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Abstract

Objectives

To determine oxygen metabolism, permeability, and blood flow in isolated joints in response to interleukin 1β (IL-1β) and contribution of innervation.

Sample Population

One metacarpophalangeal (MCP) joint of 24 adult horses.

Procedure

The MCP joint was isolated for 6 hours in a pump-perfused, auto-oxygenated, innervated or denervated preparation. Isolated joints were assigned to the following 4 groups: control, control-denervated, inflamed, and inflamed-denervated, and inflammation was induced by intra-articular injection of IL-1β. Circuit arterial and venous pressures, flows, and blood gas tensions, synovial fluid production, and intra-articular pressure were measured. Total vascular resistance; oxygen delivery, consumption, and extraction ratio (ER); and permeability surface area product were calculated. Synovial membrane blood flow was determined at 0, 60, and 330 minutes. Synovial membrane wet-to-dry ratio was obtained, and permeability to macromolecules was determined by intra-articular injection of Evans blue albumin and fluorescein isothiocyanate-conjugated dextran.

Results

Oxygen delivery and synovial membrane blood flow progressively increased but were not different among groups. Oxygen consumption and ER significantly increased in inflamed joints, as did intraarticular pressure and synovial fluid production. Inflamed joints had greater wet-to-dry ratio. Albumin permeability significantly increased in the villous synovial membrane of the inflamed groups, and dextran permeability was increased in the innervated groups, with a trend toward increased permeability in inflamed groups.

Conclusion

Inflammation significantly increased oxygen demand, which was initially met by increased ER. Permeability to small molecules was increased with inflammation; innervation increased permeability to large molecules. Use of an isolated joint model enabled documentation of the physiologic responses of the joint to acute inflammation. (Am J Vet Res 1998;59:1307–1316)

Free access
in American Journal of Veterinary Research

SUMMARY

Six horses were subjected to 3 hours of low-flow ischemia and 3 hours of reperfusion of the large colon. After induction of anesthesia, the large colon was exteriorized through a ventral midline celiotomy. Colonic blood flow was measured continuously, using Doppler ultrasonic flow probes placed on the colonic arteries supplying the dorsal and ventral colons and was allowed to stabilize for 15 to 30 minutes after instrumentation. Low-flow ischemia was induced by reducing colonic arterial blood flow to 20% of baseline (bl) flow. Colonic mucosal, seromuscular, and full-thickness blood flow were determined on a tissue-weight basis by injecting colored microspheres proximally into the colonic artery supplying the ventral colon. Reference blood samples were obtained at a known flow rate from the colonic artery and vein at a site more distal to the site of injection. Left ventral colon biopsy specimens were harvested at bl, 3 hours of ischemia, and 15 minutes of reperfusion. Blood and tissue samples were digested and filtered to collect the microspheres, and dimethylformamide was added to release the colored dyes. Dye concentration in blood and tissue samples was measured by use of spectrophotometry, and tissue-blood flow was calculated. Data were analyzed, using two-way anova for repeated measures; statistical significance was set at P < 0.05. Doppler blood flow decreased to approximately 20% of BL, whereas microsphere blood flow ranged between 13.7 and 15.5% of bl at 3 hours of ischemia. Doppler-determined blood flow increased immediately on restoration of blood flow, reached 183% of bl at 15 minutes of reperfusion, and remained at or above bl throughout 3 hours of reperfusion. This reactive hyperemia was also detected, using the colored microspheres; blood flow increased to 242 and 327% of bl at 15 minutes of reperfusion in the mucosal and seromuscular layers, respectively. Mucosal blood flow was not different from seromuscular blood flow at any time, indicating relatively equal distribution of blood flow between these 2 layers. As determined from the venous reference samples, there was no evidence of arteriovenous anastomoses.

Free access
in American Journal of Veterinary Research

SUMMARY

The effects of single iv injections of sodium bicarbonate (0.5 mEq/kg of body weight, 1 mEq/kg, 2 mEq/kg, and 4 mEq/kg) on serum osmolality, serum sodium, chloride, and potassium concentrations, and venous blood gas tensions in 6 healthy cats were monitored for 180 minutes.

Serum osmolality increased and remained significantly (P < 0.05) increased for 120 minutes in cats given 4 mEq of sodium bicarbonate/kg. Serum sodium was increased significantly (P < 0.05) for 30 minutes in cats given 4 mEq of sodium bicarbonate/kg. Serum sodium decreased and remained significantly (P < 0.05) decreased for 120 minutes in cats given 1 g of 20% mannitol/kg, and serum osmolality was significantly (P < 0.05) decreased at 30 and 60 minutes. Serum chloride decreased significantly (P < 0.05) for 10 minutes in cats given 1 mEq of sodium bicarbonate/kg, and was significantly decreased for 30 minutes in cats given 2 mEq and 4 mEq of sodium bicarbonate/kg. Serum chloride decreased and remained significantly (P < 0.05) decreased for 30 minutes in cats given 1 g of 20% mannitol/kg. Serum sodium and serum osmolality did not change significantly (P < 0.05) in cats given 4 ml of 0.9% sodium chloride/kg.

Serum potassium decreased significantly (P < 0.05) for 10 minutes in cats given 1 mEq of sodium bicarbonate/kg, and for 120 minutes in cats given 2 mEq/kg or 4 mEq/kg. There was a significantly (P < 0.05) greater decrease in serum potassium that lasted for 30 minutes after giving sodium bicarbonate at the dosage of 4 mEq/kg, compared with other dosages given. Serum potassium did not change significantly in cats given 1 g of 20% mannitol/kg, but was significantly (P < 0.05) decreased 10 minutes following 4 ml of 0.9% sodium chloride/kg.

Sodium bicarbonate infusion significantly (P < 0.05) increased venous blood pH and plasma bicarbonate concentration in all cats. The magnitude and duration of these changes were significantly greater following administration of sodium bicarbonate at dosages of 2 mEq/kg and 4 mEq/kg. Significant (P < 0.05) increases in Pco2 were associated only with the highest dosage of sodium bicarbonate (4 mEq/kg). Base excess increased significantly (P < 0.05) in all cats following sodium bicarbonate infusion. There were significantly (P < 0.05) greater increases in base excess lasting 30 minutes following administration of sodium bicarbonate at dosages of 2 mEq/kg and 4 mEq/kg. Significant (P < 0.05) changes in venous blood pH, Pco2 , or bicarbonate were not observed in cats given 4 ml of 0.9% sodium chloride/kg, or in cats given 1 g of 20% mannitol/kg. Base excess was significantly (P < 0.05) increased for 10 minutes in cats given 1 g of 20% mannitol/kg.

As expected, 4 mEq of sodium bicarbonate/kg induced the most time- and dosage-related effects. Caution should be used when administering sodium bicarbonate iv to cats at dosages > 2 mEq/kg, because of the potential for important acid-base and electrolyte changes.

Free access
in American Journal of Veterinary Research

SUMMARY

Eight adult female cattle (6 Holstein, 1 Jersey, 1 Brown Swiss) were used to determine the antagonistic effects of tolazoline, an α2-adrenoceptor antagonist, on xylazine-induced (via caudal epidural administration) depression of cns, respiratory, and cardiovascular activity and rumen motility. A 2% solution of xylazine HCl was injected into the epidural space at the first coccygeal interspace, using a dosage of 0.05 mg/kg of body weight, diluted to a 5-ml volume with sterile water, and administered at a rate of approximately 1 ml/30 s. Eight minutes after xylazine injection, either tolazoline (0.3 mg/kg) or saline solution (4 ml) was administered iv. All 8 cattle were treated, using both regimens in a random sequence; at least 1 week elapsed between treatments. Epidurally administered xylazine induced caudal analgesia (S3 to coccyx), as evaluated by no response to superficial and deep muscular pinprick, and induced sedation, cardiopulmonary depression, and inhibition of rumen motility, but all cattle remained standing. Tolazoline effectively reversed xylazine-induced rumen hypomotility, and partially antagonized xylazine-induced cardiopulmonary depression without affecting sedation and desirable local (S3 to coccyx) analgesic effects.

Free access
in American Journal of Veterinary Research

Abstract

Objective

To provide quantitative assessment of forces affecting filtration of synovial fluid in response to incremental changes in arterial and venous hemodynamics.

Animals

7 clinically normal adult horses.

Procedure

Using a stationary, isolated metacarpophalangeal joint preparation, blood flow (Qacir), tissue perfusion, arterial pressure (Pacir), venous pressure (Pvcir), transsynovial fluid flow, total vascular resistance, vascular compliance, and tissue compliance were evaluated before and after arterial and venous pressure manipulations. At isogravimetric conditions, pre- and postcapillary resistance and ratios, osmotic reflection coefficient (σd), capillary pressure, net filtration pressure, and transitional microvascular pressure were determined.

Results

Synovial tissue blood flow was similar before, immediately after, and 3.5 hours after joint isolation. The σd for the joint was low, owing to the high oncotic pressure of synovial fluid at filtration-independent states. Transsynovial flow occurred in preference to lymph flow because of the high permeability of synovial tissue (low σd). Synovial fluid production and transfluid flow (synovium weight gain) increased at Pacir > 200 mm of Hg, indicating a threshold phenomenon for synovial filtration. Net filtration pressure > 6 mm of Hg is needed to effect an increase in synovial fluid flow, and pressure of approximately 11 mm of Hg is necessary to increase lymphatic flow. Vascular compliance in the joint was low, but increased markedly with Pvcir. Vascular and tissue compliance increased with increased Pacir. Vascular compliance changes caused by increased arterial pressure were minimal, compared with those caused by increased venous pressure owing to the greater elastance of arteries and the larger muscular arterial wall.

Conclusion

This isolated joint preparation permitted evaluation of codependent hemodynamic, microvascular, and transsynovial flow responses to hemodynamic manipulations. Synovial tissue permeability was markedly affected by increased vascular forces altering filtration pressures toward synovial fluid production. (Am J Vet Res 1998;59:495–503)

Free access
in American Journal of Veterinary Research

SUMMARY

The effects of hypertonic saline solution (hss) and hyperosmotic dextrose (hd; 2,400 mosm/L, 4 mV kg of body weight) on left ventricular afterload were determined in normovolumic, chloralose-anesthetized, autonomically blocked dogs (n = 8). Solutions were infused iv over 3 minutes. Left ventricular afterload was assessed by use of a dual-tipped micromanometer catheter with an electromagnetic fluidvelocity sensor located in the ascending aorta, and the impedance spectrum was calculated after Fourier analysis of signal-averaged aortic pressure and flow signals. Hypertonic saline solution and hd decreased peripheral resistance, reflection coefficient at zero frequency, and frequency of the first zero crossing of the phase angle for 3 to 5 minutes after either fluid was administered. Characteristic impedance was not altered by hss or hd. These impedance spectrum changes indicate transient vasodilatation and afterload reduction. We conclude that the vascular effect of an ionic hyperosmotic solution (hss) is similar to that of a nonionic hyperosmotic solution (hd), and that hss and hd transiently decrease afterload in normovolumic dogs. The duration of the afterload reduction after hss administration appeared to be too short to be of great clinical benefit.

Free access
in American Journal of Veterinary Research

Abstract

Objective

To evaluate the effect of high-molecular weight (MW) dextran macromolecules on low-flow ischemia and reperfusion of the large colon in horses.

Design

Horses subjected to low-flow ischemia and reperfusion of the large colon were treated with either 0.9 NaCI (group 1, n = 6) or high-MW dextran (group 2, n = 6) solutions.

Animals

12 adult horses.

Procedure

Horses were subjected to 3 hours' low-flow ischemia followed by 3 hours' reperfusion. A dose of either 0.9% NaCI or a 6% solution of high-MW (250,000) dextran (10 ml/kg of body weight) was administered IV, 30 minutes prior to reperfusion. Hemodynamic variables were recorded at 30-minute intervals. Systemic arterial and colonic venous blood were collected for determination of PCV, plasma total protein, and whole blood lactate concentrations, and for blood gas and oximetry analyses. Histologic examination of large-colon biopsy specimens was performed.

Results

Mean arterial pressure was greater in group-2 horses, compared with group-1 horses, from 3 to 3.25 hours, but there were no significant differences between groups for any of the other hemodynamic variables. Compared with baseline values, colonic blood flow was significantly lower from 0.5 to 3 hours and was significantly greater from 3.25 to 6 hours. Arterial and colonic venous PCV were significantly lower than baseline values from 3 to 3.25 hours, and at 3 hours, respectively, in group-2 horses. These values were significantly lower in group-2 horses, from 3 to 6 and 3 to 5 hours, respectively. There was significant mucosal necrosis, hemorrhage, edema, and neutrophil infiltration in horses of both groups; however, there were no significant differences between the 2 groups.

Conclusions

High-MW dextran did not protect the colonic mucosa from low-flow ischemia and reperfusion; there were no deleterious effects on colonic mucosa or on systemic hemodynamic or metabolic variables.

Clinical Relevance

Reperfusion with high-MW dextran solution probably would not protect the large colon from ischemia-reperfusion injury associated with large-colon volvulus. (Am J Vet Res 1996;57:1067–1073)

Free access
in American Journal of Veterinary Research

Summary

Effects of low-flow ischemia and reperfusion of the large colon on systemic and colonic hemodynamic and metabolic variables were determined in horses. Twenty-four adult horses were randomly allocated to 3 groups: sham-operated (n = 6), 6 hours of ischemia (n = 9), and 3 hours of ischemia and 3 hours of reperfusion (n = 9). Low-flow ischemia was induced in groups 2 and 3 by reducing colonic arterial blood flow to 20% of baseline. Heart rate, arterial blood pressures, cardiac index, pulmonary artery pressure, right atrial pressure, and colonic blood flow were monitored. Arterial, mixed-venous, and colonic venous blood gas and oximetry analyses; PCV; and blood lactate and pyruvate and plasma total protein concentrations were measured. Data were recorded, and blood samples were collected at baseline and at 30-minute intervals for 6 hours; additionally, data were collected at 185, 190, and 195 minutes (corresponding to 5, 10, and 15 minutes of reperfusion in group-3 horses). There were no differences among groups at baseline or across time for any systemic hemodynamic or metabolic variable. Colonic blood flow did not change across time in group-1 horses. Colonic blood flow significantly (P < 0.05) decreased to 20% of baseline at induction of ischemia in horses of groups 2 and 3 and remained significantly decreased throughout the ischemic period in horses of groups 2 (6 hours) and 3 (3 hours). Colonic blood flow significantly (P < 0.05) increased above baseline by 5 minutes of reperfusion in group-3 horses. Colonic oxygen delivery and oxygen consumption, and colonic venous pH, Po2 percentage saturation of hemoglobin, and oxygen content were significantly (P < 0.05) decreased within 30 minutes after induction of ischemia in horses of groups 2 and 3; colonic venous Po2 colonic oxygen extraction ratio, and lactate and pyruvate concentrations were significantiy (P < 0.05) increased by 30 minutes of ischemia. These alterations continued throughout ischemia, but within 5 minutes of reperfusion in group-3 horses, these variables either returned to baseline (pH, Pco2 lactate, pyruvate), significantly (P < 0.05) increased above baseline (Po2 oxygen content, % saturation of hemoglobin), or significantly (P < 0.05) decreased below baseline (colonic oxygen extraction ratio). Colonic oxygen consumption remained decreased during reperfusion in group-3 horses. Colonic mucosal ischemia-reperfusion injury observed in this model of ischemia was associated with local colonic hemodynamic and metabolic alterations in the presence of systemic hemodynamic and metabolic stability. Reactive hyperemia was observed at restoration of colonic blood flow in group-3 horses and persisted during reperfusion. Colonic venous metabolic alterations were corrected at reperfusion, indicating adaptation of the colon to the return of blood flow and oxygen delivery with resultant decrease in anaerobic metabolism. The early alterations in these variables may simply represent a washout of metabolic by-products.

Free access
in American Journal of Veterinary Research

SUMMARY

The hemodynamic effects of high arterial carbon dioxide pressure (PaCO2 ) during anesthesia in horses were studied. Eight horses were anesthetized with xylazine, guaifenesin, and thiamylal, and were maintained with halothane in oxygen (end-tidal halothane concentration = 1.15%). Baseline data were collected while the horses were breathing spontaneously; then the horses were subjected to intermittent positive-pressure ventilation, and data were collected during normocapnia (PaCO2 , 35 to 45 mm of Hg), moderate hypercapnia (PaCO2 , 60 to 70 mm of Hg), and severe hypercapnia (PaCO2 , 75 to 85 mm of Hg). Hypercapnia was induced by adding carbon dioxide to the inspired gas mixture. Moderate and severe hypercapnia were associated with significant (P < 0.05) increases in aortic blood pressure, left ventricular systolic pressure, cardiac output, stroke volume, maximal rate of increase and decrease in left ventricular pressure (positive and negative dP/dtmax, respectively), and median arterial blood flow, and decreased time constant for ventricular relaxation. These hemodynamic changes were accompanied by increased plasma epinephrine and norepinephrine concentrations. Administration of the β-blocking drug, propranolol hydrochloride, markedly depressed the response to hypercapnia. This study confirmed that in horses, hypercapnia is associated with augmentation of cardiovascular function.

Free access
in American Journal of Veterinary Research

Summary

The effect of xylazine on the arrhythmogenic dose of epinephrine (ade) was studied in 9 horses. Anesthesia was induced by administration of guaifenesin (50 mg/kg of body weight, iv) followed by thiamylal (4 to 6 mg/kg, iv) and was maintained at 1 minimal alveolar concentration (mac) of halothane (0.89%). Base apex ecg and facial artery pressure were recorded. Epinephrine was infused in a sequence of arithmetically spaced increasing rates (initial rate 0.25 µg/kg/min) for a maximum of 10 minutes. The ade was defined as the lowest epinephrine infusion rate to the nearest 0.25 µg/kg/min at which at least 4 premature ventricular depolarizations occurred in a 15- second period. Xylazine (1.1 mg/kg, iv) was administered after the control ade was determined. Xylazine did not significantly alter the ade (control, 1.12 ± 0.38 µg/kg/ min; xylazine, 1.21 ± 0.46 µg/kg/min). Blood pressure increased transiently for 8 minutes after xylazine administration. Baseline systolic and diastolic arterial pressures and heart rate were not significantly different from control baseline pressures and heart rate 15 minutes after xylazine administration. Blood pressure and heart rate increased significantly during control and xylazine ade determinations. Significant differences in pH, Pao2 , Paco2 , or base excess were not observed between baseline and ade in the control or xylazine groups. One horse developed atrial fibrillation, and 2 horses developed ventricular fibrillation during ade determinations.

Free access
in American Journal of Veterinary Research