Objective—To determine selected cardiopulmonary values and baroreceptor response in conscious green iguanas (Iguana iguana) and to evaluate the use of blood gas analysis and pulse oximetry in this species.
Animals—15 healthy juvenile green iguanas.
Procedures—Baseline cardiopulmonary values were determined in 15 conscious iguanas breathing room air. Effects of 100% O2 inspiration were also measured (n = 6), and the baroreceptor reflex was characterized by exponential sigmoidal curve fitting analysis.
Results—Conscious iguanas had a mean ± SD resting heart rate of 52 ± 8 beats/min, respiratory rate of 28 ± 6 breaths/min, and systolic, mean, and diastolic arterial blood pressures of 69 ± 10 mm Hg, 62 ± 12 mm Hg, and 56 ± 13 mm Hg, respectively. Mean arterial pH at 37°C was 7.29 ± 0.11, Pao2 was 81 ± 10 mm Hg, and Paco2 was 42 ± 9 mm Hg; corrected for a body temperature of 30°C, mean arterial pH at 37°C was 7.382 ±0.12, Pao2 was 54 ± 15 mm Hg, and Paco2 was 32 ± 7 mm Hg. Inspiration of 100% O2 did not change heart and respiratory rates but increased Pao2 to 486 ± 105 mm Hg (corrected value, 437 ± 96 mm Hg). A baroreceptor reflex was evident, with mean heart rates ranging from 30 ± 3 beats/min to 63 ± 5 beats/min and mean arterial blood pressures ranging from 42 ± 3 mm Hg to 58 ± 3 mm Hg.
Conclusions and Clinical Relevance—This study provided needed information on cardiopulmonary values in healthy green iguanas, the application and limitation of arterial and venous blood gas analysis, and the accuracy of pulse oximetry.
Objective—To provide insights into the role of prostaglandin F2α (PGF2α) in the developmental stages of laminitis induced in horses by ingestion of black walnut heartwood extract (BWHE).
Sample Population—10 adult mixed-breed horses.
Procedures—Horses were separated into 2 groups and were euthanatized at 12 hours after placebo (water) administration (control horses) or after BWHE administration and development of Obel grade 1 laminitis. Blood samples were obtained to determine plasma PGF2α concentrations hourly for the first 4 hours and subsequently every 2 hours after substance administration. Laminar arteries and veins were isolated, and responses to increasing concentrations of PGF2α were measured before and after preincubation of blood vessels with prostanoid and thromboxane receptor antagonists SQ 29,548, SC-19220, and AH 6809.
Results—Plasma PGF2α concentrations increased in horses given BWHE; the WBC count decreased concurrently. In control horses, PGF2α was a potent contractile agonist for laminar veins but not for laminar arteries. In horses given BWHE, PGF2α was similarly selective for laminar veins; however, the magnitude of PGF2α-induced venoconstriction was less than that in control horses. After preincubation with SQ 29,548, laminar veins from control horses responded to PGF2α with a small degree of dilation, whereas laminar veins from horses given BWHE did not.
Conclusions and Clinical Relevance—PGF2α may play a role in the inflammatory and vascular dysfunction associated with the prodromal stages of laminitis. Prostanoids such as PGF2α may be viable targets for the prevention of acute laminitis in horses.
Objective—To determine the effects of the protein kinase C (PKC) inhibitor, Ro-31-8220, on agonist-induced constriction of laminar arteries and veins obtained from horses.
Sample Population—Laminar arteries and veins obtained from 8 adult mixed-breed horses.
Procedures—Laminar arteries and veins were isolated and mounted on small vessel myographs for the measurement of isometric tension. Concentration-response curves were then obtained for the vasoconstrictor agonists phenylephrine, 5-hydroxytryptamine, prostaglandin F2α, and endothelin-1. All responses were measured with or without the addition of Ro-31-8220 (3μM).
Results—Laminar veins were more sensitive to vasoconstrictor agonists than laminar arteries, and incubation of laminar veins with Ro-31-8220 resulted in significantly smaller agonist-induced contractile responses for all agonists tested. In contrast, Ro-31-8220 had no effect on agonist-induced contractile responses of laminar arteries.
Conclusions and Clinical Relevance—Results of the study were consistent with activation of PKC being confined to agonist-induced contraction of laminar veins isolated from the laminar dermis of horses. Consequently, the possible involvement of PKC in the venoconstriction observed during the development of laminitis is worthy of further investigation.
Objective—To determine the effects of inhibition of Rho-kinase or Src-family protein tyrosine kinases (srcPTK) on agonist-induced contractile responses in equine laminar arteries and veins.
Sample Population—Laminar arteries and veins obtained from 13 adult mixed-breed horses.
Procedures—Laminar vessels were mounted on myographs and exposed to phenylephrine (PE), 5-hydroxytryptamine (5-HT), prostaglandin F2α (PGF2α), and endothelin-1 (ET-1) with or without the Rho-kinase inhibitor Y-27632 (10μM), srcPTK inhibitor PP2 (10μM), or a negative control analogue for PP2 (PP3; 10μM).
Results—Responses to PE were reduced by use of Y-27632 in laminar vessels (approx inhibition, 55%). However, Y-27632 reduced responses to 5-HT to a greater degree in veins than in arteries (approx inhibition of 55% and 35%, respectively). The Y-27632 also reduced responses of laminar veins to ET-1 by approximately 40% but had no effect on maximum responses of laminar arteries to ET-1, although a rightward shift in the concentration response curve was evident. Addition of PP2 reduced responses to PE, 5-HT, and PGF2α in laminar veins by approximately 40%, 60%, and 65%, respectively, compared with responses after the addition of PP3; PP2 had no effect on responses to ET-1. In laminar arteries, PP2 reduced 5-HT–induced contractions by approximately 50% but did not affect responses to PE or ET-1.
Conclusions and Clinical Relevance—Results of the study were consistent with activation of Rho-kinase being important during agonist-induced constriction in laminar vessels, activation of srcPTK being an agonist-dependent event, and more prominent roles for Rhokinase and srcPTK in veins than in arteries.
Objective—To characterize the relative contributions of voltage-gated and capacitative Ca2+ entry to agonist-induced contractions of equine laminar arteries and veins.
Animals—16 adult mixed-breed horses.
Procedures—Laminar arteries and veins were isolated and mounted on small vessel myographs for the measurement of isometric tension. Concentration-response curves were obtained for the vasoconstrictor agonists phenylephrine, 5-hydroxytryptamine (5-HT), prostaglandin F2α (PGF2α), and endothelin-1 (ET-1) either in the absence of extracellular Ca2+ or in the presence of the voltage-gated Ca2+ channel inhibitor diltiazem or the putative inhibitor of capacitative Ca2+ entry, trifluoromethylphenylimidazole.
Results—In the absence of extracellular Ca2+, maximal responses of veins to 5-HT, phenylephrine, ET-1 and PGF2α were reduced by 80%, 50%, 50%, and 45%, respectively; responses of arteries to 5-HT, phenylephrine, and ET-1 were reduced by 95%, 90%, and 20%, respectively. Although diltiazem did not affect the maximal responses of veins to any agonist, responses of arteries to 5-HT, phenylephrine, and ET-1 were reduced by 40%, 50%, and 27%, respectively. Trifluoromethylphenylimidazole did not affect maximal responses of veins, but did reduce their contractile responses to low concentrations of ET-1 and PGF2α.
Conclusions and Clinical Relevance—Results suggested that the contribution of extracellular Ca2+ to laminar vessel contractile responses differs between arteries and veins and also between contractile agonists, voltage-gated Ca2+ entry is more predominant in laminar arteries than in veins, and capacitative Ca2+ entry has a minor role in agonist-induced contractile responses of laminar veins.
Objective—To determine the effects of induction of
capacitative Ca2+ entry on tone in equine laminar arteries
Sample Population—Laminar arteries and veins
from 6 adult mixed-breed horses.
Procedure—Arteries and veins were isolated and
mounted on small vessel myographs for the measurement
of isometric tension. Capacitative Ca2+ entry was
induced by incubating the vessels with the specific
Ca2+-ATPase inhibitor thapsigargin (100nM) in a Ca2+-
free physiologic salt solution. Capacitative Ca2+
entry–associated contractile responses were determined
by the subsequent addition of 2mM Ca2+ to the
solution bathing the vessels; in some experiments,
either the voltage-gated Ca2+ blocker diltiazem (10µM)
or the putative capacitative Ca2+ entry inhibitor trifluoromethylphenylimidazole
(300µM) was added to the
bathing solution 15 minutes prior to a second 2mM
Ca2+ exposure. The Sr2+ permeability of the capacitative
Ca2+ entry pathway in laminar vessels was assessed by
exposing the vessels to 4mM Sr2+ after induction of
capacitative Ca2+ entry with thapsigargin.
Results—Induction of capacitative Ca2+ entry elicited
robust contractile responses in laminar veins but did not
increase tone in laminar arteries. In laminar veins, capacitative
Ca2+ entry–induced contractile responses were unaffected
by preincubation with diltiazem, attenuated by trifluoromethylphenylimidazole,
and were impermeable to Sr2+.
Conclusions and Clinical Relevance—Results indicated
that induction of capacitative Ca2+ entry elicits
vasoconstriction in equine laminar veins but not in
laminar arteries and should therefore be considered a
potential mechanism by which selective venoconstriction
occurs in horses during the development of
acute laminitis. (Am J Vet Res 2005;66:1877–1880)