A rabbit ear model for cold stress testing

Tl, Smith; Gordon, Stan; Mb, Holden; Bp, Smith; Gb, Russell; La, Koman

doi:10.1002/micr.1920150808

Cited by 9 publications

(6 citation statements)

References 11 publications

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“…The rabbit ear model permits dircct microvascular observations of arteriovenous anastomoses (19). Following a cold thermal stress, the auricular circulation in normal rabbits is characterized by an overall reduction in blood flow in the ear and cutancous perfusion similar to that observed in human digits (22). Recent in vivo studies of the rabbit have identified specific receptor innervation of the ear microvasculature, with a,-adrenoceptor control predominating over arteriovenous anastomosis regulation (18).…”

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confidence: 99%

Effect of cooling on cutaneous microvascular adrenoceptors in vivo in the rabbit ear

Koman

Rosencrance

et al. 1998

Journal Orthopaedic Research

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Previous studies have suggested that moderate cooling increases the responsiveness of vascular alpha2-adrenoceptors. However, limited information is available documenting the influence of temperature changes on adrenoceptor responses in the microvasculature of thermoregulatory organs (e.g., the human digit and the rabbit ear) subjected to a wide range of temperatures. In the present study, the effect of local cooling (24 degrees C) on cutaneous microvascular adrenoceptors in the ear was observed in vivo in male New Zealand White rabbits (total: 66 ears). The rabbit ear was studied in a temperature-controlled tissue bath; the ear preparation was pretreated with terazosin (an alpha1-adrenoceptor antagonist) (10(-5) M) or a combination of terazosin (10(-5) M) and propranolol (a beta-adrenoceptor antagonist) (10(-6) M). The microvascular diameter responses of the ear to norepinephrine (10(-11)-10(-4) M) then were determined at 24 or 34 degrees C, respectively, to determine the influences of low temperature on adrenoceptor responses to norepinephrine stimulation. The results demonstrated that low concentrations of norepinephrine induced vasodilation in arterioles and arteriovenous anastomoses. This vasodilation was followed by vasoconstriction with an increased concentration of norepinephrine in animals with alpha1-adrenergic blockade at 34 degrees C. Moderate tissue cooling increased the microvascular maximal response of the rabbit ear to norepinephrine and abolished the vasodilatation induced by a low concentration of norepinephrine. There was no significant difference in the microvascular response to norepinephrine between the two temperature conditions after simultaneous blockade of alpha1-adrenoceptors and beta-adrenoceptors. Data from the present study indicate that moderate cooling does not enhance the responsiveness of alpha2-adrenoceptors to norepinephrine. In contrast, cooling reduced the beta-adrenergic activity of arterioles and arteriovenous anastomoses after norepinephrine stimulation.

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Effect of cooling on cutaneous microvascular adrenoceptors in vivo in the rabbit ear

Koman

Rosencrance

et al. 1998

Journal Orthopaedic Research

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“…This system allows the dual microvascular functions of maintenance of tissue nutrition (through the capillaries) and temperature regulation (through the arteriovenous anastomoses) (5). Thermoregulatory blood vesscls of the skin mediate homeostasis of body temperature by dilating in response to heating and constricting in response to cooling (19). Dilation of the arteriovenous anastomoses causes warm blood from the arterial circulation to pass into the deep venous plexus of the dermis.…”

Section: Discussionmentioning

confidence: 99%

Role of Alpha-1 Adrenoceptor Subtypes Mediating Constriction of the Rabbit Ear Thermoregulatory Microvasculature

Silver

Koman

et al. 2000

The Journal of Bone and Joint Surgery-American Volume

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Summary: An acute in vivo preparation of the microvasculature of the rabbit ear was used to evaluate the functional role of alpha, (al)-adrenoceptor subtypes in thermoregulatory microcirculation. The effect of al-adrenoceptor subtype blockade on phenylephrine-induced vasoconstriction was assessed with the alA, alB, and alD-adrenoceptor-selective antagonists 5-methyl-urapidil M ) . chloroethylclonidine (1 0-j M ) , and X-[2-[4(2-methoxyphenyl)-l-piperazinyl]ethyl]-8-azaspirol[4.S]decane-7,9-dione dihydrochloride (BMY7378) (10-6 M ) , respectively. The results demonstrated that pretreatment of the ear microvasculature with 5-methylurapidil or BMY7378 shifted the phenylephrine concentration-response curve rightward and significantly changed the log of the phenylephrine concentration, causing half-maximum stimulation (EC,,) in arterioles (p < 0.05). BMY7378 shifted the phenylephrinc concentration-response curve of the arteriovenous anastomoses about 100-fold rightward (p < 0.05). All three a,-adrenoceptor antagonists eliminated the vasoconstrictive effects of phenylephrine on venules. The results indicate that the ear microvasculature has a heterogenous distribution of ul-adrenoceptor subtypes. The alA and alD-adrenoceptor subtypes appear to have a greater influence on constrictive function in arterioles, whereas the alD-adrenoceptor is the dominant constrictor of arteriovenous anastomoses. In general, the al-adrenoceptor does not play a major vasoconstrictor role in venules. Chloroethylclonidine, an irreversible alB-adrenoceptor antagonist, induced contractile responses in the ear microvasculature, probably due to its a2-adrenoceptor agonist effects. This study extended our understanding of the adrenergic receptor control mechanisms of a cutaneous thermoregulatory end organ characterized by two parallel perfusion circuits providing nutritional and thermoregulatory functions.The microvasculature of the rabbit ear, like that of the human digit, consists of terminal arterioles, capillary loops, postcapillary venules, and arteriovenous anastomoses. The arteriovenous anastomoses allow blood to bypass the capillaries to flow directly into the deep venous plexus and are believed to be involved in thermoregulation (5). Skin blood vessels affect homeostasis of body temperature by dilating in response to heating and constricting in response to cooling. Changes in tonic sympathetic outflow are largely responsible for control of these vessels. The vasoconstrictor responses induced by exogenous norepinephrine, norepinephrine-like compounds, or sympathetic activation are mediated by alpha, (a1) and a,-adrenoceptors. Previous studies in our laboratory demonstrated that the resistance arterioles and arteriovenous anastomoses have different adrenoceptor control mechanisms (9,16): a,-adrenoceptors dominate arteriolar constriction, whereas the arteriovenous anastomoses are dually regulated by a, and a2-adrenoceptors (9,16). These findings provide a possible explanation of how blood flow in the ear is distributed between two parallel ...

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“…Surgical instrumentation procedures were performed as described previously. 21 Briefly, a transit time flow probe (model 1 RB; Transonic Systems, Inc., Ithaca, NY) was placed around the central auricular artery near the base of the ear. The electrical connector was passed under the skin across the cranium and held within an anchor button sutured to the rabbit's skin.…”

Section: Instrumentation Techniquesmentioning

confidence: 99%

“…One week after instrumentation, the rabbits were subjected to a three-phase testing procedure. 21 Baseline measurements were recorded for 20 minutes at ambient room temperature (23 to 25°C) to complete the first phase of this testing procedure. The rabbits were then placed in a cooling unit (5 to 8°C) for 10 minutes to determine their physiological response to a cold stress test.…”

Section: Experimental Protocolmentioning

confidence: 99%

“…Previous work has demonstrated that this test procedure is reproducible in rabbits and evokes a vascular response similar to that observed in patients. 21 Following the collection of baseline presurgery data, the animals were divided into three experimental groups: 1) rabbits undergoing auricular peripheral sympathectomy (n ‫ס‬ 9), 2) rabbits undergoing complete sympathectomy (amputation/replantation; n ‫ס‬ 13), and 3) surgical controls: rabbits which had undergone instrumentation only (n ‫ס‬ 5).…”

Section: Experimental Protocolmentioning

confidence: 99%

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Effects of peripheral sympathectomy on thermoregulatory vascular control in the rabbit ear

et al. 1998

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A rabbit ear model of the human digit was utilized to determine the vascular response to peripheral sympathectomy. Vascular responses were evaluated by subjecting chronically instrumented rabbits to a cold stress before and after sympathectomy surgery. The typical response to cold stress is for ear temperatures and auricular cutaneous perfusion to decrease during the cooling phase of the test and to increase toward baseline levels during the rewarming phase after cold exposure. Following peripheral sympathectomy, ear temperatures were significantly increased during both the cooling and rewarming phase of the cold stress test although overall ear perfusion and skin perfusion were not different from sham-operated rabbits. The responses observed in the rabbit ear following peripheral sympathectomy appear to mimic those noted in patients receiving digital peripheral sympathectomies for the treatment of refractory pain and ulceration. Peripheral sympathectomy may result in clinical improvements in patients because it improves both total digital and nutritional cutaneous blood flow. Peripheral sympathectomy in normal rabbit ears does not result in altered perfusion patterns with cold exposure although ear temperature is significantly higher. This pattern of changes suggests that the distribution of extremity perfusion is altered even though overall extremity perfusion and cutaneous perfusion per se are not significantly different from sham-operated controls. Complete sympathectomy was accompanied by a persistent increase in ear temperature and a dissociation between conductance and microvascular perfusion. Auricular conductance was transiently increased and then decreased to levels below preoperative control values. Microvascular perfusion is decreased immediately following amputation/replantation and thereafter increases.

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A rabbit ear model for cold stress testing

Cited by 9 publications

References 11 publications

Effect of cooling on cutaneous microvascular adrenoceptors in vivo in the rabbit ear

Effect of cooling on cutaneous microvascular adrenoceptors in vivo in the rabbit ear

Role of Alpha-1 Adrenoceptor Subtypes Mediating Constriction of the Rabbit Ear Thermoregulatory Microvasculature

Effects of peripheral sympathectomy on thermoregulatory vascular control in the rabbit ear

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