Xylazine hydrochloride-ketamine hydrochloride immobilization of wolves and its antagonism by tolazoline hydrochloride

Fourteen wolves (Canis lupus L.) were singularly or repeatedly immobilized with 30 mg xylazine hydrochloride (HCl) and 400 mg ketamine HCl. Mean induction time was 5.3 +/- 4.6 min (mean +/- SD). Administration of 8.0 mg/kg tolazoline HCl as an antagonist significantly reduced immobilization times from 148.0 +/- 52.7 to 47.9 +/- 8.9 min (F = 63.69, df = 1,17, P less than 0.05). The average times from injection to ambulation for 2.0, 4.0, and 8.0 mg/kg tolazoline HCl were 35.2 +/- 31.8, 18.5 +/- 11.7, and 10.2 +/- 9.1 min. Tolazoline HCl increased heart rates significantly (P less than 0.001) from 75 +/- 14 to 120 +/- 23 beats/min, reversing a xylazine HCl-induced bradycardia. Respiratory rates also increased significantly (P less than 0.01) after tolazoline HCl injection from 19 +/- 7 to 28 +/- 8 breaths/min. Immobilization resulted in an initial hypertension which was normalized after tolazoline HCl administration. One female wolf had a single sinoatrial block within 1 min of receiving tolazoline HCl. Tolazoline HCl appears to be an effective antagonist for xylazine HCl-ketamine HCl immobilization of wolves.     

Cardiopulmonary, hemocytologic and biochemical effects of xylazine in goats

Intramuscular administration of xylazine at the rate of 0.22 mg/kg body weight caused a significant reduction in respiratory rates. Mean arterial blood pressure and rectal temperature were not altered. Preadministration of atropine did not affect the depth and pattern of respiration; however, the heart rate increased. A significant reduction in pH and arterial oxygen tension and an increase in carbon dioxide tension was observed after xylazine and xylazine following atropine treatment. Hemocytologic changes included a decrease in total erythrocytes, leukocytes, hematocrit and hemoglobin concentration and a rise in neutrophils with relative decrease in lymphocytes. Biochemical changes included a slight rise in potassium and a decrease in sodium concentration. Glucose level was significantly increased at maximum depth of sedation. The changes in hemocytologic and biochemical parameters returned to near preadministration level in 24-72 hours. No alteration was observed in the electrocardiogram. Xylazine was well tolerated, and the sedation was rapid in onset and lasted for about 30 minutes. The recovery was uneventful.     

Effects of yohimbine on bradycardia and duration of recumbency in ketamine/xylazine anesthetized ferrets

Eleven adult ferrets (Mustela putorius furo) were anesthetized with ketamine hydrochloride (25 mg/kg, IM) and xylazine hydrochloride (2 mg/kg, IM). Fifteen minutes post-ketamine/xylazine injection, ferrets were treated with yohimbine hydrochloride at a dose of 0.5 mg/kg, or an equal volume of physiologic saline, intramuscularly. Each ferret served as its own control by randomly receiving both treatments with a minimum interval of 2 weeks between treatments on any one ferret. At 15 minutes post-ketamine/xylazine injection, mean heart rate measurements for both treatment groups were 27% less than the mean heart rate measurement reported for unanesthetized ferrets. Intramuscular administration of yohimbine antagonized the ketamine/xylazine induced bradycardia in 10 of the 11 ferrets, (p = 0.0001). In yohimbine treated ferrets, an increase in mean heart rate measurement was noted 5 minutes after the intramuscular administration of yohimbine, and followed, over the next 15 minutes, by a progressive increase in mean heart rate. However, a corresponding decrease in mean heart rate measurement was observed in saline treated controls. Fifteen minutes after the injection of yohimbine, the mean heart rate measurement of yohimbine treated animals had increased to 194 beats per minute. This mean heart rate measurement is nearly 30% greater than the mean heart rate of 150 beats per minute measured at 15 minutes post-saline injection in saline treated controls. Also, yohimbine treatment significantly reduced duration of recumbency in 10 of 11 ferrets (p = 0.0001). Mean duration of recumbency for yohimbine treated ferrets was 41 +/- 9.7 minutes, whereas mean duration of recumbency for saline treated ferrets was determined to be 80 +/- 11.4 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)     

Central control of cardiac baroreflex responses during peripheral hyperosmolality

Acute increases in peripheral osmolality evoke a pressor response and baroreflex-mediated bradycardia. These experiments were designed to determine if the fall in heart rate during peripheral sodium loading is 1) equivalent to bradycardia accompanying phenylephrine (PE) infusion, 2) mediated by the parasympathetic (PSNS) or sympathetic (SNS) nervous system, and 3) controlled by the median preoptic nucleus (MnPO). Male rats received an intravenous infusion of isotonic saline, hypertonic saline (2.5 M NaCl), or PE for 30 min. Blood pressure increased equivalently in the hypertonic NaCl and PE groups. However, heart rate fell more in animals infused with PE. Furthermore, pretreatment with methylatropine to block the PSNS had no effect on bradycardia, whereas blocking SNS influences on cardiac function significantly attenuated the fall in heart rate during peripheral hyperosmolality. Finally, kainic acid administration in the MnPO before testing increased bradycardia observed during hypertonic saline loading. Taken together, these data suggest that acute peripheral hyperosmolality acts at the MnPO to reduce cardiac SNS withdrawal during the pressor response that reduces the associated baroreflex bradycardia.     

Blood pressure and other physiological responses in awake and anesthetized guinea pigs

The effect of combinations of injectable anesthetics on mean arterial blood pressure, blood gases, heart rate and respiration of the guinea pig (NIH Outbred strain) was investigated. After a 30 minute period in which baseline resting cardiorespiratory measurements were obtained, five groups of six pigmented animals having indwelling carotid cannulas were anesthetized with (a) ketamine hydrochloride (30 mg/kg, im)/xylazine (5 mg/kg, im); (b) sodium pentobarbital (15 mg/kg, ip)/fentanyl-droperidol (0.4 mg/kg, im); (c) diazepam (5mg/kg, ip)/fentanyl citrate (0.32 mg/kg, im); (d) diazepam (5 mg/kg, ip)/alphaxalone-alphadolone acetate (45 mg/kg, im); or (e) 1% alpha-chloralose-40% urethane (0.8 ml/100g, ip). Animals were not respirated artificially and no supplemental doses of anesthetic were given. Resting blood pressure in awake animals was measured over time for as long as cannulas remained patent (109 measurements). Mean resting blood pressure, for this strain of guinea pigs, was determined to be 53.1 +/- 4.2 mmHg. There was no indication that mean arterial blood pressure changed with age in animals varying in weight from 215 g to 550 g. Under diazepam/fentanyl, blood pressure rose significantly above resting level to a mean of 71.1 +/- 6.1 mmHg. With the other four combinations, blood pressure stabilized near, but below pre-anesthesia levels (ketamine/xylazine 47.1 +/- 6.8 mmHg; pentobarbital/fentanyl-droperidol, 46.9 +/- 3.2 mmHg; diazepam/alphaxalone-alphadolone, 47.8 +/- 4.8 mmHg; chloralose-urethane, 51.0 +/- 1.2 mmHg). Under diazepam/alphaxalone-alphadolone and chloralose-urethane, respiration was depressed and blood gas levels deviated from normal to the extent that artificial ventilation would be necessary to maintain an adequate physiological state.     

Blood pressure and heart rate response to vasoactive agents in conscious diabetic rats.

Blood pressure and heart rate responses to different vasoactive agents were observed in conscious streptozotocin-diabetic rats. An indwelling femoral artery catheter was used for direct measurement of arterial pressure and heart rate. The femoral vein was cannulated for drug administration. In a resting state diabetic rats showed lower heart rates and lower systolic blood pressure. The vasodepressor response to both acetylcholine and sodium nitroprusside was decreased, while the heart rate increase induced by the baroreceptor reflex was not altered. Both the increase in blood pressure and the reflex bradycardia to norepinephrine were decreased in the diabetic group. When the change in heart rate was plotted against blood pressure in response to norepinephrine, there was no difference in the two groups of animals. The vasodepressor response to isoproterenol, hydralazine, and verapamil in diabetic rats was unchanged. The results demonstrate a decreased vascular responsiveness in diabetic rats to norepinephrine, acetylcholine, and nitroprusside. The diabetes-induced vascular system changes require further study to understand the mechanisms involved.     

A comparison of two subarachnoid α2-agonists,xylazine and clonidine,with respect to duration of antinociception,and hemodynamic effects in goats

Subarachnoid administration of clonidine and xylazine produces antinociception in several species and in humans. The present study compares these two drugs administered by the subarachnoid route to goats. Goats (n=6) were randomly assigned to three treatment groups. All animals of each group received 0.06 mg kg⁻¹ clonidine (CLO), 0.1 mg kg⁻¹ xylazine (XIL) and 0.9% saline solution (SS), with a minimum interval of 1 week between treatments. All injections were made into the subarachnoid space between the last lumbar vertebra and the first sacral vertebra. Analgesia, ataxia, sedation, cardiovascular and respiratory effects, and rectal temperature were evaluated at predefined regular time intervals before drug administration (baseline) and after administration. The onset of analgesia by clonidine and xylazine was observed in 6.8±1.8 and 9.5±2.6 min (mean±S.D.), respectively. Both α₂-agonists produced analgesia of dorsocaudal rib areas, flanks, hind limbs, perineum and tail, sedation and ataxia. The duration of antinociception after clonidine administration was 118.8±24 min and after xylazine 88.3±15 min (mean±S.D.). Clonidine and xylazine subarachnoidally administered induced a significant (P<0.05) decrease in heart and respiratory rates and hypothermia in relation to the basal value. Neither drug significantly altered blood pressure. Both α₂-agonist drugs induced frequent diuresis and an increase in salivation. We conclude that subarachnoid clonidine produces longer antinociception with less ataxia than xylazine in goats. However, the drug induced bradycardia, a decrease in the respiratory rate and hypothermia, with a small compromise in the blood pressures at the doses studied. Further studies should be done to determine whether this analgesia is sufficient for surgical procedures.     

Giraffe restraint,habituation, and desensitization at the Cheyenne Mountain Zoo

The giraffe restraint device manufactured at the Cheyenne Mountain Zoo has the capability to fully support the weight of an immobilized adult giraffe in an upright posture and allow physical restraint of giraffe. The unit has been used for either chemical or physical restraint 74 times, in 22 months, on seven different adult giraffe, without animal or personnel injuries. Habituation and desensitization of the giraffe are critical prerequisites for the successful use of the giraffe restraint device. Yohimbine effectively reversed the effects of xylazine sedation of giraffe. A drug combination of detomidine and azaperone offers promise as an alternative to either physical restraint or immobilization of giraffe for selected clinical and investigative procedures. Using the restraint device it has been possible to perform tuberculin testing, venipuncture, vaginal examination, rectal palpation, rectal ultrasound, cervical catheterization, hoof-trimming, and placement of a hoof block on awake, habituated, and desensitized giraffe.     

Females of the marine amphipod Jassa marmorata mate multiple times with the same or different males

Cardiovascular and respiratory variables were recorded in the blue crab, Callinectes sapidus, during injury and subsequent autotomy of a chela. Cardiac function and haemolymph flow rates were measured using a pulsed-Doppler flowmeter. Oxygen uptake was recorded using an intermittent flow respirometry system. Crabs reacted to the loss of a chela with a rapid increase in heart rate, which was sustained for 2?h. Stroke volume of the heart also increased after the chela was autotomized. A combined increase in heart rate and stroke volume led to an increase in cardiac output, which was maintained for an hour after the loss of a chela. There was also differential haemolymph perfusion of various structures. There was no change in perfusion of the anterolateral arteries or posterior and anterior aortae, during injury of the chela or subsequent autotomy. Haemolymph flow rates did increase significantly through the sternal artery during injury and immediately following autotomy of the chela. This was at the expense of blood flow to the digestive gland: a sustained decrease in haemolymph flow through the hepatic arteries occurred for 3?h following autotomy. Fine-scale cardiac changes associated with the act of autotomy included a bradycardia and/or associated cardiac pausing before the chela was shed, followed by a subsequent increase in cardiac parameters. Changes in the cardiovascular physiology were paralleled by an increase in oxygen uptake, which was driven by an increased ventilation of the branchial chambers. Although limb loss is a major event, it appears that only acute changes in physiology occur. These may benefit the individual, allowing rapid escape following autotomy with a subsequent return to normal activity.     

Cardiovascular and respiratory responses associated with limb autotomy in the blue crab, Callinectes sapidus

Cardiovascular and respiratory variables were recorded in the blue crab, Callinectes sapidus, during injury and subsequent autotomy of a chela. Cardiac function and haemolymph flow rates were measured using a pulsed-Doppler flowmeter. Oxygen uptake was recorded using an intermittent flow respirometry system. Crabs reacted to the loss of a chela with a rapid increase in heart rate, which was sustained for 2 h. Stroke volume of the heart also increased after the chela was autotomized. A combined increase in heart rate and stroke volume led to an increase in cardiac output, which was maintained for an hour after the loss of a chela. There was also differential haemolymph perfusion of various structures. There was no change in perfusion of the anterolateral arteries or posterior and anterior aortae, during injury of the chela or subsequent autotomy. Haemolymph flow rates did increase significantly through the sternal artery during injury and immediately following autotomy of the chela. This was at the expense of blood flow to the digestive gland: a sustained decrease in haemolymph flow through the hepatic arteries occurred for 3 h following autotomy. Fine-scale cardiac changes associated with the act of autotomy included a bradycardia and/or associated cardiac pausing before the chela was shed, followed by a subsequent increase in cardiac parameters. Changes in the cardiovascular physiology were paralleled by an increase in oxygen uptake, which was driven by an increased ventilation of the branchial chambers. Although limb loss is a major event, it appears that only acute changes in physiology occur. These may benefit the individual, allowing rapid escape following autotomy with a subsequent return to normal activity.     

Effects of epidural administration of xylazine or lidocaine on bovine uterine motility and perineal analgesia

The objective of this study was to evaluate and compare the effects of caudal epidural (sacral-coccygeal interspace) administration of xylazine or lidocaine on uterine motility and perineal analgesia in the cow. Six Holstein cows (7 d post estrus) were assigned to one of three treatment groups: control (5 ml saline); lidocaine (0.2 mg/kg, 2% solution); and xylazine (0.06 mg/kg suspended in 5 ml saline), with each cow randomly assigned to each treatment over a period of three estrous cycles. Uterine motility, perineal analgesia, electrocardiography, and overt signs of sedation were recorded. Data were collected at 10-min intervals starting 10 min before treatment and continuing until 60 min post treatment. At 60 min post treatment, oxytocin (20 USP units) was administered i.v. to serve as a positive control for uterine motility. In the xylazine group, uterine motility significantly (P < 0.05) increased at 20 min post treatment, peaked at 30 min, and gradually decreased to non-significant levels at 50 min post treatment when compared with the lidocaine and control groups. Additionally, xylazine produced a higher degree and longer duration of perineal analgesia than lidocaine. Systemically, epidural xylazine produced signs of sedation, salivation, vocalization and bradycardia. Ataxia was also observed in the xylazine-treated group which may have been induced through a local and/or systemic effect. The individual properties of xylazine and lidocaine should be taken into consideration when performing an obstetrical procedure requiring the use of an epidural analgesic agent, and they should be utilized to benefit the clinician in performing the procedure.     

Reflex changes in heart rate during chemoreceptor stimulation in monkeys

The changes in heart rate induced by the stimulation of arterial chemoreceptors by apneic asphyxia and left atrial - intracarotid injections of sodium cyanide were investigated in anesthetized artificially ventilated and paralysed monkeys. Apneic asphyxia and sodium cyanide injection caused tachycardia, bradycardia, or both in monkeys paralysed with decamethonium bromide and tachycardia only, in monkeys paralysed with gallamine. In both groups, the tachycardia was abolished by prior administration of propranolol and the bradycardia, by atropine. Prior ventilation with 100% O2 abolished the heart rate responses produced by apnea. Recording of phrenic efferent activity showed that the neural discharge increased in response to apneic asphyxia and sodium cyanide injections. It remained so during the manifestation of tachycardia, bradycardia, or no change in heart rate, suggesting that even though "higher centres" may have an important influence in the heart rate responses elicited, central respiratory drive may not be the only mechanism. The present results show that in the nonhuman primate, arterial chemoreceptor stimulation elicits both cardioacceleratory and cardioinhibitory reflexes, and the net effect of their stimulation on heart rate depends upon the balance between these opposing mechanisms.     

Immobilization of swift foxes with ketamine hydrochloride-xylazine hydrochloride

There is an increasing need to develop field immobilization techniques that allow researchers to handle safely swift foxes (Vulpes velox) with minimal risk of stress or injury. We immobilized captive swift foxes to determine the safety and effectiveness of ketamine hydrochloride and xylazine hydrochloride at different dosages. We attempted to determine appropriate dosages to immobilize swift foxes for an adequate field-handling period based on three anesthesia intervals (induction period, immobilization period, and recovery period) and physiologic responses (rectal temperature, respiration rate, and heart rate). Between October 1998-July 1999, we conducted four trials, evaluating three different dosage ratios of ketamine and xylazine (2.27:1.2, 5.68:1.2, and 11.4:1.2 mg/kg ketamine:mg/kg xylazine, respectively), followed by a fourth trial with a higher dosage at the median ratio (11.4 mg/kg ketamine: 2.4 mg/kg xylazine). We found little difference in induction and recovery periods among trials 1-3, but immobilization time increased with increasing dosage (P < 0.08). Both the immobilization period and recovery period increased in trial 4 compared with trials 1-3 (P < or = 0.03). There was a high variation in responses of individual foxes across trials, making it difficult to identify an appropriate dosage for field handling. Heart rate and respiration rates were depressed but all physiologic measures remained within normal parameters established for domestic canids. We recommend a dosage ratio of 10 mg/kg ketamine to 1 mg/kg xylazine to immobilize swift foxes for field handling.     

DEVELOPMENT OF A BIMODAL HEART RATE PATTERN IN UNDISTURBED FETAL HARBOR SEALS

Fetal and maternal heart rates were studied in unrestrained, pregnant harbor seals during the last third of gestation. Heart rates were recorded while the mothers were resting on land or performing trained simulated dives of up to 2.25 min. Data from resting mothers showed the development of a bimodal or two-speed fetal heart rate pattern during late gestation. The mean faster and slower fetal heart rates at term were 125 ± 3.7 and 79 ± 3.1 (mean + SEM) respectively. The amount of fetal bradycardia observed increased steadily towards term, and fetal heart rate changes were not correlated with changes in maternal heart rate or maternal respiration. The bimodal fetal heart rate was also seen during the simulated dives, and no decrease in either the faster or slower heart rate was found. Heart rates from resting, unrestrained harbor seal pups were also studied. The pups displayed a bimodal heart rate similar to the fetuses' with the slower rate occurring during breath-holds. The bradycardia in the pups was equivalent to the slower fetal heart rate. These findings suggest that the regulatory mechanism that determines the apneic bradycardia in young harbor seals during non-stressful conditions develops in the last quarter of gestation.     

Physiologic and electrocardiographic responses of American river otters (Lutra canadensis) during chemical immobilization and inhalation anesthesia

Rectal temperatures and heart rates of American river otters (Lutra canadensis) decreased significantly (P less than 0.05) during chemical immobilization with i.m. ketamine hydrochloride in combination with xylazine hydrochloride and acepromazine and during inhalation anesthesia with isoflurane. Anesthetized otters showed a tendency for apnea during induction and while dorsally recumbent, which was reflected by a respiratory acidosis on arterial blood gases. Declines in rectal temperatures and heart rates were not found to be a function of dosage (mg/kg) of the ketamine combination used except for rectal temperatures of otters in relatively poor body condition (inanition). The electrocardiograms of isoflurane-anesthetized otters were similar to those recorded on immobilized otters with the exception of an r' deflection in the ventricular depolarization complex (RSr'). Electrocardiographic criteria were not found which predicted the degree of right ventricular or generalized cardiac enlargement seen radiographically.     

Effects of diabetes mellitus on salivary secretion and its composition in the human

Calreticulin is a Ca2+ binding/storage chaperone resident protein of the endoplasmic reticulum. This protein plays a key role in the calreticulin/calnexin cycle and the quality control pathways in the endoplasmic reticulum. Calreticulin deficiency is lethal due to impaired cardiac development. However, over-expression of the protein in developing and postnatal heart leads to bradycardia, complete heart block and sudden death. Ultrastructural evidence indicates that the deficiency associated with the absence of calreticulin in the heart may be due to a defect in the development of the contractile apparatus and/or a defect in development of the conductive system as well as a metabolic abnormality. Collectively, we postulate that calreticulin and endoplasmic reticulum plays an important role in cardiac development and postnatal pathologies.     

The relationship between FTL and NA, DMV or CVLM in central cardiovascular control

The aim of the present study was to examine the relationship between the lateral tegmental field (FTL), a cardioinhibitory area, with other cardioinhibitory areas, i.e., the ambiguus nucleus (NA) and the dorsal motor nucleus of vagus (DMV) and the caudal ventrolateral medulla (CVLM), a vasopressor inhibitory area. In 55 cats anesthetized with chloralose (40 mg/kg) and urethane (400 mg/kg), the cardiovascular responses of heart rate (HR), systemic arterial blood pressure (SAP) and vertebral nerve activity (VNA) were recorded. The FTL, NA, DMV and CVLM were identified first by stimulation (rectangular pulses in 80 Hz, 0.5 ms, 50-100 microA) and then confirmed by microinjection of sodium glutamate (Glu, 0.25M, 70 nl). In studying the influence of NA, DMV, or CVLM lesion on the Gluinduced responses in FTL, kainic acid (KA, 24 mM, 100 nl) was microinjected into the NA, DMV or CVLM. FTL stimulation produced an average decrease of HR by 55%. After KA lesioning of the ipsilateral NA or the DMV, the decreased HR induced by FTL was significantly diminished. After subsequent lesion of the contralateral DMV or NA, the bradycardia of FTL was abolished. The reduction of resting HR was more intense after lesioning the NA than DMV and with the left side more than that of the right side. These studies suggest that the cardioinhibitory responses of FTL are mediated through both NA and DMV with predominance of the former, while the hypotensive effect of FTL is mediated through CVLM. The precise pathway responsible for the FTL-induced bradycardia and hypotension is to be determined.     

Effect of caffeine sodium benzoate, ketamine hydrochloride, and yohimbine hydrochloride on xylazine hydrochloride-induced anorexia in white-tailed deer

Fifteen male white-tailed deer (Odocoileus virginianus) were administered xylazine hydrochloride (1 mg/kg BW i.m.), xylazine hydrochloride (1 mg/kg i.m.) followed by caffeine sodium benzoate (10 mg/kg i.m.), xylazine hydrochloride (0.5 mg/kg i.m.) and ketamine hydrochloride (4.5 mg/kg i.m.), and xylazine hydrochloride (1 mg/kg i.m.) followed by yohimbine hydrochloride (0.125 mg/kg i.m.), in a Latin Square design. Mean dry matter intake (DMI) for 4 days pre-treatment was compared to each of 4 days post-treatment. A significant (P less than 0.01) decrease in DMI was found only on the first day following treatment for each of the four drug combinations. The percent decreases in DMI on the first 24-hr period after immobilization were: xylazine hydrochloride 47%, xylazine hydrochloride/caffeine sodium benzoate 36%, xylazine hydrochloride/yohimbine hydrochloride 36%, and xylazine hydrochloride/ketamine hydrochloride 31%. The xylazine hydrochloride/ketamine hydrochloride combination was found to be insufficient to adequately sedate the deer. The use of caffeine or yohimbine hydrochloride is recommended to reduce recumbency time, but offers no improvement in xylazine hydrochloride-induced anorexia.     

The effects of breathing different levels of O2 and CO2 on the diving responses of ducks (Anas platyrhynchos) and cormorants (Phalacrocorax auritus)

Summary The effects of breathing different levels of O₂ and CO₂ before forced dives were investigated in 5 dabbling ducks (White Pekin) and 5 deep divers (Double Crested Cormorants). Breathing and heart rates, blood gases, and blood pH, were monitored. After breathing air before diving, ducks exhibited a slow decrease in heart rate that reached a minimum of 20 beats·min⁻¹ after 50 s submergence. The development of bradycardia was retarded if the duck breathed a hyperoxic gas mixture before diving and was accelerated if the gas mixture was hypoxic and hypercapnic. The cormorants' diving heart rate decreased to a minimum of about 60 beats·min⁻¹ in less than 20 s and development of bradycardia was unaffected by different levels of O₂ and CO₂ breathed before diving. Consequently, bradycardia in forced dived cormorants was unrelated to changes in blood gases in the dives which suggests that intravascular chemoreceptors are unimportant in initiating diving bradycardia in cormorants.     

Changes in heart rate during progressive hyperoxia in the dogfish Scyliorhinus canicula L.: evidence for a venous oxygen receptor

Progressive hyperoxia caused a gradual increase in arterial blood oxygen tension (PaO2). Initially there was no change in venous O2 tension (PvO2) but in extreme hyperoxia (PO2 650 mmHg) it increased to 2.5 times the normoxic (PO2 150 mmHg) level (Table 1). Ventilation frequency gradually decreased down to 73% of the normoxic value as PO2 rose towards a maximum at 700 mmHg (Fig. 1). In moderately hyperoxic water (mean PO2 233 mmHg) heart rate (fH) increased significantly above the normoxic level. Further increases in ambient PO2 caused a progressive reduction in fH to a level significantly below the normoxic rate in extreme hyperoxia (Fig. 2). Injection of atropine abolished these changes, and the atropinized fH was similar to that measured during moderate hyperoxia. The initial increase in fH during progressive hyperoxia is attributed to release of vagal tone, due to removal of normoxic stimulation of peripheral oxygen receptors; whereas, the secondary bradycardia is attributed to the stimulation of oxygen receptors located in the venous system. Injection of 5 ml of hyperoxaemic blood into the venous system of normoxic fish caused a transient bradycardia (Fig. 3), lasting a mean of 73 sec, which is the approximate time for passage of the blood volume of the venous system through the heart. This bradycardia was neither pH dependent nor a pressor response and provides supporting evidence for the existence of a venous oxygen receptor.