ISSN:0425-1644    

DOI:10.1111/j.2042-3306.1996.tb01578.x

出版商:Blackwell Publishing Ltd    

年代:1996

数据来源: WILEY

ISSN:0425-1644    

DOI:10.1111/j.2042-3306.1996.tb01579.x

出版商:Blackwell Publishing Ltd    

年代:1996

数据来源: WILEY

ISSN:0425-1644    

DOI:10.1111/j.2042-3306.1996.tb01580.x

出版商:Blackwell Publishing Ltd    

年代:1996

数据来源: WILEY

ISSN:0425-1644    

DOI:10.1111/j.2042-3306.1996.tb01581.x

出版商:Blackwell Publishing Ltd    

年代:1996

数据来源: WILEY

ISSN:0425-1644    

DOI:10.1111/j.2042-3306.1996.tb01582.x

出版商:Blackwell Publishing Ltd    

年代:1996

数据来源: WILEY

ISSN:0425-1644    

DOI:10.1111/j.2042-3306.1996.tb01583.x

出版商:Blackwell Publishing Ltd    

年代:1996

数据来源: WILEY

ISSN:0425-1644    

DOI:10.1111/j.2042-3306.1996.tb01585.x

出版商:Blackwell Publishing Ltd    

年代:1996

数据来源: WILEY

摘要:

SummaryThe potential for participation of the arginine‐nitric oxide system in the aetiology of acute equine laminitis has been assessed. Nitric oxide (NO), produced by the action of NO synthase (NOS) on its substratel‐arginine, relaxes vascular smooth muscle to cause vasodilatation. An attenuated normal vasodilatory tone may characterise the pathogenesis of acute equine laminitis. An intravenous infusion of 10%l‐arginine in 0.9% saline caused vasodilatation in the hoof of a normal pony and immediate reperfusion of laminal tissues in an acutely laminitic pony, detected noninvasively by near infrared spectroscopy (NIRS), but the amino acid had little effect on systemic blood pressure. Treatment of acute laminitis with glyceryl trinitrate applied topically to the pasterns reduced the typical ‘bounding pulses’ in treated limbs, reduced lameness and lowered systemic blood pressure. Nitric oxide is likely to participate in the multifactorial pathogenesis of equine

ISSN:0425-1644    

DOI:10.1111/j.2042-3306.1996.tb01586.x

出版商:Blackwell Publishing Ltd    

年代:1996

数据来源: WILEY

摘要:

SummaryThe highest no effect doses (HNEDs) for the local anaesthetic (LA) effects of procaine, cocaine, bupivacaine and benzocaine were determined using the heat lamp/hoof withdrawal model of Kamerlinget al. (1985b) and the abaxial sesamoid block model of local anaesthesia. The heat lamp rapidly (4 or 5 s) increased the temperature of the superficial skin layers of the pastern to about 90°C, at which point the animal sharply withdrew its hoof. Effective LA blockade precluded this response and superficial skin temperatures exceeded 120°C. Thermal stimulus experiments were routinely terminated after 10 s of exposure to prevent undue tissue damage.Following abaxial sesamoid block with bupivacaine, the HNED for that drug was about 0.25 mg/site. Increasing the dose to 2 mg/site apparently produced complete and prolonged LA blockade.Analogous work showed that the HNED for procaine was about 2.5 mg/site. Similarly, the dose response curve for procaine was parallel with that of bupivacaine but was shifted 10‐fold to the right The duration of the LA response following procaine injection was less than for bupivacaine with the statistically significant response following 40 mg/site injection lasting less than 45 min.Cocaine was less potent than procaine, showing a shallower dose response curve. The HNED for cocaine was less than 5 mg/site, although at this dose the duration of action was extremely short (<7.5 min). Benzocaine had no significant LA action when a dose of 800 mg was applied topically as a 5% preparation.These results show that the HNEDs for bupivacaine and procaine are remarkably low, that cocaine is somewhat less potent as a LA than might be expected, and that 5% topical benzocaine has no significant pharmacology. The small doses of bupivacaine and procaine producing effective local anaesthesia suggests that developing plasma thresholds for these agents is likely to be very challeng

ISSN:0425-1644    

DOI:10.1111/j.2042-3306.1996.tb01587.x

出版商:Blackwell Publishing Ltd    

年代:1996

数据来源: WILEY

摘要:

SummaryThirty‐two dorsal, mid‐hoof wall, lamellar sections from 8 Standard bred horses, humanely killed 48 h after the administration of an alimentary carbohydrate overload, were sectioned and examined by light microscopy. Sections were stained with the connective tissue and basement membrane stains periodic acid‐Schiff (PAS), Azan and periodic acid silver methanamine (PASM) and with routine haematoxylin and eosin (H&E). Lesions of the epidermal lamellae, attributable to laminitis, were graded in order of increasing severity fromGrade N(normal),Grade 1(mild),Grade 2(moderate) toGrade 3(severe and extensive). The grading system was based principally on changes to lamellar basement membrane (BM) which were clearly visible when the connective tissue stains PAS and PASM were used. Earliest changes were rounding of the basal cell nuclei and elongation of secondary epidermal lamellae (SELs). Secondary epidermal lamellae tips were pointed instead of round and the basement membrane had separated from the lamellae. In earlyGrade 1lesions, this was obvious at the tips of the SELs where the BM had lifted to form teat‐shaped bubbles. The absence of BM at the tips of secondary dermal lamellae, along with varying amounts of connective tissue, was considered a progression in severity and classified asGrade 2. Eventually, even the primary epidermal and primary dermal lamellae separated from each other and the empty shells of isolated BM, in what was once the tip of the primary epidermal lamella, signified that a global separation of the epidermal and dermal lamellae had occurred (Grade 3lesion). The histopathological grading system correlated well with the degree of lameness at the time of euthanasia, (r2= 0.94) and apparently described the severity of laminitis accurately. Disintegration of the BM and failure of its attachment to the basal cells of the epidermis appears to be one of the earliest pathological events to occur in acute laminitis and could be the change that initiates the collapse of the lamellar architecture. Histopathological diagnoses of laminitis are strengthened when based on sections stained with at least PAS, in addition to routine H&E and should exhibit evidence of the BM pathology describ

ISSN:0425-1644    

DOI:10.1111/j.2042-3306.1996.tb01588.x

出版商:Blackwell Publishing Ltd    

年代:1996

数据来源: WILEY