb with acceleromyography when ventilation had spontaneously returned to pre-vecuronium values. Monitoring spontaneous ventilation, including end-tidal CO₂, expired tidal volume, peak inspiratory flow or minute ventilation cannot be used as a surrogate for objective neuromuscular monitoring, and this practice may increase the risk of postoperative residual paralysis.     

Myophosphorylase deficiency (glycogen storage disease Type V) in a herd of Charolais cattle in New Zealand: Confirmation by PCR-RFLP testing

AIM: To describe a disease of muscle in Charolais calves and confirm the putative diagnosis of inherited myophosphorylase deficiency.

METHODS: Variously stained paraffin sections of muscle prepared from affected calves were used to describe the lesions. A polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) test was developed and applied to affected calves, their sires, dams and other individuals.

RESULTS: The lesions were those of rhabdomyolysis of skeletal muscles and sub-sarcolemmal spaces in normal fibres. The PCR-RFLP test confirmed the expected mutation for phosphorylase deficiency of Charolais cattle in two affected calves. In addition, sires, dams and other closely-related individuals of four affected calves tested as heterozygous for the mutation. Other apparently unrelated animals also tested as heterozygous.

CONCLUSIONS: The diagnosis of myophosphorylase deficiency was confirmed. The PCR-RFLP test is suitable for use in controlling this recessively-inherited disorder as it can diagnose heterozygous individuals that are otherwise clinically normal.     

Cardiovascular effects of sevoflurane in Holstein calves

Objective The purpose of this study was to determine the cardiovascular effects of sevoflurane in calves. Study design Prospective experimental study. Animals Six, healthy, 8–12‐week‐old Holstein calves weighing 80 ± 4.5 (mean ± SEM) kg were studied. Methods Anesthesia was induced by face‐mask administration of 7% sevoflurane in O₂. Calves tracheae were intubated, placed in right lateral recumbency, and maintained with 3.7% end‐tidal concentration sevoflurane for 30 minutes to allow catheterization of the auricular artery and placement of a Swan‐Ganz thermodilution catheter into the pulmonary artery. After instrumentation, administration of sevoflurane was temporarily discontinued until mean arterial pressure was > 100 mm Hg. Baseline values were recorded and the vaporizer output increased to administer 3.7% end‐tidal sevoflurane concentration. Ventilation was controlled to maintain normocapnia. The following were recorded at 5, 10, 15, 30 and 45 minutes after collection of baseline data and expressed as the mean value (± SEM): direct systolic, diastolic, and mean arterial blood pressures; cardiac output; mean pulmonary arterial pressure; pulmonary arterial occlusion pressure, heart rate; and pulmonary arterial temperature. Cardiac index and systemic and pulmonary vascular resistance values were calculated using standard formulae. Arterial blood gases were analyzed at baseline, and at 15 and 45 minutes. Differences from baseline values were determined using one‐way analysis of variance for repeated measures with post‐hoc differences between mean values identified using Dunnet's test (p < 0.05). Results Mean time from beginning sevoflurane administration to intubation of the trachea was 224 ± 9 seconds. The mean end‐tidal sevoflurane concentration at baseline was 0.7 (± 0.11)%. Sevoflurane anesthesia was associated with decreased arterial blood pressure at all sampling times. Mean arterial blood pressure decreased from a baseline value of 112 ± 7 mm Hg to a minimum value of 88 ± 4 mm Hg at 5 minutes. Compared with baseline, arterial pH was decreased at 15 minutes. Pulmonary arterial blood temperature was decreased at 15, 30 and 45 minutes. Arterial CO₂ tension increased from a baseline value of 43 ± 3 to 54 ± 4 mm Hg (5.7 ± 0.4 to 7.2 ± 0.3 kPa) at 15 minutes. Mean pulmonary arterial pressure was increased at 30 and 45 minutes. Pulmonary arterial occlusion pressure increased from a baseline value of 18 ± 2 to 23 ± 2 mm Hg at 45 minutes. There were no significant changes in other measured variables. All calves recovered from anesthesia uneventfully. Conclusion We conclude that sevoflurane for induction and maintenance of anesthesia was effective and reliable in these calves and that neither hypotension nor decreased cardiac output was a clinical concern. Clinical relevance Use of sevoflurane for mask induction and maintenance of anesthesia in young calves is a suitable alternative to injectable and other inhalant anesthetics.     

Prickly paddy melon (Cucumis myriocarpus) poisoning of cattle

Twenty-six Hereford heifers died after eating mostly ripe fruit of Cucumis myriocarpus growing in a fallowed cultivation paddock. Four affected cattle were dehydrated and apparently had abdominal pain. Necropsy of three revealed intense congestion with haemorrhage of the alimentary tract, numerous C. myriocarpus seeds in ruminal contents, pulmonary congestion and oedema and, in two, swollen livers. Midzonal swelling and vacuolation of hepatocytes occurred in these two. C. myriocarpus fruit (83% by weight ripe) were dosed to two calves at 60 g wet weight/kg live weight. Both collapsed with tachycardia and dyspnoea and died within 6 h. Their packed cell volumes just before death had increased to 0.7. They had hydropic degeneration and necrosis of the ruminal mucosa, intense congestion and oedema of the rumen, abomasum and intestines, swollen and vacuolated hepatocytes and foci of myocardial degeneration and necrosis. Two other calves were dosed daily with 20 g fruit/kg for three days, then 40 g/kg for three days. One calf received a further 40 g/kg next day. Both calves developed persistent diarrhoea and neutrophilia, and their plasma gamma glutamyltransferase and bilirubin concentrations increased. Necropsy revealed necrosis and oedema of the rumen and swollen degenerate hepatocytes.     

Blood supply of the ovine adrenal gland and its relevance in adrenal autotransplantation

SUMMARY The arterial supply and venous drainage of 62 left and 5 right ovine adrenal glands is described, and the contribution of individual arteries to successful adrenal gland autotransplantation was evaluated. Arterial flow was measured by direct collection from the draining adrenal vein. Assessment of function of the transplanted adrenal gland was made from survival of the sheep and by the cortisol response to infusion of ACTH and the aldosterone secretory response to infusion of angiotensin II or potassium. For the left adrenal, the principal arterial supply was from the renal artery in 21 (34%), a lumbar artery in 32 (52%), and the anterior mesenteric artery in 3. The total blood flow was 5.0 ± SEM 0.4 mL/min, the flow from the renal branch 2.3 ± 0.3 mL/min, and the principal lumbar branch 2.6 ± 0.3 mL/min. Venous drainage from the left adrenal was via a major adrenal vein to the left renal vein, but additional tributaries to the renal vein were present in 26% . The arterial supply to the adrenal is regional and omission of a branch at transplantation could result in infarction of portion of the gland. By defining arterial supply and measuring blood flow, selection of the appropriate artery or multiple arteries can achieve an adrenal gland autotransplant survival of 90% .     

Segmental axonopathy of Merino sheep in New Zealand

AIM: To investigate an axonopathy of Merino sheep that caused progressive hindlimb ataxia and slight to moderate paresis, with the purpose of understanding its pathogenesis.

METHODS: Tissues were fixed in buffered paraformaldehyde or paraformaldehyde and glutaraldehyde, processed into wax and epoxy resin, respectively, and examined by light and electron microscopy. Fresh frozen spinal cord and trigeminal nerve roots were subjected to homogenisation, centrifugation and two-dimensional electrophoresis. Selected protein spots were identified using matrix-assisted laser desorption ionisation (MALDI) mass spectrometry.

RESULTS. By light microscopy, there were large pale foamy spheroidal axonal swellings affecting peripheral as well as central axons. By electron microscopy, these were shown to contain many membrane-bound vesicles. The main abnormalities in expressed proteins involved cytoskeletal elements and myosin heavy chain, the latter interpreted as associated with the molecular motor myosin Va.

CONCLUSIONS: The disorder is the same as that described in Merinos in Australia as segmental axonopathy, and believed to have an inherited aetiology. The lesions and protein changes indicate abnormalities of the cytoskeleton, its relationship with the myelin sheath, and myosin Va molecular motor. The consequence appears to be abnormal axonal transport and inability to maintain the integrity of axons and their myelin sheaths.