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Abstract

OBJECTIVE To establish a study cutoff for evidence of glaucoma on the basis of IOP measurements from a large population of healthy dogs and to assess the effects of IV propofol administration on IOPs in premedicated and nonpremedicated dogs with and without glaucoma defined by this method.

DESIGN Prospective, descriptive study.

ANIMALS 234 client-owned dogs.

PROCEDURES IOPs measured in 113 healthy dogs (226 eyes) were used to calculate an IOP value indicative of glaucoma. The IOPs were measured in an additional 121 dogs (237 eyes) undergoing ophthalmic surgery. Midazolam-butorphanol was administered IV as preanesthetic medication to 15 and 87 dogs with and without glaucoma, respectively. A placebo (lactated Ringer solution) was administered IV to 8 and 11 dogs with and without glaucoma, respectively. Anesthesia of surgical patients was induced with propofol IV to effect. The IOPs and physiologic variables of interest were recorded before (baseline) and after preanesthetic medication or placebo administration and after propofol administration.

RESULTS An IOP > 25 mm Hg was deemed indicative of glaucoma. Compared with baseline measurements, mean IOP was increased after propofol administration in nonpremedicated dogs without glaucoma and unchanged in nonpremedicated dogs with glaucoma. Propofol-associated increases in IOP were blunted in premedicated dogs without glaucoma; IOP in affected eyes of premedicated dogs with glaucoma was decreased after preanesthetic medication and after propofol administration.

CONCLUSIONS AND CLINICAL RELEVANCE Results indicated that preexisting IOP influences the response to anesthetic drugs, and administration of preanesthetic medication with muscle-relaxing properties may blunt or reduce propofol-induced increases in IOP. Further research with a larger number of dogs is needed to confirm our results in dogs with glaucoma.

Full access
in Journal of the American Veterinary Medical Association

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

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 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

Objective—

To compare the efficacy of 7% NaCI solution (hypertonic saline) in 6% dextran 70 solution (HSD) with that of lactated Ringer's solution (LRS) for treatment of dogs in traumatic shock.

Design—

Prospective, randomized, clinical study.

Animals—

16 traumatized adult dogs with clinical signs of shock.

Procedure—

Physical, hemodynamic, blood gas, and clinical chemistry measurements were performed prior to treatment. Initial treatment consisted of HSD (n = 8) or LRS (n = 8) administered as a bolus (5 ml/kg of body weight, IV) over a 3-minute period, followed by administration of additional LRS and other treatments to restore hemodynamic and physical criteria to within reference limits. Measurements were repeated for 3 hours after initial treatment. The volumes of LRS and HSD administered were recorded hourly. Degree of injury was scored by using a trauma severity index.

Results—

Dogs responded similarly to the treatments, and all but 3 dogs survived to be discharged. The amount of fluid administered to dogs in the HSD group over the final 2 hours of the study was significantly less than that administered to the dogs in the LRS group. Serum sodium concentration and osmolality of the dogs in the HSD group were not significantly greater than those values in the LRS group. Bradyarrhythmias were observed in 2 dogs in the HSD group.

Clinical Implications—

Hypertonic sodium chloride/ dextran solution is safe and effective for resuscitating dogs in traumatic shock. Seven percent NaCI in 6% dextran 70 may reduce the need for isotonic fluids in the hours after initial resuscitation. (J Am Vet Med Assoc 1996;208:366-370)

Free access
in Journal of the American Veterinary Medical Association

Summary:

An in-circuit vaporizer for delivery of isoflurane was evaluated. The isoflurane concentration within an isolated circle breathing circuit was determined for 1 hour in 6 in-the-circuit vaporizers with the wicks removed. A mechanical ventilator and artificial lung were connected to the circuit. Isoflurane concentration increased as vaporizer setting increased, and delivered concentration (%) at 60 minutes ( X ¯ ± sem) ranged from 0.46 ± 0.10 at tap setting 1 to 3.67 ± 0.30 at setting 5. Temperature of the isoflurane did not change.

Cardiovascular and respiratory function were maintained within a clinically acceptable range in 6 dogs anesthetized with thiamylal and maintained with 1.87% end-tidal isoflurane delivered from the in-circuit vaporizer during spontaneous ventilation, controlled ventilation, and closed-circuit anesthesia. The range of vaporizer tap settings ( X ¯ ± sem) was lower during closed-system anesthesia (2.5 ± 0.1 to 3.5 ± 0.6) and during controlled ventilation (2.6 ± 0.2 to 3.3 ± 0.2) than during semi-closed system anesthesia (5.4 ± 0.3 to 6.8 ± 0.4).

The in-circuit vaporizer was used to deliver isoflurane to 36 dogs anesthetized for a variety of surgical and medical procedures. Ventilation was spontaneous, assisted, and in 1 instance, controlled. Cardiovascular function, respiratory function, and recovery times were within clinically acceptable ranges. The initial vaporizer tap setting ( X ¯ ± sem) was 8.2 ± 0.4, and this corresponded to an end-tidal isoflurane concentration of 3.5 ± 0.6. The range of vaporizer settings during the maintenance phase ( X ¯ ± sem) was 2.8 ± 0.5 to 4.6 ± 1.9. This corresponded to an end-tidal isoflurane concentration of 1.2 ± 0.1 to 1.8 ± 0.1%.

This study documents that when appropriate guidelines are followed and limitations understood, the in-circle vaporizer is suitable for delivery of isoflurane to dogs undergoing a variety of surgical and medical procedures. Guidelines include removal of the wick, attention to the relatively rapid increase of anesthetic depth during the first 5 minutes of anesthesia, and the need to decrease the setting of the vaporizer control lever if assisted or controlled ventilation is used, or if closed system flow rates are used. Limitations include unpredictability of output with changing ambient temperature and difficulty adapting its use with semi-open breathing systems such as the t-piece or Bain coaxial circuit.

Free access
in Journal of the American Veterinary Medical Association

SUMMARY

The effect of hypercapnia on the arrhythmo-genic dose of epinephrine (ADE) was investigated in 14 horses. Anesthesia was induced with guaifenesin and thiamylal sodium and was maintained at an end-tidal halothane concentration between 0.86 and 0.92%. Base-apex ECG, cardiac output, and facial artery blood pressure were measured and recorded. The ADE was determined at normocapnia (arterial partial pressure of carbon dioxide [Paco2 = 35 to 45 mm of Hg), at hypercapnia (Paco2 = 70 to 80 mm of Hg), and after return to normocapnia. Epinephrine was infused at arithmetically spaced increasing rates (initial rate = 0.25 μg/kg of body weight/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 4 premature ventricular complexes occurred in a 15-second period. The ADE (mean ± SD) during hypercapnia (1.04 ± 0.23 μg/kg/min) was significantly (P < 0.05) less than the ADE at normocapnia (1.35 ± 0.38 μg/kg/min), whereas the ADE after return to normocapnia (1.17 ± 0.22 μg/kg/min) was not significantly different from those during normocapnia or hypercapnia. Baseline systolic and diastolic arterial pressures and cardiac output decreased after return to normocapnia. Significant differences were not found in arterial partial pressure of O2 (PaO2) or in base excess during the experiment. Two horses developed ventricular fibrillation and died during normocapnic determinations of ADE. Hypercapnia was associated with an increased risk of developing ventricular arrhythmias in horses anesthetized with guaifenesin, thiamylal sodium, and halothane.

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

Abstract

Objective

To determine cardiorespiratory effects of a tiletamine/zolazepam-ketamine-detomidine (TZKD) combination in horses.

Animals

8 healthy adult horses.

Procedure

Horses were instrumented for measurement of cardiorespiratory, acid-base, and electrolyte values. Each horse was given xylazine (0.44 mg/kg of body weight, IV) 10 to 15 minutes prior to induction of recumbency by administration of the TZKD combination. Cardiorespiratory, acid-base, and electrolyte values were measured at 5-minute intervals for ≥ 30 minutes.

Results

All horses became recumbent within 1 minute after IV administration of TZKD. Mean ± SD duration of recumbency was 40 ± 8 minutes. All horses regained standing position after ≤ 2 attempts. Quality of anesthesia and analgesia was determined to be satisfactory in all horses. Xylazine induced decreases in respiratory rate, heart rate, cardiac output, maximum rate of increase of right ventricular pressure, and rate pressure product. The PaCO2, right atrial pressure, and peripheral vascular resistance increased, whereas blood temperature, PO2, pHa, HCO3 , PCV, total solids, Na, and K values remained unchanged. Subsequent administration of TZKD caused right atrial pressure and PaCO2 to increase and PaO2 to decrease, compared with values obtained after xylazine administration. Remaining cardiorespiratory, acid-base, hematologic, and electrolyte values did not differ from those obtained after xylazine administration.

Conclusion

IV administration of TZKD induces short-term anesthesia in horses. Potential advantages of this drug combination are the small volume of drug administered; minimal cardiorespiratory depression; quality of induction and maintenance of, and recovery from, anesthesia; and duration of drug effects. (Am J Vet Fles 1999;60:770–774)

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