Capillary permeability to endogenous macromolecules in the equine digit

Microvascular permeability characteristics were evaluated in digits of 7 adult horses. After capillaries were isolated and an extracorporeal perfusion circuit for the digit was established, a lymphatic vessel draining the distal portion of the phalangeal region was cannulated at the level of the coronary band. Venous pressure was increased in a stepwise manner, and lymph flow, lymph protein concentration (Cl), and plasma protein concentration (Cp) were determined after measured variables were allowed to reach steady state. Lymph-to-plasma protein concentration ratios (Cl/Cp) and lymph and plasma oncotic pressures were determined from samples collected during steady state. The osmotic reflection coefficient was determined after Cl/Cp became constant, regardless of increasing lymph flow, and was expressed as 1--Cl/Cp. The osmotic reflection coefficient for the digit was 0.67. Seemingly, the microvasculature bed of the digit was relatively permeable and could maintain only 67% of the endogenous macromolecules within the vasculature.     

Ultrastructural mucosal injury after experimental ischemia of the ascending colon in horses.

The ultrastructural injury that develops sequentially in the ascending colon during experimentally induced ischemia was examined in 6 halothane-anesthetized horses. Colonic ischemia was created by 2 types of vascular occlusion 24 cm proximal and distal to the pelvic flexure. In all horses, transmural vascular compression was created. The colonic venous circulation was obstructed in 3 horses, whereas in the other 3 horses, arterial and venous circulation was obstructed. Two additional horses were anesthetized as controls for determination of any morphologic alterations associated with the experimental protocol. Full-thickness colonic biopsy specimens were obtained from the antimesenteric border of the pelvic flexure at 0, 0.25, 0.5, 1, 1.5, 1.75, 2, 2.25, 2.5, 3, 3.5, 4, 4.5, and 5 hours during occlusion, and were studied by light and transmission electron microscopy. Morphologic alterations did not develop in the colon of control horses. Mucosal congestion was observed by light microscopy in the colon of horses with experimentally induced ischemia, but congestion developed early in those with obstructed colonic venous circulation, compared with those having arterial and venous obstruction. Inter- and intracellular vacuolation and loss of staining initially resulted in groups of 3 to 5 superficial luminal epithelial cells. Alterations in the glandular epithelium lagged behind those in the superficial epithelium, but were observed in both groups by 2 hours of obstruction. These changes progressed to 100% sloughing of all epithelium by 4.5 to 5 hours. The initial cellular alterations, which were observed by transmission electron microscopy, developed at 0.25 hour in horses with colonic venous obstruction and was characterized by inter- and intracellular edema.(ABSTRACT TRUNCATED AT 250 WORDS)     

The Effects of Ischemia and Reperfusion on Mucosal Respiratory Function, Adenosine Triphosphate, Electrolyte, and Water Content in the Ascending Colon of Ponies

Objective- The purpose of this study was to examine the effects of ischemia and reperfusion on the biochemical integrity of equine colonic mucosa to assess the relative roles of ischemic- and reperfusion-induced damage.
Study Design- Two hours of no-flow ischemia experimentally induced by 720° counterclockwise ascending colon volvulus followed by 2 hours reperfusion after derotation.
Animals- Ten ponies.
Methods- Ascending colon biopsies were obtained every hour for measurement of mucosal adenosine triphosphate (ATP), water, sodium, and potassium content. Additional samples were homogenized for assay of mitochondrial respiratory function.
Results- ATP content diminished 92% after ischemia and recovered to only 44% of control levels ( P <.001 versus controls) after 2 hours reperfusion. Reperfusion increased mucosal water and decreased sodium and potassium content for the duration of the experiment. Both NADH- (pyruvate) and FADH-linked (succinate) respiration decreased after ischemia and did not recover during reperfusion indicating electron transport chain dysfunction.
Conclusions- Two hours ischemia induced severe metabolic dysfunction in equine colon mucosa which persisted throughout reperfusion. Unequivocal evidence of injury specific to reperfusion was not observed in this study suggesting that much of the damage observed during reperfusion may be a continuation of injury induced during the ischemic period and not specific to reperfusion per se.
Clinical Relevance- This study suggests that greater efforts to metabolically support ischemically injured mucosa may be an important aspect of obtaining improved survival of horses affected by ascending colon volvulus (ACV).     

Strangulating volvulus of the ascending colon in horses

Of 57 horses with strangulating volvulus of the ascending colon, 42 were mares (including 21 postparturient mares), 8 were stallions, and 7 were geldings. Volvulus occurred most frequently in the summer (n = 24) and spring (n = 17). Pain was evaluated as severe in 41 horses, moderate in 9, and mild in 4. The abdominal fluid from 30 horses varied from clear yellow in 19 horses, to cloudy yellow in 3 horses, and serosanguineous in 8 horses. Protein content and nucleated cell count in the abdominal fluid were 2.5 +/- 1 g/dl and 1,000 +/- 900 microliters, respectively. Fifty horses had greater than or equal to 360 degrees volvulus and 7 had a 270 degrees volvulus, with 49 occurring in a counterclockwise direction. The site of volvulus in all horses was at the mesenteric attachment of the colon, except for a 360 degrees volvulus at the sternal and diaphragmatic flexures in 1 horse. Survival rates for horses with a greater than or equal to 360 degrees and a 270 degrees volvulus were 36% and 71%, respectively. The difference in survival rates reflected the severe vascular occlusion in the colon of horses with greater than or equal to 360 degrees volvulus. In nonsurvivors, hemorrhage in the submucosa and lamina propria (P less than 0.005) and edema in the submucosa (P less than 0.01) were greater than those in survivors. In nonsurvivors, greater than 97% of the superficial epithelium was lost. In horses that survived, only 60% of the cells were lost or degenerated.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of Carolina rinse solution, dimethyl sulfoxide, and the 21-aminosteroid, U-74389G, on microvascular permeability and morphology of the equine jejunum after low-flow ischemia and reperfusion

OBJECTIVE: To evaluate effects of Carolina rinse solution, dimethyl sulfoxide (DMSO), and 21-aminosteroid, U-74389G, on microvascular permeability and morphology of the equine jejunum after low-flow ischemia and reperfusion. ANIMALS: 20 healthy adult horses. PROCEDURE: Under anesthesia, full-thickness biopsy specimens of a distal portion of the jejunum were obtained for baseline measurements. In addition to a control segment, 2 jejunal segments were identified as sham-operated or experimental segments. Experimental segments underwent 60 minutes of low-flow ischemia and 3.5 hours of reperfusion. Treatments were as follows: U-74389G (3 mg/kg, IV; 6 horses), DMSO (20 mg/kg, IV; 6) diluted in 1 L of saline (0.9% NaCl) solution, local perfusion (via jejunal artery) of Carolina rinse solution (0.5 mL/kg; 4), and local perfusion of lactated Ringer's solution (0.5 mL/kg; 4). RESULTS: Jejunal microvascular permeability was significantly lower after treatment with Carolina rinse solution or DMSO, compared with U-74389G or lactated Ringer's solution treatments. After DMSO treatment, serosal- and submucosal-layer edema was significantly increased in experimental segments, compared with control or sham-operated segments; however, edema increases were significantly less than for lactated Ringer's solution or U-74389G treatments. Significant decreases in intestinal wet weight-to-dry weight ratio were found following Carolina rinse solution or DMSO treatments, compared with lactated Ringer's solution or U-74389G treatments. Edema formation and leukocyte infiltration in jejunal segments of horses treated with lactated Ringer's solution or U-74389G were increased, compared with Carolina rinse solution or DMSO treatments. CONCLUSIONS AND CLINICAL RELEVANCE: Carolina rinse solution and DMSO may be protective against ischemia-reperfusion injury in the equine jejunum.     

Serosal injury in the equine jejunum and ascending colon after ischemia-reperfusion or intraluminal distention and decompression

OBJECTIVE: To document morphologic changes that occur in equine intestinal serosa after experimentally induced ischemia and subsequent reperfusion (jejunum, ascending colon) or after intraluminal distention and decompression (jejunum). STUDY DESIGN: Morphologic effects of ischemia-reperfusion or intraluminal distention-decompression determined on the serosal layer of the equine jejunum. The large colon serosa was evaluated after ischemia-reperfusion injury. ANIMALS OR SAMPLE POPULATION: Seven adult horses. METHODS: After induction of general anesthesia and ventral median celiotomy, ischemia was created by arteriovenous (AVO) and lumen occlusion of a 20-cm segment of jejunum and ascending colon for 70 minutes, followed by a 60-minute reperfusion period. Intraluminal distention (25 cm H2O) was created in a second 20-cm jejunal segment and maintained within the abdomen for 120 minutes, followed by a 120-minute decompression period. Seromuscular biopsies were obtained upon entering the abdomen and after the ischemic and reperfusion periods, and after the distention and decompression periods along with corresponding control seromuscular biopsies. Samples were processed and examined by light microscopy, transmission electron, and scanning electron microscopy. RESULTS: Ischemia and reperfusion, and intraluminal distention and decompression, resulted in severe morphologic changes in the seromuscular layer of equine jejunum. A similar period of ischemia-reperfusion caused minimal changes in the ascending colon serosa. CONCLUSION: Adult equine jejunum sustains more serosal damage than the ascending colon after similar periods of ischemia-reperfusion injury. Intraluminal distention and subsequent decompression causes serosal damage in the equine jejunum. CLINICAL RELEVANCE: The small intestine is more susceptible to seromuscular layer damage than the ascending colon.     

Systemic and colonic venous plasma biochemical alterations in horses during low-flow ischemia and reperfusion of the large colon.

The purpose of this study was to determine the effects of low-flow ischemia and reperfusion (I-R) of the large colon on 16 systemic venous (SV) and colonic venous (CV) plasma biochemical variables in horses. Horses (n = 24) were randomly allocated to 3 groups: sham-operated (n = 6), 6 h ischemia (n = 9), and 3 h ischemia followed by 3 h reperfusion (n = 9). SV and CV heparinized blood was collected at 0, 1, 3, 3.25, 4, and 6 h. The SV-CV difference was calculated for each variable. The SV, CV, and SV-CV difference for albumin, total protein, and calcium decreased significantly (P < 0.05) across time in horses of all groups, but there were no differences among groups. SV phosphorous was significantly increased from baseline (BL) at 1 to 6 h in horses of all groups, but there were no differences among groups. CV phosphorous was significantly greater than BL from 1 to 6 h in group-2 horses and from 1 to 3 h in group-3 horses. SV potassium was not different among groups, but was significantly higher at 6 h, compared with BL in horses of all groups. CV potassium was significantly greater than BL from 1 to 6 h in horses of groups 2 and 3. SV glucose was greater at 6 h compared with all previous times in horses of all groups, but there were no difference among groups. CV glucose was significantly lower than BL and group-1 values in horses of groups 2 and 3 during ischemia, but returned to BL during reperfusion in group-3 horses. CV anion gap was significantly greater and SV-CV anion gap was significantly more negative in horses of groups 2 and 3, compared with group-1 horses during ischemia. The biologic relevance of these alterations is unknown, but they may contribute to histopathologic, hemodynamic, and metabolic alterations characteristic of low-flow I-R. Alternatively, these alterations may simply reflect colonic injury sustained during I-R. Results suggest that the colon utilizes glucose as a fuel and generates acid anions during low-flow ischemia. Increased CV phosphorous and potassium during I-R likely occurs as a result of leakage of intracellular stores subsequent to cellular damage.     

Effect of Platelet-Activating Factor Antagonist L-691,880 on Low-Flow Ischemia-Reperfusion Injury of the Large Colon in Horses

Objective—To determine the effect of platelet-activating factor (PAF) antagonist L-691,880 on low-flow ischemia and reperfusion (I-R) of the large colon in horses. Animals —12 adult horses. Experimental Design—Horses were anesthetized, and the large colon was exteriorized through a ventral median celiotomy and instrumented. Colonic arterial blood flow was reduced to 20% of baseline (BL) and maintained for 3 hours; flow was then restored, and the colon was reperfused for 3 hours. One of two solutions was administered intravenously 30 minutes before reperfusion: group 1, 10 mL/kg 0.9% NaCl; and group 2, 5 mg/kg PAF antagonist L-691,880 in 0.9% NaCl. Hemodynamic variables were monitored and recorded at 30-minute intervals. Systemic arterial and colonic venous blood were collected for measurement of blood gas tensions, oximetry analyses, packed cell volume, and total plasma protein concentrations. Colonic venous blood was collected for determination of lactate, 6-keto prostaglandin F_1α (6-kPG), prostaglandin E₂ (PGE₂), and thromboxane B₂ (TXB₂) concentrations. Full-thickness biopsy specimens were harvested from the left ventral colon for histological evaluation. Results—There were no significant differences between the two groups for any hemodynamic or metabolic variables. Colonic venous pH decreased, and carbon dioxide tension and lactate concentration increased during ischemia but returned to BL values during reperfusion. Colonic venous 6-kPG concentration was significantly increased above BL value at 2 hours and remained increased through 6 hours in horses of both groups. Colonic venous PGE₂ concentration was significantly greater in group 2 compared with group 1 throughout the study. Colonic venous PGE₂ concentration was increased above BL value from 3 to 6 hours in horses of both groups. Colonic venous TXB₂ concentration was not different between groups but was significantly increased above the BL value for the first hour of reperfusion. Low-flow I-R of the large colon caused significant mucosal necrosis, hemorrhage, edema, and neutrophil infiltration; however, there were no differences in histological variables between vehicle-control and PAF antagonist-treated horses. Conclusion—No protective effects of PAF antagonist L-691,880 were observed on colonic mucosa associated with low-flow I-R. Additionally, deleterious drug-induced effects on hemodynamic and metabolic variables and colonic mucosal injury were not observed.     

In vivo investigation of the efficacy of a customized solution to attenuate injury following low-flow ischemia and reperfusion injury in the jejunum of horses

OBJECTIVE: To evaluate the efficacy of a customized solution to attenuate intestinal injury following 20% low-flow ischemia and reperfusion in the jejunum of horses. ANIMALS: 10 healthy adult horses. PROCEDURE: Two 30.5-cm-long segments of jejunum were exteriorized through a ventral midline incision and the mesenteric artery and vein supplying that portion of the intestine were instrumented with flow probes. Blood flow was decreased to 20% of baseline for 90 minutes followed by 90 minutes of reperfusion. In 5 horses, 60 mL of the customized solution was placed in the lumen of each segment (treatment-group horses), and 60 mL of lactated Ringer's solution was placed in the lumen of 5 additional horses (control-group horses). Biopsy specimens were obtained from 1 segment in both groups for histologic evaluation. Aliquots of luminal fluid were obtained from the other segment in both groups for determination of albumin concentrations as an index of mucosal permeability. RESULTS: Compared with control-group horses, treatment-group horses had a significant decrease in luminal albumin concentration following reperfusion. Although differences in mucosal grades were not significantly different between control- and treatment-group horses, treatment-group horses had significantly greater jejunal villous length and area, compared with that of control-group horses. CONCLUSIONS AND CLINICAL RELEVANCE: Intraluminal administration of the customized solution in the jejunum, compared with lactated Ringer's solution, results in an improvement in histologic findings and mucosal translocation of albumin in horses with mild intestinal injury.     

Effects of intraluminal distention and decompression on microvascular permeability and hemodynamics of the equine jejunum

OBJECTIVE: To determine whether intraluminal distention and subsequent decompression of the equine jejunum affects intestinal blood flow, hemodynamics, and microvascular permeability. ANIMALS: 5 healthy adu t horses. PROCEDURES: Horses were anesthestized and underwent exploratory laparotomy. Two jejunal segments were identified as sham-operated or instrumented segments. After baseline values were obtained, intraluminal distention was created in the experimental segment to induce an ntraluminal pressure of 18 cm H2O. After 120 minutes of distention, the intestine was decompressed for 120 minutes. Mesenteric blood flow, oxygen delivery, oxygen consumption, microvascular permeability, wet weight-to-dry weight ratio, neutrophil infiltration, and vascular resistance were determined and comparisons made among control, sham-operated, and experimental segments. RESULTS: Mean jejunal blood flow was 21.4 ml/min per kg. There was a significant decrease in mesenteric bood flow to the distended intestine (13.4 ml/min per kg). Blood flow increased significantly during the decompression period (340% of baseline blood flow). Intraluminal distention and subsequent decompression resulted in a significant increase in microvascular permeability, as determined by the osmotic reflection coefficient. Oxygen delivery and oxygen content decreased significantly during the distention period and increased during decompression. Morphologic evaluation revealed a significant increase in edema and neutrophil infiltration after distention and decompression, compared with results for the sham-operated or control segments. CONCLUSIONS AND CLINICAL RELEVANCE: Intraluminal distention and decompression of the equine jejunum results in low-flow ischemia and edema, which may contribute to adhesions and ileus in the postoperative period after surgery for obstructions of the small intestines.     

Mechanisms of Gastrointestinal Ischemia-Reperfusion Injury and Potential Therapeutic Interventions: A Review and Its Implications in the Horse

Restoration of blood flow after a period of intestinal ischemia is necessary to maintain cell function and viability; however, the reintroduction of oxygen can initiate a cascade of events that exacerbates tissue injury. Intestinal I-R injury is manifested as increased microvascular and mucosal permeability, and mucosal necrosis. Reperfusion injury begins with the accumulation of hypoxanthine from ATP metabolism and the conversion of XDH to XO during ischemia. Upon reperfusion, the XO catalyzes the conversion of hypoxanthine to superoxide radicals in the presence of oxygen. Superoxide radicals are further reduced to highly reactive hydroxyl radicals, which initiate lipid peroxidation. Lipoperoxidation causes functional and structural alterations in cell membrane lipids and can release numerous inflammatory mediators, which exacerbate tissue damage. Neutrophils are recruited into tissues during ischemia and on reperfusion; then they undergo degranulation and release destructive products (proteases and OFRs), which mediate further tissue injury. A limited number of experimental studies in the gastrointestinal tract of horses have shown I-R injury. Additional studies are necessary to further elucidate and sequence the precise pathophysiologic mechanisms occuring in the equine intestine during I-R. Therapy should be focused on prevention of I-R injury by pharmacologic or chemical inhibition or modification of these pathophysiologic pathways. Selected pharmacologic agents or drug combinations may offer novel, scientifically relevant and yet practical approaches to alleviating intestinal I-R injury in horses. This may improve survival of horses with naturally acquired intestinal strangulation obstruction.     

In vitro evaluation of an intraluminal solution to attenuate effects of ischemia and reperfusion in the small intestine of horses

OBJECTIVE: To evaluate the efficacy of intraluminal administration of a customized solution during low-flow ischemia and reperfusion in the jejunum of horses. SAMPLE POPULATION: Segments of jejunum obtained from 13 healthy adult horses. PROCEDURE: In isolated segments of jejunum maintained in an extracorporeal circuit, arterial flow was reduced to 20% of baseline for 40 minutes (ischemia) followed by 60 minutes of reperfusion. In 2 groups, a customized solution (concentrations, 12.5 and 25%, respectively) was placed in the lumen prior to low-flow ischemia and maintained during reperfusion. The control group received intraluminal lactated Ringer's solution for the same duration. Various metabolic, hemodynamic, histologic, and permeability variables were recorded. RESULTS: The 12.5% solution resulted in less histomorphologic injury and reduced mucosal permeability to albumin, compared with the 25% solution and the lactated Ringer's solution. Morphologic injury and permeability were reduced in tissues that received the 25% solution, compared with the control group, but this difference was not significant. CONCLUSIONS AND CLINICAL RELEVANCE: Use of a 12.5% customized solution appeared to minimize injury in the isolated extracoporeal jejunal loop, which provides some indication that it might be useful in clinical situations.     

The pathophysiology of intestinal damage: effects of luminal distention and ischemia

Intestinal edema, luminal distention, and ischemia are common pathologic processes involved in producing the intestinal damage found during surgical exploration for acute abdominal disorders in the horse. The severity of intestinal edema depends on the degree of altered intravascular forces and changes in capillary permeability. Capillary hydrostatic pressure rises as the less pliable venules and veins become occluded during intestinal obstruction. Concurrently, the production of various endogenous products that damage the vascular wall leads to increases in capillary permeability and protein exudation, causing fluid movement into the interstitium and consequent tissue edema. The information presently available indicates that luminal distention does not produce the morphologic damage observed during natural conditions. However, slight intestinal edema was observed with experimental distention of the equine small intestine. Although the effects of increased luminal pressure appear minor, in the overall scheme of intestine damage, many processes are occurring together, and the luminal distention may be additive in the production of intestinal damage. The intestinal damage occurring during natural obstructions is most likely related to both the severity of the ischemia and the subsequent reperfusion injury. Experimentally, an ischemic insult produces a consistent sequence of mucosal alterations to both the equine small and large intestine. Severity of ischemia may be the limiting factor in determining the clinical outcome in cases in which the ischemic insult is irreversible; however, if the intestinal tissue survives the ischemia, the reperfusion injury may substantially increase the damage, producing an irreversible injury. The proposed mechanisms responsible for the reperfusion injury include the presence of highly reactive cytotoxic oxygen radicals. The intestinal epithelium and vascular endothelium are both capable of producing these unstable compounds. Secondly, the influx and activation of neutrophils may also release oxygen radicals. During experimental ischemia, neutrophils gradually move to the affected area; however, during reperfusion their numbers dramatically increase and may play a significant role in producing intestinal damage. Therapy for intestinal damage involves first determining the viability of the affected intestine. All nonviable bowel should be resected and viable intestine anastomosed. The care and maintenance of intestine of questionable viability are presently based on therapy in humans and experimental information concerning the pathophysiologic mechanisms of intestinal ischemia.(ABSTRACT TRUNCATED AT 400 WORDS)     

In vitro evaluation of a customized solution for use in attenuating effects of ischemia and reperfusion in the equine small intestine.

OBJECTIVE: To determine whether a customized solution could attenuate the effects of low-flow ischemia and reperfusion injury of the equine jejunum. SAMPLE POPULATION: A segment of jejunum obtained from 21 healthy adult horses. PROCEDURE: A segment of jejunum was maintained in an isolated extracorporeal circuit, and arterial flow was reduced to 20% of baseline for 40 minutes (ischemia) followed by 60 minutes of reperfusion. In 1 group, a customized solution was infused at a rate of 1 ml/min during low-flow ischemia and 3 ml/min during reperfusion. In a second group, the solution was infused at the same rate during low-flow ischemia, but it was infused at a rate of 7 ml/min during reperfusion. Control groups received lactated Ringer's solution administered at the same rates as for the customized solution. Various metabolic, hemodynamic, histologic, and permeability variables were recorded. RESULTS: A lower flow rate during reperfusion (3 ml/min) had a beneficial effect, compared with lactated Ringer's solution or the higher flow rate (7 ml/min). Use of the solution at this rate resulted in less histomorphologic injury and reduced mucosal permeability to albumin. CONCLUSIONS AND CLINICAL RELEVANCE: Use of a customized solution at a lower flow rate during repurfusion appeared to have a protective effect on equine jejunum when administered IV during low-flow ischemia and reperfusion.     

Effect of Ischemia and Reperfusion on Neutrophil Accumulation in Equine Microvascular Tissue Flaps

Objective— To investigate neutrophil accumulation after ischemia and reperfusion (IR) in microvascular tissue flaps in horses.
Study Design— Randomized controlled experiment.
Sample Population— A total of 8 horses between 1 and 10 years of age, 4 of each sex.
Methods— Control and experimental myocutaneous island flaps based on the superficial branch of the deep circumflex iliac vessels were dissected on each horse. Atraumatic vascular clamps were applied to the pedicle of the experimental flap for 90 minutes and then removed to allow reperfusion. Based on the assumption that rapid infiltration of neutrophils into affected tissues is a hallmark of IR injury, radiolabeled autogenous leukocytes were used to indirectly quantify neutrophil accumulation in flap tissues. Labeled leukocytes were administered through a jugular catheter 30 minutes before flap reperfusion. Biopsies were collected from each flap over a 6 hour postischemia time period; in group 1 (  n = 4  ) from 0 to 6 hours postischemia, and in group 2 (  n = 4  ) from 24 to 30 hours postischemia. Biopsies were examined scintigraphically and histologically for evidence of neutrophil infiltration.
Results— All control flaps survived and 6 of 8 experimental flaps survived. There was no significant evidence of acute neutrophil infiltration into flap tissues after reperfusion in either group.
Conclusions— The results of this study suggest that equine myocutaneous flap tissues can survive a 90-minute ischemic period and reperfusion. No significant evidence of the occurrence of IR injury in flap tissues was found.
Clinical Relevance— The reasons for the previously reported failures of equine free tissue transfer remain uncertain, but they do not appear to be caused by neutrophil mediated injury associated with ischemia and reperfusion.     

Pathologic changes associated with induced small intestinal strangulation obstruction and nonstrangulating infarction in horses

Arteriovenous (ischemic strangulation obstruction, ISO) or venous (hemorrhagic strangulation obstruction, HSO) occlusions were created in the jejunum of 5 anesthetized horses and were left in situ for 1-, 2-, or 3-hour intervals. Segments were evaluated grossly for color, thickness, and motility. The horses were euthanatized, and the degree of mucosal slough, edema, congestion, and hemorrhage was determined histologically. Segments subjected to ISO became dark, but did not contain edema or hemorrhage. Segments subjected to HSO were characterized by progressive congestion, edema, and hemorrhage especially in the mucosal layer. Histologically, the mucosal epithelium was affected approximately equally by ISO or HSO, although more gross changes were evident in segments subjected to HSO.     

Treatment of ischaemic jejunum with topical and intraluminal Carolina Rinse

Carolina Rinse Solution (CRS) was applied topically and intraluminally to ischaemic (Group 1; n = 5) and distended equine jejunum (Group 2; n = 5). Mesenteric blood flow, ORC (osmotic reflection coefficient), wet weight to dry weight ratios (WW/DW), serosal thickness, and neutrophil accumulation in the serosa were measured. After 60 min ischaemia followed by reperfusion (Group 1), mesenteric blood flow remained greater than baseline values. The mean ORC was similar to that previously reported in normal bowel or ischaemic intestine treated with CRS by arterial perfusion. The ORC after distention and decompression (Group 2) increased and was similar to that previously reported in a comparable untreated experimental model. The WW/DW after both ischaemia and distention increased compared to specimens collected from noninstrumented jejunum proximal to the experimental segments in the same horses. There was no difference in neutrophil numbers in the serosa of either ischaemic or distended intestine compared to the noninstrumented proximal jejunum. CRS-treated ischaemic intestine maintained microvascular permeability similar to that reported for normal intestine whereas treated distended intestine did not. Combined topical and intraluminal application of CRS to ischaemic intestine may reduce complications due to acute inflammation during reperfusion.     

Ionized calcium concentration in horses with surgically managed gastrointestinal disease: 147 cases (1988-1990).

Packed cell volume, total plasma protein, serum sodium, potassium, and ionized Ca2+ concentrations, and blood pH were determined at the time of admission and following surgery in 147 horses with acute abdominal crisis. Horses were allotted to 3 categories on the basis of the surgical lesion: (1) nonstrangulating obstruction of the ascending or descending colon (category A, n = 76), (2) strangulating and nonstrangulating infarction of the cecum or ascending colon (category B, n = 37), and (3) strangulating and nonstrangulating infarction of the small intestine (category C, n = 25). Horses with low serum ionized Ca2+ concentration following surgery were given 23% calcium gluconate (100 to 300 ml) IV to effect, and ionized Ca2+ concentration was determined following treatment. The serum ionized Ca2+ concentrations of horses in categories A, B, and C before and after surgery were lower than our normal laboratory reference range. Prior to surgery, serum ionized Ca2+ concentration measured from horses in category B and C was lower than that in horses in category A. There was no difference in ionized Ca2+ concentration in serum samples obtained before surgery in horses from category B and C, and in serum samples obtained following surgery. There was a decrease in ionized Ca2+ concentration during surgery in horses in category A. There was no change between preoperative and postoperative ionized Ca2+ concentration in the samples obtained from horses in category B and C. After calcium gluconate administration, all horses with low serum ionized Ca2+ after surgery had concentrations within our normal range. Measurement of serum ionized Ca2+ in horses with an acute abdominal crisis is recommended.(ABSTRACT TRUNCATED AT 250 WORDS)     

Plasma lactate as a predictor of colonic viability and survival after 360 degrees volvulus of the ascending colon in horses

Objectives— To determine the relationship between plasma lactate concentration and colonic viability and survival in horses with ≥360° volvulus of the ascending colon.
Study Design— Retrospective study.
Animals— Horses (n=73) with ≥360° volvulus of the ascending colon.
Methods— Medical records (January 2000–November 2005) of all horses examined for colic at Michigan State University Veterinary Teaching Hospital were reviewed. Horses were included only if plasma lactate concentration was measured preoperatively and a diagnosis of ≥360° volvulus of the ascending colon was confirmed by surgery or necropsy. Non-survivors were only included if the ascending colon was evaluated histopathologically. Logistic regression analysis was used to model the relationship between lactate, colonic viability, and survival.
Results— Of 73 horses, 61 were discharged. Mean (±SD) plasma lactate concentration was significantly lower in survivors (2.98±2.53 mmol/L) compared with non-survivors (9.48±5.22 mmol/L; odds ratio [OR]=1.628, 95% confidence limit [CI]=1.259–2.105). Plasma lactate concentration was significantly lower in horses with a viable colon (3.30±2.85 mmol/L) compared with horses with a non-viable colon (9.1±6.09 mmol/L; OR=1.472, 95% CI=1.173–1.846). Plasma lactate concentration <6.0 mmol/L had a sensitivity of 84% and a specificity 83% for predicting horse survival.
Conclusions— Our results demonstrate a strong association between plasma lactate concentration at the time of hospital admission and outcome in horses with ≥360° volvulus of the ascending colon.
Clinical Relevance— Plasma lactate concentration may help predict colonic viability and horse survival after ascending colon volvulus in horses.     

Equine Large Intestinal Volvulus A Review of 124 Cases

The average age of 122 horses with ascending colon volvulus was 6.6 +/- 0.4 years. Gastric reflux was a presenting sign in 35% of the cases. Peritoneal fluid protein levels had a mean of 2.54 +/- 0.14 g/dl and 20 horses had grossly normal peritoneal fluid at the time of presentation. Ascending colon volvulus was most commonly found at the level of the cecocolic fold with the initial ventral colon movement in a dorsomedial direction about the ascending mesocolic axis. The overall survival rate was 34.7% with a recurrence rate of only 4.9%.