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  • Author or Editor: Ryohei Nishimura x
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Abstract

Objective—To determine the effects of nitrous oxide (N2O) on the speed and quality of mask induction with sevoflurane or isoflurane in dogs.

Animals—7 healthy Beagles.

Procedure—Anesthesia was induced with sevoflurane or isoflurane delivered in 100% oxygen or in a 2:1 mixture of N2O and oxygen via a face mask. Each dog received all treatments with at least 1 week between treatments. Initial vaporizer settings were 0.8% for sevoflurane and 0.5% for isoflurane (0.4 times the minimum alveolar concentration [MAC]). Vaporizer settings were increased by 0.4 MAC at 15-second intervals until settings were 4.8% for sevoflurane and 3.0% for isoflurane (2.4 MAC). Times to onset and cessation of involuntary movements, loss of the palpebral reflex, negative response to tail-clamp stimulation, and endotracheal intubation were recorded, and cardiopulmonary variables were measured.

Results—Administration of sevoflurane resulted in a more rapid induction, compared with isoflurane. However, N2O had no effect on induction time for either agent. Heart rate, mean arterial blood pressure, cardiac output, and respiratory rate significantly increased and tidal volume significantly decreased from baseline values immediately after onset of induction in all groups. Again, concomitant administration of N2O had no effect on cardiopulmonary variables.

Conclusions and Clinical Relevance—Administration of N2O did not improve the rate or quality of mask induction with sevoflurane or isoflurane. The benefits provided by N2O attributable to concentrating and second gas effects appear minimal in healthy dogs when low solubility inhalation agents such as isoflurane and sevoflurane are used for mask induction. (Am J Vet Res 2001;62:1727–1733).

Full access
in American Journal of Veterinary Research

Abstract

Objective—To characterize the effects of medetomidine- midazolam, midazolam-butorphanol, or acepromazine- butorphanol as premedicants for mask induction of anesthesia with sevoflurane in dogs.

Animals—10 healthy Beagles.

Procedure—The following premedicants were administered intramuscularly: medetomidine-midazolam (20 µg/kg and 0.3 mg/kg, respectively), midazolambutorphanol (0.1 and 0.2 mg/kg, respectively), and acepromazine-butorphanol (0.05 and 0.2 mg/kg, respectively). Saline (0.9% NaCl) solution (0.1 ml/kg) was administered intramuscularly as a control. Anesthesia was induced in each dog with sevoflurane in a 100% O2 at a flow rate of 4 L/min developed by a facemask. Vaporizer settings were increased by 0.8% at 15-second intervals until the value corresponding to 4.8% sevoflurane was achieved. Time to onset and cessation of involuntary movements, loss of the palpebral reflex, negative response to tail-clamp stimulation, and endotracheal intubation were recorded, and the cardiopulmonary variables were measured.

Results—Mask induction with sevoflurane in dogs that received each premedicant resulted in a shorter induction time and milder changes in heart rate, mean arterial blood pressure, cardiac output, and respiratory rate, compared with mask induction without premedicants. Treatment with medetomidine-midazolam resulted in a shorter and smoother induction, compared with acepromazine-butorphanol or midazolambutorphanol treatment, whereas the cardiovascular changes were greater. Cardiopulmonary variables of dogs during induction following treatment with acepromazine- butorphanol or midazolam-butorphanol were maintained close to the anesthetic maintenance values for sevoflurane, with the exception of mild hypotension that was observed in dogs following acepromazine-butorphanol treatment.

Conclusion and Clinical Relevance—In dogs use of premedicants provides a smoother and better quality mask induction with sevoflurane. (Am J Vet Res 2002;63:1022–1028)

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in American Journal of Veterinary Research

Abstract

Objective—To characterize and determine the sensory innervation of respiratory reflexes elicited by nasal administration of halothane to dogs.

Animals—10 healthy Beagles.

Procedure—Dogs underwent permanent tracheostomy and, 2 to 3 weeks later, were anesthetized with thiopental and α-chloralose administered IV. The nasal passages were functionally isolated so that halothane could be administered to the nasal passages while dogs were breathing 100% O2 via the tracheostomy. Respiratory reflexes in response to administration of halothane at concentrations of 1.25, 1.75, and 2.5 times the minimum alveolar concentration (MAC), and 5% (administered in 100% O2 at a flow rate of 5 L/min) were recorded. Reflexes in response to administration of 5% halothane were also recorded following transection of the infraorbital nerve, transection of the caudal nasal nerve, and nasal administration of lidocaine.

Results—Nasal administration of halothane induced an inhibition of breathing characterized by a dosedependent increase in expiratory time and a resultant decrease in expired volume per unit time. Effects were noticeable immediately after the onset of halothane administration and lasted until its cessation. Reflex responses to halothane administration were attenuated by transection of the caudal nasal nerve and by nasal administration of lidocaine, but transection of the infraorbital nerve had no effect.

Conclusions and Clinical Relevance—Nasal administration of halothane at concentrations generally used for mask induction of anesthesia induces reflex inhibition of breathing. Afferent fibers in the caudal nasal nerve appear to play an important role in the reflex inhibition of breathing induced by halothane administration. (Am J Vet Res 2000;61:260–267)

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in American Journal of Veterinary Research

Abstract

Objective—To evaluate dose-sparing effects of medetomidine-midazolam (MM), acepromazinebutorphanol (AB), and midazolam-butorphanol (MB) on the induction dose of thiopental and propofol and to examine cardiopulmonary changes in dogs.

Animals—23 healthy Beagles.

Procedure—Dogs were administered MM, AB, MB, or physiologic saline (0.9% NaCl) solution (PS) IM, and anesthesia was induced with thiopental or propofol. Cardiopulmonary measurements were obtained before and after administration of medication and 0, 5, 10, and 15 minutes after endotracheal intubation.

Results—Induction doses were reduced significantly by preanesthetic administration of MM, AB, and MB (thiopental, 20, 45, and 46% after administration of PS; propofol, 42, 58, and 74% after administration of PS, respectively). Recovery time in dogs administered MM-thiopental or MM-propofol and AB-propofol were significantly prolonged, compared with recovery time in dogs administered PS-thiopental or PS-propofol. Relatively large cardiovascular changes were induced by administration of MM, which were sustained even after the induction of anesthesia. Administration of AB and MB induced cardiovascular changes during and immediately after endotracheal intubation that were significantly decreased by induction with thiopental or propofol. However, mild hypotension developed with AB-propofol. Apnea was observed in dogs administered MM during induction of anesthesia, but most respiratory variables did not change significantly.

Conclusions and Clinical Relevance—Preanesthetic medication with MM greatly reduced the anesthesia induction dose of thiopental and propofol but caused noticeable cardiopulmonary changes. Preanesthetic medication with AB and MB moderately reduced the induction dose of thiopental and propofol and ameliorated cardiovascular changes induced by these anesthetics, although AB caused mild hypotension. (Am J Vet Res 2002;63:1671–1679)

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in American Journal of Veterinary Research

Abstract

Objective—To determine differentiation and growth inhibition effects of retinoids on canine osteosarcoma cells.

Sample Population—3 osteosarcoma cell lines established from osteosarcomas in dogs.

Procedure—Osteosarcoma cells were incubated with various concentrations of all-trans-retinoic acid and 9-cis-retinoic acid or control medium, counted daily for 10 days, and evaluated for morphologic changes. Synthesis of DNA was measured by use of a cell proliferation ELISA. To analyze effect of retinoids on colony formation on plastic dishes, cells were cultured for 14 days, fixed, and stained; number of colonies was counted.

Results—In a dose-dependent manner, both retinoids induced morphologic differentiation and growth inhibition in the 3 osteosarcoma cell lines and inhibited each cell's ability to form anchorage-dependent colonies.

Conclusion and Clinical Relevance—Retinoids induced differentiation of osteosarcoma cells of dogs, resulting in altered expression of their malignant phenotype. Induction of differentiation by retinoids may have potential as an adjunctive treatment for osteosarcoma in dogs. (Am J Vet Res 2000;61:69–73)

Full access
in American Journal of Veterinary Research

Abstract

Objective—To determine effects of all-trans and 9-cis retinoic acid (RA) on tumor growth and metastatic ability of canine osteosarcoma cells transplanted into athymic (nude) mice.

Animals—Forty-five 5-week-old female BALB/c nude mice.

Procedure—1 × 107 POS osteosarcoma cells were transplanted subcutaneously into the intrascapular region of mice. All-trans RA (3 or 30 µg/kg of body weight in 0.1 ml of sesame oil), 9-cis RA (3 or 30 mg/kg in 0.1 ml of sesame oil), or sesame oil (0.1 ml; control treatment) were administered intragastrically 5 d/wk for 4 weeks beginning 3 days after transplantation (n = 4 mice/group) or after formation of a palpable tumor (5 mice/group). Tumor weight was estimated weekly by measuring tumor length and width, and retinoid toxic effects were evaluated daily. Two weeks after the final treatment, mice were euthanatized, and number of mice with pulmonary metastases was determined.

Results—Adverse treatment effects were not detected. Tumor weight was less in mice treated with either dose of 9-cis RA than in control mice, although this difference was not significant. Treatment with 30 mg of 9-cis RA/kg initiated after tumor formation significantly reduced the incidence of pulmonary metastasis, compared with the control group.

Conclusions and Clinical Relevance—9-cis RA decreased the incidence of pulmonary metastasis in nude mice transplanted with canine osteosarcoma cells and may be a potential adjunct therapy for treatment of osteosarcoma in dogs. (Am J Vet Res 2000; 61:1241–1244)

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in American Journal of Veterinary Research

Abstract

Objective—To characterize respiratory reflexes elicited by nasal administration of sevoflurane (Sevo), isoflurane (Iso), or halothane (Hal) in anesthetized dogs.

Animals—8 healthy Beagles.

Procedure—A permanent tracheostomy was created in each dog. Two to 3 weeks later, dogs were anesthetized by IV administration of thiopental and α-chloralose. Nasal passages were isolated such that inhalant anesthetics could be administered to the nasal passages while the dogs were breathing 100% O2 via the tracheostomy. Respiratory reflexes in response to administration of each anesthetic at 1.2 and 2.4 times the minimum alveolar concentration (MAC) and the full vaporizer setting (5%) were recorded. Reflexes in response to administration of 5% of each anesthetic also were recorded following administration of lidocaine to the nasal passages.

Results—Nasal administration of Sevo, Iso, and Hal induced an immediate ventilatory response characterized by a dose-dependent increase in expiratory time and a resulting decrease in expired volume per unit of time. All anesthetics had a significant effect, but for Sevo, the changes were smaller in magnitude. Responses to administration of each anesthetic were attenuated by administration of lidocaine to the nasal passages.

Conclusions and Clinical Relevance—Nasal administration of Sevo at concentrations generally used for mask induction of anesthesia induced milder reflex inhibition of breathing, presumably via afferent neurons in the nasal passages, than that of Iso or Hal. Respiratory reflexes attributable to stimulation of the nasal passages may contribute to speed of onset and could promote a smoother induction with Sevo, compared with Iso or Hal. (Am J Vet Res 2001;62:311–319)

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in American Journal of Veterinary Research

Abstract

Objective—To characterize the clinical features of visceral mast cell tumors (MCT) without associated cutaneous involvement in dogs.

Design—Retrospective study.

Animals—10 dogs with histologically confirmed MCT without associated cutaneous lesions.

Procedure—Information on signalment, clinical signs, laboratory examinations, and time from first admission to death was obtained from the medical record of each dog.

Results—Purebred male dogs of miniature breeds appeared to have a higher prevalence of visceral MCT. Clinical signs included anorexia, lethargy, vomiting, and diarrhea. Anemia (n = 7), hypoproteinemia (5), and mastocythemia (5) were detected. Treatments, including glucocorticoids, were not successful. Primary sites of tumors were the gastrointestinal tract (n = 6) and the spleen or liver (1); the primary site was not confirmed in the remaining 3 dogs. In 7 dogs, tumors were categorized as grade II or III, on the basis of histologic findings. The prognoses were poor, and all dogs died within 2 months after first admission.

Conclusions and Clinical Relevance—Visceral MCT is uncommon in dogs, and the prognosis is extremely poor. Biological behavior and drug susceptibility of visceral MCT may be different from cutaneous MCT. The lack of specific clinical signs may result in delay of a definitive diagnosis. The rapid progression of clinical signs and difficulty in diagnosis contributes to a short survival time. ( J Am Vet Med Assoc 2000;216: 222–226)

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in Journal of the American Veterinary Medical Association

Abstract

Objective—To measure telomere length and telomerase activity in naturally occurring canine mammary gland tumors.

Sample Population—27 mammary gland tumor specimens obtained during resection or necropsy and 12 mammary gland tissue specimens obtained from healthy (control) dogs.

Procedure—Telomere length in tissue specimens was measured by use of restriction endonuclease digestion and Southern blot analysis. Telomerase activity was measured by use of a telomeric repeat amplification protocol assay.

Results—Telomere length in mammary gland tumors ranged from 11.0 to 21.6 kilobase pairs (kbp; mean ± SEM, 14.5 ± 0.5 kbp) but did not differ among tumor types. Telomeres in mammary gland tumors were slightly shorter than in normal tissue specimens, but telomere length could not be directly compared between groups, because mean age of dogs was significantly different between groups. Age was negatively correlated with telomere length in control dogs but was not significantly correlated with length in affected dogs. Telomerase activity was detected in 26 of 27 mammary gland tumors and in 4 of 12 normal tissue specimens. However, telomerase activity and telomere length were not correlated in tumor specimens.

Conclusion and Clinical Relevance—Telomere length is maintained in canine mammary gland tumors regardless of the age of the affected dog. Measurement of telomere length may be a useful tool for monitoring the in vivo effects of telomerase inhibitors in dogs with tumors. (Am J Vet Res 2001; 62:1539–1543)

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in American Journal of Veterinary Research

Abstract

Objective—To evaluate aberrations of the p53 tumor suppressor gene in naturally developing tumors in dogs.

Sample Population—Tumor specimens from 15 dogs with various tumors, including malignant lymphoma (7 dogs), monocytic leukemia (1), mammary gland adenoma (1), mammary gland benign mixed tumor (1), rhabdomyosarcoma (1), colon cancer (1), and osteosarcoma (3).

Procedure—Aberrations of the p53 gene in these tumor tissues were examined by reverse transcriptase- polymerase chain reaction and single-strand conformation polymorphism analysis, using 3 fragments that covered the entire open reading frame of the canine p53 gene, followed by nucleotide sequencing of the abnormal bands.

Results—Point mutations, deletions, and insertions resulting in a number of amino acid substitutions of wild-type p53 were detected in 7 of the 15 tumor specimens from dogs with malignant lymphoma, monocytic leukemia, rhabdomyosarcoma, colon cancer, and osteosarcoma. Of these 7 dogs, 2 had aberrations of the p53 gene on both alleles, whereas 5 had aberrations of the p53 gene on 1 allele and concurrently lacked the wild-type p53 transcript. Many of the aberrations of the p53 gene detected in these tumors were located in the transactivation, DNA binding, and oligomerization domains.

Conclusions and Clinical Relevance—Various naturally developing tumors in dogs often have inactivation of the p53 tumor suppressor gene, which may be 1 of the multiple step-wise genetic changes during tumorigenesis. This study indicates that p53 gene can be a target for gene therapy for tumors in dogs. (Am J Vet Res 2001;62:433–439)

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in American Journal of Veterinary Research