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Long-term experience with spring-assisted surgery has facilitated the development of standardized, reproducible techniques allowing spring design modifications to optimize clinical outcome.

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A rabbit ear model resembling the human digit was studied to determine the vascular response of the rabbit ear to a cold stress. Following moderate cooling (10 minutes at 5 degrees - 8 degrees C), auricular blood flow and cutaneous perfusion were reduced. This decrease was reversed by 30 minutes of warming. The response in the rabbit ear to cold stress is similar to that of normal human digits. The similarities between the control of the circulation in human digits and rabbit ears may result from the similarities in digital and auricular vascular receptors and receptor subtypes. Verification of the rabbit model provides an experimental method for obtaining important data regarding digital pathophysiology and the treatment of cold intolerance. Further study with this model will provide clinically relevant information regarding the pathophysiology of digital thermoregulatory abnormalities.

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 ...

BBB, Basso, Beattie, and BresnahanDTI, diffusion tensor imagingFA, fractional anisotropyMTR, mechanical tissue resuscitationMTR50, mechanical tissue resuscitation with 50-mm Hg subatmospheric pressureMTR75, mechanical tissue resuscitation with 75-mm Hg subatmospheric pressureROI, region of interestSCI, spinal cord injury.

An acute in vivo preparation of the microvasculature of the rabbit ear was used to evaluate the functional role of alpha1 (alpha1)-adrenoceptor subtypes in thermoregulatory microcirculation. The effect of alpha1-adrenoceptor subtype blockade on phenylephrine-induced vasoconstriction was assessed with the alpha1A, alpha1B, and alpha1D-adrenoceptor-selective antagonists 5-methyl-urapidil (10(-8) M), chloroethylclonidine (10(-5) M), and 8-[2-[4(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspirol[4.5]deca ne-7,9-dione dihydrochloride (BMY7378) (10(-6) M), respectively. The results demonstrated that pretreatment of the ear microvasculature with 5-methyl-urapidil or BMY7378 shifted the phenylephrine concentration-response curve rightward and significantly changed the log of the phenylephrine concentration, causing half-maximum stimulation (EC50) in arterioles (p < 0.05). BMY7378 shifted the phenylephrine concentration-response curve of the arteriovenous anastomoses about 100-fold rightward (p < 0.05). All three alpha1-adrenoceptor antagonists eliminated the vasoconstrictive effects of phenylephrine on venules. The results indicate that the ear microvasculature has a heterogenous distribution of alpha1-adrenoceptor subtypes. The alpha1A and alpha1D-adrenoceptor subtypes appear to have a greater influence on constrictive function in arterioles, whereas the alpha1D-adrenoceptor is the dominant constrictor of arteriovenous anastomoses. In general, the alpha1-adrenoceptor does not play a major vasoconstrictor role in venules. Chloroethylclonidine, an irreversible alpha1B-adrenoceptor antagonist, induced contractile responses in the ear microvasculature, probably due to its alpha2-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.