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Tuesday December 7, 2021
Category: Hoof Anatomy & Physiology
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The microcirculation of the dermal laminae and papillae of the equine foot from seven clinically normal Australian ponies was studied using an improved microvascular casting corrosion technique and scanning electron microscopy. Casts of veins, arteries, capillaries and arteriovenous anastomoses (AVAs) were readily identified by their characteristic surface morphology. Arteries entered the laminar circulation axially, between pairs of axial veins, and were connected to each other by smaller calibre interconnecting arteries. Short abaxial branches of the axial interconnecting arteries gave rise to tufts of predominantly, proximodistally orientated, capillaries arranged abaxially in rows. The laminar veins anastomosed with each other extensively (the axial venous plexus) and formed most of the vascular skeleton of casts of the dermal laminae. AVAs were found throughout the laminar circulation but the largest and longest (40p diameter) were found clustered close to the origin of the axial arteries. The density of the laminar AVAs was estimated to be 500 AVAs/cmz. Blood vessels of the dermal papillae of the periople, coronary band, distal laminae, sole and frog shared a basic structural organization. The cast of each papillary unit consisted of a central artery and vein enmeshed in a sheath of fine capillaries. At intervals along the length of the central artery were short branches which gave rise to tufts of capillaries. The capillaries formed a tortuous anastomosing plexus which encircled the papillary unit and drained into the central vein at intervals along its length. ÃVAs were always present at the base of the papillary units and anastomoses connected the central artery and vein. ÃJAs are important components of the dermal microcirculation of the equine foot and their distribution and density is compatible with their proposed role in the pathophysiology of equine laminitis.


VASOCONSTRICTION and ischaemia of the peripheral dermal microcirculation of the equine foot have been in criminated in the pathophysiology of laminitis (Hood et al 1989; Garner 1975; Coffman 1972; Ackerman, Garner, Coffman and Clement 1975; Coffman, Johnson, Guffy and Finocchio 1970). In contrast, acute laminitis is recognized clinically by a bounding digital pulse (Colles and Jeffcott 1977; Yelle 1986), as a result of increased total blood flow to the digit (Robinson, Scott and Dabney 1976). The simultaneous presence, in the digit, of ischaemia despite increased blood flow, has been rationalized by the proposal that ischaemia results because blood is shunted away from the dermal capillary circulation through dilated arteriovenous anastomoses (Hood and Stephens 1981; Coffman 1984). Significant arteriovenous shunting of blood occurs during the developmental stages of laminitis, as capillary sized radioactive particles are diverted from the peripheral capillary bed of the digital dermis (Hood et al 1978).

Arteriovenous anastomoses (AVAs) have been described in the hoof wall laminae, in the papillae of the coronet and sole and in the terminal papillae of the laminae (Schummer, Wilkens, Vollmerhaus and Habermehl 1981; Talukdar et al 1972; Rooney l984; Pollitt and Molyneus 1987). Estimates of the density of laminar AVAs differ widely (50 per cm=, Rooney 1984; 500 per cm=, Pollitt and Molyneux 1987).

The equine digital microcirculation has to be understood before the pathophysiological mechanism responsible for laminitis can be fully elucidated. Recent technological advances in producing microvascular corrosion casts of the entire circulation of organs (Gannon 1978; Kardon and Kessel 1979) combined with scanning electronmicroscopy, has enabled the microcirculation of the equine digit and the surface markings of vessels to be studied in detail. This investigation characterizes the microcirculation of the dermal laminae and papillae and offers a new theory correlating the distribution and density of AVAs with the pathophysiology of developmental laminitis.

Materials & Methods

Seven clinically normal Australian ponies (two male, four geldings and one female) ranging in age from one to 15 years (mean 3.5 years) and weighing from 330 to 420 kg were used in the study. The ponies were destroyed with an intravenous (iv) injection of pentabarbitone sodium and the forelimbs were immediately amputated at the carpal joint. A 12g plastic cannula was inserted into the common digital artery of each limb, firmly ligated and perfused with one liter of warm, normal saline containing 5000 units of heparin. During the perfusion the limb was flexed, extended and made to bear weight until the perfusate was clear of red blood cells. The heparinised saline was held 200cm above the cut end of the common digital artery and the perfusate entered the circulation of the limb at maximal flow rate.

After perfusing the amputated limb with heparinised saline a modified, partially polymerized, red pigmented, methacrylate corrosion compound (Batson's No.l7 anatomical corrosion compound, Polyscience Inc.) was then injected using a 25ml automatic vaccinating syringe (Hauptner-Muto, Germany). The Batson's No.l7 anatomical casting compound was diluted with methyl methacrylate monomer (BDH Chemicals Ltd., Poole, England) to reduce the viscosity. The amount of accelerator (component B) recommended by the distributors was reduced by 80 per cent (Gannon 1978). The final injection mixture consisted of l00ml methyl methacrylate monomer, 150ml Batson's No.l7 component A, 20ml component B and 5.0ml component C (Amevo 1984). This prolonged the monitoring time and permitted the injection of the large volume (275m1) of the vascular casting mixture required to perfuse an equine digit without early polymerization causing any apparent increase in viscosity. Saline flowed from the cut ends of the veins during the initial stage of injection of the casting compound. Later, globules of red liquid plastic, suspended in the saline, flowed from the veins, but during injection of the last l00mls the venous effluent appeared uncontaminated with saline. While injecting the last 20mls of plastic, the cut ends of the major veins were ligated and when the injection was completed, the arterial cannula was clamped to prevent backflow. The leg was them immersed in hot water to polymerize the plastic. The next day a band saw was used to cut lcm thick sections from the toe and heel regions which were incubated (37C) for three days, in lolo trypsin dissolved in phosphate buffered saline (pH 7.5). The partially digested dermis was carefully separated from the keratinized tissue and examined with a dissecting microscope. Sections showing good filling of small blood vessels were immersed in 30ml potassium hydroxide for 2 to 3 days to macerate the soft tissue. The vascular casts were then placed in distilled water and cleaned ultrasonically for 3 to 5 minutes. After immersion in absolute alcohol the casts were air dried and prepared for further dissection.

Casts of the blood vessels of the dermal laminae were glued with the laminar surface uppermost to the surface of 70 x 70 x 4mm pieces of opaque acrylic plastic (Perspex, ICI). With a dissecting microscope, fine dissecting needles and microsurgery instruments, intact sheets of the casts of laminar vessels (10 x 4mm) complete with the casts of the underlying dermal arteries and veins were cut free and mounted on scanning electron microscopy stubs coated with double sided adhesive tape (Cellotape, 3M).

Casts of the vessels of the coronary band, distal laminae, sole and frog were reimmersed in distilled water and placed wet, onto. pieces of the opaque acrylic plastic. The water surround the cast was then frozen to -70 degrees C and sections of the vascular casts were cut using steel backed razor blade. The casts were then immersed in alcohol, dried and mounted as before. The mounted plastic specimens were rendered conductive by sputtering with gold in a Denton Vacuum (Denton Vacuum, Inc., Cherry Hill, New Jersey) Desk I coating unit for 30 seconds.

The specimens were examined and photographed using a Cambridge SS 600 stereo-scanning electron microscope at an accelerating voltage of 7.5 to l5kv. Stereo photographs using an 8 degree angle of tilt were used to perceive the third dimension of the micrographs. Enlarged photographic mosaics of the casts of entire laminae were constructed so that AVAs could be counted.


The injection technique using a modified low viscosity plastic (Batson's 17 compound diluted with methyl methacrylate monomer) produced complete casts of most of the dermal vascular bed of the digit, except in the demial laminae of the mid- dorsal toe. The casts of the dermal laminae from the heel regions were complete (Fig la and 1b) and it was assumed that the anatomical pattern of the mid dorsal toe was similar (Mishra and Leach 1983b).


Fig 1: (a) [left] Vascular corrosion cast of three adjacent primary dermal laminae (PDL). Spaces between parallel sheets of laminar vessel casts would normally be occupied by primary epidermal laminae of hoof wall. The vessels at top of picture are marginal veins, the most peripheral elements of the laminar circulation (bar = 400u) (b) [right] A single sheet of laminar vessel casts showing the laminar marginal vein (MV) and mesh of fine interconnected capillaries adjacent to axially located laminar arteries and veins. Boxed area shows cluster of AVAs at base of axial artery. On either side of the artery are prominent axial axial veins (V). The hoof wall was to the left of the picture and the pedal bone to the right (bar = 1mm)

Casts made with the improved plastic formulation (Amevo 1984) had a soft, flexible consistency and could be cut and dissected into small portions without fracturing. Using the SEM at 7.5kv the vascular casts showed neither distortion nor charging. Stabilizing the delicate vascular casts in blocks of frozen water prior to sectioning with a razor blade enabled the study of delicate regions such as the blood vessels of the coronary band. The routine examination of stereo pair micrographs conveyed more anatomical information about the spatial relationships of interconnecting blood vessels than single micrographs. Enzyme digestion of hoof sections prior to maceration in saturated potassium hydroxide prevented the hoof wall from collapsing onto the vascular cast during corrosion and preserved the finest elements of the capillary bed (Figs 2, 11 and 12).


Fig 2: Corrosion cast of dermal laminar vessels. A mesh of fine interconnected capillaries (C) overlies the axially located laminar arteries (A) and veins (V). Segments directly connecting arteries to veins (AVAs) were recognized by characteristically alveolate surface morphology (arrows). The peripheral hoof wall was to the left of picture. Large AVAs were always located at the base of axial arteries and veins and had an average diameter of 40 u (bar = 100u)

The shape of a digital vascular cast reflected the anatomy of the internal surface of the hoof wall, with perioplic and coronary sphincter regions forming a convex brush border made up of numerous tapering cone shaped papillae (Fig 6). The laminar region consisted of approximately 600 thin parallel sheets arranged in vertical rows (Fig 1 a). At the distal tip of each lamina, a row of terminal papillae merged with the papillae on the surface of the sole and frog.


Fig 3: Corrosion cast of laminar vessels showing morphological differences between arteries and veins. Casts of veins (V) show oval shallow pavement depressions. Arteries (A) show fusiform depressions. On the laminar artery are the impressions of rings of constriction which are shown arrowed near an arteriolar side branch which shows sphincter-like impression at its origin (bar = 40u)

In this study distinction between the arterial and venous divisions of the circulation was made using the criteria of Kardon and Kessel (1979) who also made vascular casts using a mixture of low viscosity and showed that the different morphology of the endothelial cells lining the lumina of arteries and veins was reflected in the depressions on the surface of vascular casts. Casts of the venous divisions typically possessed numerous oval, shallow 'pavement', surface depressions, whereas fusiform depressions, with their long axis aligned in the direction of blood flow, characterized the surface of arterial casts (Figs 3, 4 and 12). Arterioles showed the impressions of rings of constriction along their lengths, particularly prominent near arteriolar side branches (Fig 3). Venous casts branched and anastomosed profusely, had greater luminal diameters with frequent dilations and were flatter in cross section than adjacent arteriolar casts. Direct vascular connections (AVAs) between arterial and venous divisions were readily identified because their luminal morphology was different from any other elements of the dermal vascular bed (Fig 4). The AVA surface was alveolate and the cavities were surrounded by interconnecting, irregular shaped walls. On some segments, the walls were hexagonal, while in others they were irregular and resembled rough, overlapping scales. This characteristic surface morphology ended abruptly at the junction between arterial and venous ends of the AVA. The arterial junction was neck shaped with a sphincter-like ring of constriction (Fig 4). At the venous end there was a small diameter wide-arm with branches which merged into the general capillary network (Fig 4). Some AVAs, in particular those arising from the first branch of the parietal artery or at the base of papillae, shared a common arterial origin, but then branched into two and resembled the double AVAs described in sheep skin (Molyneux 1965). Each branch entered the venous circulation at a different level (Fig 5). The AVAs of the deeper dermis were longer, of wider diameter (average diameter ~40) and more branched than those of the peripheral layers.


Fig 4: Corrosion cast of laminar dermal vessels showing direct connection between an artery and vein. The surface of the cast of the arteriovenous anastomosis (AVA) is deeply pitted (alveolate) and the pits are surrounded by irregular shaped walls. At the arterial (A) end of the AVA the junction shows a sphincter-like ring of constriction (arrowed). A venous (V) side arm close to the AVA leads to a venular-capillary (C) network (bar = 100 u)


Fig 5: Corrosion cast of dermal vessels at base of terminal papillae. Both arms of a double AVA are shown (arrows) entering the venous (V) circulation at different levels. In this preparation some of the finer vessel casts have been removed to show deeper structures. Arteries (A), bar= 100u

The vascular skeleton of dermal papiflae

The vessels of the dermal papillae of the periople, coronary band, distal laminae, sole and frog regions shared a basic structural organization (Fig 9). The cast of each papillary unit consisted of a central artery and vein enmeshed in a sheath of fine capillaries (Fig 6 and 7). At intervals along the artery, short side-arms gave rise to capillary tufts, which formed a tortuous anastomosing plexus, encircling the papillary unit before draining into the central vein at intervals along its length (Fig 7 and 9).


Fig 6: Vascular cast of the vessels of dermal coronary papillae (CP). in life, each papilla fit into a socket in the epidermis of the enmeshed in a sheath of coronary groove of the proximal hoof wall. The arrows show arteries crossing a large collecting vein (V). Each papillary unit contains a central artery and vein surrounded by a meshwork of capillaries (bar = 1mm)


Fig 7: Corrosion cast of a terminal papilla showing central artery (A) and vein (V) enmeshed in a sheath of capillaries (C). The capillary plexus drains into the central papillary vein (arrowed), bar = 200u

Examination of stereo pair micrographs of papillary vascular units showed that the central artery was circular and the vein was ovoid in cross-section and that the two vessels spiralled around each other. The terminal portions of the casts of these vessels were usually devoid of endothelial mall impressions probably because of low perfusion pressure. Several AVAs were always present at the base of the papillary using units directly connecting the arterial and venous divisions of the circulation prior to its entering the papillary capillary bed. I into Smaller and shorter AVAs connected the central artery and vein. skin within the proximal third of each papillary vascular unit (Fig 8)


Fig 8: Vascular cast of the vessels of dermal coronary papilla. An AVA is shown arising from the central papillary artery (A). The AVA drains directly into the central vein (not shown here). Capillaries (C), small vein (v) bar = 40u

The vascular skeleton of dermal laminae

The architecture of the venous laminar circulation followed the pattern described by Mishra and Leach (1983b). In the hoof wall corium, at the base of each primary dermal lamina, were vertically orientated parietal collecting veins (Fig 10). Axial veins orientated parallel to one another were distributed throughout each dermal lamina and joined the parietal veins at regular intervals. Numerous anastomoses of the large calibre axial veins: formed the axial venous plexus. Peripherally, near the exterior limits of the laminar circulation, the axial venous plexus formed either a marginal vein or a marginal plexus (Fig 10). Smaller: calibre interconnecting veins completed the axial plexus and the capillaries of the laminae drained directly into them (Fig 10 and 11).


Fig 9: Schematic diagram of the microcirculation of digital dermal papillae. Numerous AVAs connect the central artery and vein of each papilla. The largest AVAs are found (lose to the origin of the central artery and vein. Each dermal papilla fits into an epidermal socket lined with germinal cells giving rise to epidermal cells which keratinize and form the horny substance of the equine hoof. The microcirculation of the coronary, laminar terminal, and solar papillae is essentially the same.


Fig 10: Schematic diagram of the laminar dermal circulation. For reasons of clarity the capillary network is shown to six vertically oriented abaxial capillaries. Numerous AVAs are present throughout the laminar dermal circulation but the longest and largest are found close to branches of the axial arteries.

The majority of the laminar capillaries were orientated vertically and were situated in abaxial rows on either side of the axial vessels (Fig 10). The rows were more obvious distally. Some of the capillaries formed show abaxial loops which in vivo would penetrate between pairs of secondary epidermal laminae. In this study none of the capillary enlargements and sprout-like structures described by Mishra and Leach (1983b) were recognized.


Fig 11: Vascular corrosion cast of abaxial laminar capillaries (C) draining into an axial interconnecting vein (V). The pavement impression of oval endothelial cells on the surface of the venous cast (V) is artery (characteristic for veins (bar = 40 u)

Laminar aneries (branches of the anerial plexus of the wall corium) entered the laminar circulation axially between each pair of axial veins (Fig 10). Each axial anery was connected to its neighbor by smaller calibre, interconnecting branches oriented vertically. Long anerial anastomoses at the periphery of each dennal lamina appeared to be the architectural equivalents of the marginal vein. Some abaxial branches of the axial interconnecting arteries gave rise to tufts of vertically orientated capillaries arranged in rows (Fig 10 and 12).


Fig 12: Vascular corrosion cast of abaxial laminar capillaries (C) arising from a short side branch of an interconnecting artery (A). The artery is recognized by the characteristic longitudinal indentations made on the cast by the endothelial cells of the arterial lumen (bar = 40 u)

In the interior third of each lamina and in the corium proper, close to each axial artery were clusters of AVAs with an average diameter of 40t. Their venous end drained into veins of the axial plexus and not the axial vein proper. The arterial ends were situated on the vertical interconnecting branches close to their origins on the main axial arteries. Smaller calibre, shorter AVAs were present throughout the laminar circulation and were occasionally found connecting the vertical peripheral axial artery with the marginal vein. The density (number per cmz) of AVAs was estimated by counting the number of AVAs present in measured areas of vascular casts of the dermal laminae and was approximately 500 per cm.


Since the microvascular corrosion cast can be considered a three- dimensional vascular skeleton around which the extravascular components are arranged (Rogers and Gannon 1983), the characteristic patterns of the vascular skeleton reflect the anatomy of the surrounding tissues. Thus the internal surface of the coronary and perioplic grooves of the proximal hoof wall were concave and the complementary vascular casts were convex. The keratinized surfaces of the coronary and perioplic grooves were perforated by numerous small openings which received the 4 to 6mm long papillae of the coronary and perioplic dermis or corium (Sack and Habel 1977, Schummer et al 1981). The vascular casts of the coronary and perioplic papillae were cone-shaped and the tapering tips of the cones formed a brush-border. A similar anatomical relationship existed between the vascular casts of the sole and frog papillae and their complementary, keratinized structures.

Below the coronary groove the internal surface of the hoof wall bears approximately 600 keratinized, primary epidermal laminae interdigitating with an equal number of dermal laminae (Sack and Habel 1977, Schummer et al 1981). The vascular skeletons of the laminar region reflected this anatomical arrangement and were arranged in rows of thin parallel sheets (Fig 1 a). The casts of proximal laminar vessels merged with the papillae of the coronary demlis, but those of the distal laminae ended in rows of terminal papillae which resembled vascular casts of coronary and sole papillae. The epidermis of the terminal papillae continually produces pigmented horn which fills the spaces (originally occupied by dermal laminae) between the distal ends of the unpigmented epidermal laminae as they grow downwards to form the inner border of the white zone (Sack and Habel 1977, Schummer et a1 1981).

The characteristic surface marking of the vascular cohesion casts of the digital dermis clearly differentiates AVAs from ins arterial and venous vessels (Figs 2, 3, 4 and 5). Less prominent in surface markings have been reported on the surface of AVAs in vascular casts of the rabbit's ear (Monis and Bevan 1984; Amevo 1984; Amevo and Molyneux 1985). In transmission electron microscopy studies of the digital dermis of the horse (Molyneux and Pollitt 1987) the endothelium of AVAs is very prominent and ally. protrudes into the lumen of the anastomoses forming an undercut into and tunnel-like areas which correlate with the alveoli. Appearance of AVAs in vascular casts. Prominent endothelial-like cells, but less so than in the foot of the horse, are a usual feature were of cutaneous AVAs and have been observed in AVAs in the leg of the sheep and the ear of the rabbit (Molyneux, unpublished wall observations). The significance of this distinguishing feature of a pair AVA structure remains obscure, although such an arrangement to its could be advantageous in completely occluding the lumen on ended closure of the anastomoses, particularly as they lack an internal each elastic lamina.

The density of laminar AVAs at 500 AVAs/cm2 is probably an underestimate as only one surface of each dermal lamina could be clearly examined. Nevertheless, it is a tenfold increase on the density reported by Rooney (1984) using light microscopy and serial sections. AVA densities greater than this have only been reported in the flipper skin of marine animals such as the Weddel seal (Leptonychote.s weddelli) (1000 AVAs/cmz) and the Southern elephant seal (Mirounga leonina) (1200 AVAs/cmz) (Molyneux and Bryden 1981) so the horse is comparatively well endowed with digital AVAs, The large number of laminar AVAs may be an adaptation preventing cold induced tissue damage in horses standing for long periods in ice and snow. A similar explanation has been proposed for the large number of AVAs in the naked feet and legs of polar birds (Munish and Guard 1977). When environmental temperatures drop below 0C, the feet are prevented from freezing by periodic vasodilatation of AVAs. This allows warm blood to bypass the capillary bed and enter the digits quickly to maintain their temperatures above the freezing point.

Consideration of the enormous pressure fluctuations which must develop within the equine hoof capsule during galloping and jumping supports the proposal that "bypasses", such as digital AVAs, act as vascular safety valves (Schummer et al 1981). Instead of blood being forced into the high resistance capillary bed (which has a relatively slow circulation time) during peaks of high pressure, blood can be shunted safely from artery to vein via periodically open AVAs, Blood may even flow back and forth from vein to artery when AVAs are open, a phenomenon seen in the dermal microcirculation of conscious rabbit's ears through transparent chambers (Molyneux, unpublished data). If this occurs in the equine digit it may explain why there are no valves found in the veins of the dermal laminae, (Mishra and Leach 1983a).

The dermal microcirculation of the equine digit contains a large number of anastomoses in all divisions of its vascular organization. In the laminar circulation, arteries anastomose with each other at regular intervals along the vertical length of each of the 600 or so dermal laminae (from the level of the coronary papillae down to the terminal papillae). The laminar veins also anastomose extensively (the axial venous plexus) and form the bulk of the vascular skeleton of casts of the dermal laminae (Schummer et al 1981). Such a large number of anastomoses would probably impart resistance to infarction so that intravascular coagulation alone cannot be the primary cause of the peripheral digital ischaemia stated to occur during the pathogenesis of early laminitis (Hood et al 1979; Coffman 1972; Ackerman et al 1975; Coffman et al 1970).

The inappropriate activity of arteriovenous anastomoses has been said to decrease digital capillary perfusion and cause degeneration of dermal-epidermal tissues (Coffman et al 1970; Coffman 1972; Ackerman et al 1975; Garner 1975; Hood et al 1978; Hood and Stephens 1981; Coffman 1984; Yelle 1986) although the precise anatomical location of such AV shunts was unknown (Hood and Stephens 1981; Mishra and Leach 1983b). Experiments using radioactive particles (Hood et a! 1978) have shown the digital AV shunting does occur during the onset of laminitis and have explained how unchanged or increased total digital blood flow (Robinson et a1 1976) can occur simultaneously with capillary ischaemia of the digit.

Since this study has shown that AVAs occur extensively in the dermal circulation in the coronary and terminal papillae as well as in the laminae, the AVA mediated ischaemia of developmental laminitis may affect not only the laminae, but the coronary and terminal papillae as well. Failure of coronary papillae to receive adequate perfusion would result in cessation of hoof wall growth and, if severe enough, coronary band necrosis. This may explain the disturbed hoof and coronary band growth patterns which follow laminitis (Colles and Jeffcott 1977; Yelle 19A6). Weakening or necrosis of the epidermis supplied by the terminal papillae would contribute to separation of the sole wall junction and may account for the sudden appearance of the air or gas line visible in the laminar region of the hoof wall on lateral radiographs made during acute laminitis (Yelle 1986).

The presence of large numbers of AVAs directly connecting arteries to veins allows the following pathophysiological mechanism to be proposed. During the developmental stage of laminitis the digital AVAs come under the influence of humoral or neuronal factors which induce their prolonged dilatation. Arterial blood flows rapidly into the venous system, instead of slowly perusing the high resistance capillary bed of the coronary papillae, dermal laminae and terminal papillae. If this inappropriate dilatation of AVAs proceeds for long enough, capillary ischaemia causes epidermal necrosis and disintegration of the hoof-pedal bone bond. After AV shunting has initiated laminitis the disease enters the painful, acute phase and a number of overlapping pathological phenomena follow. Coagulation dysfunction (Hood et al 1979), hypertension (Garner et al 1975), catecholamine release (Amoss, Gremmel and Hood 1982) occur and clinically their effect can be ameliorated with drugs such as the alpha-blockers acepromazine or phenoxybenzamine (Hood, Stephens and Amoss (1982a) and the anticoagulant heparin (Hood, Stephens and Amoss 1982b).

If this theory is correct it implies that epidermal cell damage must be one of the earliest lesions of developmental laminitis, universally affecting the entire hoof wall of all four feet. Why then is laminitis usually confined to the toes of the front feet? Perhaps the mechanical factors which cause tearing of the laminae at the toe of the forelegs in 'road founder' (Rooney 1984) also operate during developmental and acute laminitis. The degree of rotation of the hoof wall as it is tom away from the third phalanx (P3) and the amount of sinking of P3 within the hoof capsule vary according to the extent of epidermal cell damage and the interplay of mechanical forces such as weight, centre of gravity, hoof-pastern conformation, amount of forced exercise and the break-over forces of locomotion. This explains why a properly applied Heart-bar Shoe (Chapman and Platt 1994) which stabilized the third phalanx and to some extent neutralizes the angular forces tearing the laminae from P3 can be so efficacious if applied in the early stages of the laminitis syndrome (Pollitt, unpublished data).

The bounding digital pulse which is a characteristic clinical finding of laminitis (Colles and Jeffcott 1977; Yelle l996) is probably the result of a change in the dynamics of the pulse wave when the arterial blood bypasses high resistance dermal capillary bed via dilated dermal AVAs. Experiments demonstrating that horses with laminitis have more radioactive cystine in the venous return of their digits than normal horses (Larsson, Obel and Aberg 1956) has suggested that a failure of keratinization or onychogenesis in the cystine dependent cells of the stratum spinosum plays a primary role in the development of laminitis (Coffman 1972). However generalized digital AVA dilatation and the AV shunting of blood would also result in higher than normal concentrations of venous cystine.

It seems likely that AVAs have a specific role in the pathophysiology of developmental laminitis, because under certain conditions, over 50 per cent of the limb blood flow can pass through AVAs (Hales and Molyneux 1988) and the existence of relatively large numbers of AVAs in the dermis of the horses digit has now been established. The presence of vasodilator substances such as vasoactive intestinal polypeptide (VIP), substance P and calcitonin gene-related polypeptide (CGRP) in the dense innervation of the dermal AVAs in the digits of horses and ponies (Molyneux and Pollitt 1978) supports our contention that the triggering of perturbed AVA dilatation may be the common denominator linking the varied aetiologies of laminitis.

Trout (1987) used radionuclide angiography to show increased total laminar blood flow in the digital circulation of horses with acute laminitis. Prolonged AVA dilatation is a likely cause of this increase but the techniques used were unable to differentiate between capillary and AVA blood flow in the laminar tissues. However synthetic radioactive microspheres of known diameter have been used to partition cutaneous capillary and AVA blood flow (Hales, Fawcett and Bennett 1978; Hales 1981) and experiments in collaboration with Dr. Hales are in progress to differentiate laminar capillary from AVA flow in horses and ponies.


This study was supported by a grant from the Queensland Equine Research Foundation. The technical assistance provided by the University of Queensland Electronmicroscopy Unit is gratefully acknowledged.


Amevo, B. (1984) Micro-corrosion cast study of the luminal morphology of cutaneous orteriovenous anastomoses. MSc. thesis. Department of Anatomy, University of Queensland, Australia.

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Posted here with the permission of the authors.
First published in Equine vet. J., (1990) 22(2)79-87

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