هادی ایمانی راستابی

This study aimed to compare four pain scales, including simple descriptive scales (SDS), visual analog scale (VAS), the University of Melbourne Pain Scale (UMPS), and the short form of Glasgow Composite Pain Scale (GCPS-SF) to assess postoperative pain in dogs that underwent ovariohysterectomy (OHE). Twenty-two female mixed-breed dogs were allocated into three treatments to receive incisional (n=7), transverse abdominis plane (TAP, n=7), and rectus sheet (RS, n=8) blocks. After premedication with acepromazine (0.05 mg/kg) and morphine (0.5 mg/kg), anesthesia was induced (4 mg/kg) and maintained (0.4 mg/kg/min) with propofol. Each dog randomly received one analgesic method, and then OHE was performed. Postoperative analgesia was evaluated up to 6 hours after the operation with the above-mentioned pain scales. The results showed that with the GCPS-SF, the scores at 4, 5, and 6 hours after surgery in the Incisional and RSB were higher than the baseline. In the UMPS, in the RSB, at 2, 3, 4, 5, and 6 hours after surgery, the pain score was significantly higher than the baseline. With the VAS, the pain score in the RSB was higher than the baseline at 3, 4, 5, and 6 hours after surgery. In the SDS, the Incisional and RS pain scores were higher at 3, 4, 5, and 6 hours after surgery than the baseline values. In conclusion, the UMPS might detect pain earlier and is more sensitive than the other three methods. Further studies should be done to confirm the results.

Stanozolol and nandrolone decanoate hormones are mainly used in dogs and horses to strengthen muscle growth, increase of body weight, treatment of anemia and stimulation of appetite; nevertheless, some side effects have been reported, including testicular atrophy, and decrease of spermatozoid count in dogs. The aim of the present study is to evaluate the histopathological changes of testicular and epididymal tissues in dogs treated with stanozolol and nandrolone decanoate. The present survey was performed on sixtheen male dogs. The studied animals were divided into two equal groups of eight. Stanozolol was administered to dogs in group A with dosage of 50 mg per dog intramuscularly for 6 continuous weeks. Group B was similar to group A, but instead of stanozolol, nandrolone decanoate was injected with dosage of 1 mg/kg. To evaluate the possible side effects on the testicles, one of them was surgically removed before the investigation and the second testicle was removed on days 28 (four dogs in each group) and 42 (the remaining four of each group). Before the testes were placed in 10% formalin buffer, sperm quality in the epididymis was evaluated for indicators such as motility, morphology and number in times zero, 28 and 42 days. The results showed that destructive effects were obtained such as hyperplasia of interstitial Leydig cells, vacuolation, the presence of multinucleated cells and different stages of spermatogonia in testicular tissue; also, the destruction of duct covering cells and the detachment of cilia in the epididymal epithelium was observed. These changes were significantly greater in the stanozolol group than nandrolone decanoate. The quantitative changes were more pronounced in the stanozolol group and the qualitative changes in the nanderlone decanoate group. Although both drugs had side effects on testicular and epididymal tissues; the side effects of stanozolol were greater than nandrolone decanoate; therefore, it is recommended minimum dose of nandrolone decanate for therapeutic purposes.

It has been proposed that dose reduction via co-administration of other agents might ameliorate respiratory depression associated with ketofol.

The present study was designed to evaluate the effects of adding lidocaine, fentanyl, or dexmedetomidine on the required dose and cardiorespiratory variables in dogs undergoing total intravenous anesthesia (TIVA) with ketofol.

In phase I, twelve dogs (six per each treatment) were induced and maintained with two out of four anesthetic regimens of (1) ketofol (4 mg/kg and 0.3 mg/kg/min, respectively; KET), (2) ketofol and lidocaine (1.5 mg/kg and 0.25 mg/kg/min, respectively; KLD), (3) ketofol and fentanyl (5 µg/kg and 0.1 µg/kg/min, respectively; KFN), and (4) ketofol and dexmedetomidine (2 µg/kg and 2 mg/kg/h, respectively; KDX) with at least one-week interval. The minimum infusion rate (MIR) of ketofol was determined. In phase II, the other twelve dogs were given the same anesthetic regimens for 60 min with the determined infusion rate of ketofol, and cardiorespiratory variables were recorded.

Mean MIR of ketofol for KET, KLD, KFN, and KDX were 0.35, 0.23, 0.15, and 0.08 mg/kg/min, respectively. In phase II, the times of recovery events were shorter in KFN and KDX than KET and KLD. The heart rate was significantly higher than baseline in KET and KLD, which was also significantly lower than KFN and KDX at several time points. In all treatments, respiratory depression was detected.

Despite the decrease in the dose of ketofol, none of the added drugs attenuated respiratory depression caused by this agent.

It has been documented that hemodynamic disturbances occur in hypovolemic patients. Therefore, the early management of hypovolemia is essential to achieve optimal outcomes. Blood gas, which changes rapidly during hemodynamic instability, can be used as a diagnostic approach for monitoring emergency patients. The objective of the current study was to evaluate the results of resuscitation with hydroxyethyl starch (HES) or lactated Ringer's solution (LR) on venous and arterial blood gas. In addition, the difference between venous and arterial blood gas parameters is investigated to assess the possibility of using venous blood gas analysis as a successor for arterial blood gas analysis in the resuscitation of hypovolemic dogs. Venous and arterial pH, PO2, PCO2, HCO3-, and base excess were analyzed at the end of each study stage as follow: 1) Establishment of anesthesia, 2) Blood collection to an arterial mean pressure of 40-50 mm Hg, 3) Maintaining dogs in a hypovolemic state, 4) Resuscitation with LR (group A) or HES (group B) in four steps, and 5) One hour after the final resuscitation step. Hypovolemia decreased the studied parameters, except venous PCO2, which showed a significant increase (p < 0.05). Fluid resuscitation returned the studied parameters to the control values as venous PCO2 in group A and HCO3- in group B showed a significant change in comparison with the control values (p < 0.05). We found that venous pH, HCO3-, and PCO2 can be used as less invasive and safer alternatives to similar arterial parameters to monitor the fluid resuscitation of hypovolemic dogs.

Intermittent chest compression is still routinely used in resuscitation for hemorrhagic shock patients. There is a possibility that by using a different resuscitation method with interposed abdominal compressions, through forcing the blood from abdominal organs into the circulation and increasing intraperitoneal pressure, more blood pumps to heart. Therefore, in this study, chest compression resuscitation and interposed abdominal compressions resuscitation were compared in dogs with induced experimental hemorrhagic shock and electrocardiographic changes evaluated as an important diagnostic and monitoring tool in heart conduction and rhythm disorders. Thus hemorrhagic shock was induced by drawing blood from femoral artery in 15 dogs under anesthesia and continued until pulseless electrical activity achieved. The dogs were kept pulseless for 20 minutes, then were randomized to three treatment groups - fluid resuscitation alone with Ringer's lactate solution, chest compressions with fluid resuscitation, and interposed abdominal compression with fluid resuscitation. Resuscitation was conducted until reaching the point of return of spontaneous circulation. Electrocardiograms were recorded before the induction of hemorrhage, at the time that the pulse was lost, after 20 minutes of pulseless state and at the point of return of spontaneous circulation. Changes in P and QRS waves amplitudes, QT interval, heart rate, and electrical axis and morphology of ST segment was significant in different times within groups. but there were no significant changes in P and QRS durations and PR interval and heart rhythm. There were no significant changes in any parameter with different type of resuscitation method. Finally mixed effect of time and groups were also statistically insignificant in all parameters. In conclusion, it seems that there is no positive impact in electrocardiographic parameters using either of chest compression only or interposed abdominal compression resuscitation methods in dogs with induced hemorrhagic shock.

The aim of the present study was to evaluate the effect of midazolam on lidocaine-induced toxicity in chickens. Forty-eight healthy, Lohmann broiler chickens (Gallus gallus domesticus) divided into two groups (n=24) and four subgroups each (n=6). The birds in group I and II received lidocaine with infusion rates of 15 and 25 mg/kg/min, respectively. Ten minutes before lidocaine administration, in each subgroup, one of the treatments of normal saline or midazolam at the dose rate of 0.25, 0.5 and 1.0 mg/kg were injected into the pectoral muscle. With occurrence of the signs related to the toxicity (convulsion and/or respiratory arrest), lidocaine infusion was disrupted and the administered dose of lidocaine was calculated. In group I, convulsion was observed at the dose of 38.0 ± 13.0 mg/kg in the birds received normal saline while in midazolam-treated birds, respiratory arrest without convulsion occurred at the dose of 36.1 ± 12.4, 39.9 ± 15.3, and 37.1 ± 9.1 mg/kg, respectively. In group II, convulsion occurred saline-treated animals at the dose of 23.4 ± 4.8 mg/kg. The birds that received midazolam showed respiratory arrest without convulsion at the dose of 31.1 ± 3.8, 31.3 ± 3.8 and 28.2 ± 5.3 mg/kg, respectively. The birds which received lidocaine at the lower infusion rate showed toxicity signs at the significantly higher doses. Based on the results of the current study, at lower infusion rate, premedication with midazolam protected chickens against convulsion but it had no effect on the threshold of toxicity (respiratory arrest) following administration of high doses of lidocaine.

Stanozolol and Nandrolone decanoate are the most commonly used hormones in canine medi-cine. They are mainly administered to strengthen the muscle, gain weight, treatment of anemia and stimulate the appetite. One of the effects of hormones is to enhance the erythropoietin production and eventually an increase in the number of RBCs.

Prolonged usage of hormones may be relevant to the liver and renal disorders; therefore, the pre-sent survey was aimed to evaluate the effects of stanozolol and nandrolone decanoate on liver and kidney indices, erythropoietin and testosterone serum concentrations and hematocrit changes in healthy dogs.

Sixteen dogs were randomly categorized in two groups of A (stanozolol) and B (nandrolone decano-ate). Each group was divided into two subgroups (A1, A2 and B1, B2). The second testicle was removed on day 28 in the first subgroups (A1 and B1), and day 42 in the second subgroups (A2 and B2). The first testicle was removed at time zero. Stanozolol (50 mg per dog) was administered to all dogs of group A as IM once a week for six weeks. Group B was similar to group A with the difference that nandrolone decanoate was injected (1 mg/kg) instead of stanozolol. Blood samples were collected on days 0, 3, 14, 28 and 42.

Erythropoietin and testosterone concentrations were virtually increased in both groups A (p <0.05) and B (p <0.05). The effect of stanozolol on erythropoietin (subgroup A1) (11.35±1.31 ng/mL) was significantly higher than nandrolone decanoate (subgroup B1) (8.02±0.55 ng/mL) (p <0.05); nevertheless, the changes in testosterone levels, was not significant between groups A and B (p >0.05). The liver enzymes of ALP, ALT and AST were increased more significantly in group A than group B (p <0.05).

Erythropoietin and testosterone levels were virtually increased in both groups A and B; how-ever, stanozolol had more significant effect than nandrolone decanoate in increment of erythropoietin; nevertheless, it had more side effects on liver indices. It is suggested that nandrolone decanoate to be administered for the thera-peutic goals.

Medetomidine and dexmedetomidine are the two new alpha-2 agonists available for use in veterinary anesthesia. These drugs are employed for sedation and premedication in small animals. The present study aimed to investigate the effects of medetomidine and dexmedetomidine alone and in combination with acepromazine on sedation, cardiovascular function and electrocardiography in dogs. Sixty dogs were randomly divided into four equal groups. The dogs received one of the treatments of medetomidine (10 μg/kg), dexmedetomidine (5 μg/kg), medetomidine (10 μg/kg) with acepromazine (0.05 mg/kg) and dexmedetomidine (5 μg/kg) with acepromazine (0.05 mg/kg) intramuscularly. Sedation levels, heart rate, non-invasive arterial blood pressure, respiratory rate, body temperature and electrocardiogram were carefully recorded in dogs up to 20 minutes after administration. Sedation scores were significantly higher in groups of medetomidine with acepromazine and dexmedetomidine with acepromazine, at 5 and 20 minutes in comparison to groups of medetomidine and dexmedetomidine alone. Comparison of sedation scores in each group showed a significant increase over time. The comparison of heart rate, within the groups, showed a significant decrease when compared with the baseline value. The respiratory rate showed a decreasing trend in all groups over time. The amplitude of the P wave decreased and the P-R and Q-T intervals increased during the evaluation period in all groups. Sinus arrhythmia, AV-block grade 1, and sinus arrest were seen after the administration of sedative drugs in all groups. In conclusion, it is inferred that the addition of acepromazine to medetomidine and dexmedetomidine increases the sedation level. Heart rate decreased in medetomidine and dexmedetomidine groups and the addition of acepromazine exacerbated this decrease. The combination of acepromazine with medetomidine and dexmedetomidine did not also reduce the occurrence of arrhythmias in the dog.

Cardiac index is a criterion associated with cardiac output that measures the volume of blood pumped over time to the animal’s body surface area. Cardiac index is considered the reference standard parameter for targeting organ perfusion and oxygen delivery in shock.

For this purpose, ten mixed-breed male dogs ranging in age from 1.5 to 3.5 years were selected and after determination of body surface area, cardiac output was measured by Doppler echocardiography in eight stages. After induction of anesthesia and recording of vital signs, cardiac index evaluation was performed in control stage. Hypovolemic shock was induced by blood withdrawal to a mean arterial pressure of 40 to 50 mmHg within 30 minutes and then maintained for additional 30 minutes under hypovolemic condition. The dogs were then randomly divided into two equal groups, each group was resuscitated with Ringer's lactate solution (20 ml/kg) or 6% hydroxyethyl starch (5 ml/kg) over four 15-min intervals.

Hypovolemic shock caused significantly decrease in cardiac index (2.3±0.1) compared to control stage (4.8±0.6) (p < 0.05). Following resuscitation, cardiac index increased and returned to pre-shock values in both groups.

According to the findings of the present study, it can be concluded that echocardiographic evaluation of cardiac index is an easy, affordable and reliable method to diagnose hypovolemia and monitor patients' response to fluid therapy.Conflict of interest: None declared.

GReliable prediction of patient response to fluid resuscitation is a crucial issue in the management of hemorrhagic shock.

This study was designed to investigate vertebral heart score (VHS) variation in fluid resuscitation of hemorrhagic shock patients and the feasibility of this method in determining resuscitation endpoint. 

VHS values were assessed using previously published standard method in left to right lateral view. After induction of anesthesia (control assessments), hemorrhagic shock was induced by blood withdrawal to a mean arterial pressure of 40 to 50 mmHg within 30 minutes and then maintained in hypovolemic situation for an additional 30 minutes (second and third stages of assessments). Afterward, the dogs were randomly assigned to two groups which received 20 ml/kg lactated Ringer’s solution or 5 ml/kg Hydroxyethyl starch, in four consecutive 15 minute intervals (fourth stage of assessments). One hour after the last resuscitation step, final radiographic assessments were performed. 

Hemorrhagic shock caused significant decrease in VHS values to a mean of 7.7 vertebrae (P<0.05). Following the fluid resuscitation VHS increased and returned to pre-shock values in both groups.

This study confirms that the breed-specific VHS assessment can be a useful method in monitoring of patient’s response to fluid therapy and determination of resuscitation endpoint in dogs with hemorrhagic shock.

Hemorrhagic shock remains one of the leading causes of death following multiple organ ischemic injuries in dogs. The aim of this study was to compare tissue perfusion and electrocardiographic parameters in experimentally induced acute hemorrhagic shock in dogs before and after resuscitation with the lactated ringer and hydroxyethyl starch 6% solutions. The parameters of tissue perfusion included the gingival mucosal color, CRT, peripheral pulse quality, appendage temperature, serum lactate concentration, heart rate, mean arterial blood pressure and urine output plus ECG were evaluated in ten male adult healthy mongrel dogs which instrumented, and anesthetized (control measurement). Hemorrhage was performed with removal of up to 60% of blood volume to keep MAP between 40 and 50 mm Hg (second set of measurements). After a 30- minute stabilization period in hemorrhagic shock condition, the third set of measurements was performed. The dogs were randomly assigned to two study groups which received lactated ringer or hydroxyethyl starch solutions, 20 or 5 ml/kg respectively in four consecutive 15 –min periods (fourth to seventh measurements). One hour after the last resuscitation stage, the dogs were monitored and at the end of this time, an eighth evaluation step was carried out. Time induced a significant effect on heart rate, mean arterial blood pressure, appendage temperature, urine output, serum lactate concentration, R wave amplitude and Q-T interval. While solution type had a significant effect on serum lactate concentration, urine output and P wave amplitude. The results of this study showed that each of lactated ringer and hydroxyethyl starch solutions, has no significant effect in the short term on tissue perfusion and electrocardiogram parameters in hemorrhagic shock resuscitated dogs.

This study sought to assess the levels of cardiac troponin I, as a resuscitation end point, along with oxygen delivery (DO2) and oxygen consumption (VO2) during resuscitation of dogs with experimental hemorrhagic shock using lactated Ringer’s solution or 6% hydroxyethyl starch. After induction of anesthesia (control measurements), hemorrhagic shock was induced by rapid removal of blood to achieve a mean arterial pressure (MAP) of 40 to 50 mmHg within 30 minutes and then maintained in hypovolemic situation for additional 30 minutes (second and third stages of measurements). Afterward, the dogs were randomly assigned to two groups which received 20 ml/kg lactated Ringer’s solution or 5 ml/kg Hydroxyethyl starch, in four consecutive 15 minutes intervals (forth stage of measurements). One hour after the last resuscitation step, final measurements were performed. Hemorrhagic shock caused marked elevation in the levels of cTnI and reduction in DO2 and VO2 (p < 0.05). Following resuscitation, a significant reduction was observed in the levels of cTnI and VO2 but a significant elevation was seen in DO2 levels (p < 0.05), without significant differences between the groups (p > 0.05). The results of this study proved that cTnI can be evaluated for better monitoring during fluid therapy in hemorrhagic shock, as a novel resuscitation end point.

The aim of the present study was to determine whether the addition of dexamethasone or epinephrine to lidocaine altered the characteristics of anesthesia and cardiorespiratory variables following caudal epidural application in cows. Twenty adult dairy cows were randomly assigned to receive one of the treatments of lidocaine (LID, 0.2 mg/kg), dexamethasone (DEX, 8 mg), lidocaine-dexamethasone (LIDEX; 0.2 mg/kg and 8 mg, respectively) and lidocaine-epinephrine (LIDEP; 0.2 mg/kg and 5 µg/ml, respectively) by epidural injection with the final volume of 0.018 ml/kg and 10 ml of solution as the upper limit. The time to the onset and duration of anesthesia as well as heart rate (HR), respiratory rate (fR) and rectal temperature (RT) were recorded. No local anesthetic effects were observed in DEX. The onset of anesthesia did not show significant differences among LID, LIDEX and LIDEP. The duration of anesthesia was significantly longer in LIDEX (152.4 ± 25.8 min) as compared to LID (116.0 ± 11.5 min). Although the duration of anesthesia in LIDEP (137.7 ± 10.0 min) was longer in comparison to LID, the difference was not statistically significant. There was no significant difference regarding the onset and duration of anesthesia between LIDEX and LIDEP. HR, fR and RT did not show significant changes over time. Mild transient ataxia was observed in groups that received lidocaine-containing solutions. In conclusion, addition of dexamethasone to lidocaine, without altering the time to onset, produced more prolonged anesthesia than that of lidocaine alone following caudal epidural application in cows.

Methylphenidate (MPH) has been used to induce emergence from general anesthesia.
The objective of the present study was to evaluate the effect of MPH on recovery from propofol and ketamine anesthesia in dogs.
Six healthy male mix-breed dogs weighing 21.9 ± 3.9 kg were used in a randomized crossover design. Thirty minutes after premedication with acepromazine (0.1 mg/kg; IM), anesthesia was induced with either IV propofol or ketamine (8 and 15 mg/kg, respectively). Dogs, six minutes after induction, received either IV normal saline or methylphenidate (1 mg/kg) (propofol-saline; propofol-methylphenidate; ketamine-saline; ketamine-methylphenidate). Each dog was anesthetized four times randomly with at least one week interval.
No significant differences were observed between propofol-saline and propofol-methylphenidate as well as between ketamine-saline and ketamine-methylphenidate in the times needed for various chronological sequences of recovery (p>0.05). Recovery in the dogs that received methylphenidate was eventful and associated with some adverse effects. Heart rate showed a decrease in propofol-methylphenidate group compared to the base (p It was concluded that methylphenidate at 1 mg/kg could not shorten recovery time in the dogs premedicated with acepromazine and anesthetized with either propofol or ketamine. Testing lower doses of methylphenidate and using a different premedication agent are recommended for future studies.

The objective of the present study is to evaluate epidural application of lidocaine, lidocaine-verapamil and verapamil in buffalo calves. Sixteen buffalo calves of both sexes with 5-7 months age and 60-90 kg weight were assigned in three groups and received one of the three treatments of lidocaine (0.2 mg/kg, n=6, LID), lidocaine-verapamil (0.2 mg/kg – 2.5 mg, n=6, LID-VER) and verapamil (2.5 mg, n=4, VER). Onset and duration of tail paralysis and perineal anti-nociception as well as changes in heart rate, respiratory rate and rectal temperature were recorded. The onset of tail paralysis in LID was significantly shorter than that of LID-VER and VER (p

Nonsteroidal anti-inflammatories and opioids are of drugs that have been widely used to manage the pain after orthopedic surgery in human and animals. The purpose of this study was to compare the inhibitory effects of metamizol and tramadol on bone defect healing in rabbit tibia. In this study, thirty male New Zealand white rabbits were divided into two groups. A 5 mm in diameter circular defect was created on the medial surface of the tibial metaphyseal region of the right foot of each rabbit. Respectively, in metamizole and tramadol groups, metamizole, 5 mg / kg and tramadol 4 mg/ kg were subcutaneously administrated In a 5-day course of treatment every 12 hours and then every 24 hours during a three-day. Defect healing was assessed by obtaining radiographs on 0, 7, 14, 21, 28, 35, 42 days after surgery. Also, histopathologic evaluation was done at 7, 21 and 45 days using Goldner’s trichrome staining. It also represents a faster start filling defect in the histopathological study, following administration of tramadol compared with metamizole. Also, at the end of the study, tramadol achived more filling defect points compared with metamizole. The results of this study showed that the beginning of the process of callus formation in metamizol was later than tramadol, so there was a significant difference between groups, in the formation of callus so that in the radiographs taken on 14, 28 and 35 days. The results of this study showed that in comparison with Tramadol, metamizol has more effects in slowing bone repair.