Tear production in three captive wild herbivores in Israel

The Schirmer tear test (STT) I was performed to evaluate tear production in 12 captive Nubian ibex (Capra ibex nubiana), 10 captive Burchell's zebras (Equus burchelli) and five Arabian oryx (Oryx leucoryx) at the Tel-Aviv Ramat-Gan Zoological Center (Israel). Mean (+/- standard deviation) STT values were 13.2 +/- 5.1 mm/min in the ibex, 23.4 +/- 3.4 mm/min in the zebra and 12.7 +/- 4.8 mm/min in the oryx. There were no significant effects of gender, age, weight, or side of the eye. There were no significant differences in STT values between ibex and oryx, but tear production in both species was significantly lower than in zebras. Knowledge of normal tear production values is important for the differential diagnosis of conjunctivitis and keratitis in these species.     

Experimental surface strain mapping of porcine peripapillary sclera due to elevations of intraocular pressure

To experimentally characterize 2D surface mapping of the deformation pattern of porcine peripapillary sclera following acute elevations of intraocular pressure (IOP) from 5 mm Hg to 45 mm Hg. Four porcine eyes were obtained within 48 h postmortem and dissected to the sclera. After the anterior chamber was removed, each posterior scleral shell was individually mounted at the equator on a custom-built pressurization device, which internally pressurized the scleral samples with isotonic saline at 22 degrees C. Black polystyrene microspheres (10 microm in diameter) were randomly scattered and attached to the scleral surface. IOP was incrementally increased from 5 mm Hg to 45 mm Hg (+/-0.15 mm Hg), and the surface deformation of the peripapillary sclera immediately adjacent to the dural insertion was optically tracked at a resolution of 2 micrompixel one quadrant at a time, for each of four quadrants (superior, nasal, inferior, and temporal). The 2D displacement data of the microsphere markers were extracted using the optical flow equation, smoothed by weighting function interpolation, and converted to the corresponding Lagrangian finite surface strain. In all four quadrants of each eye, the principal strain was highest and primarily circumferential immediately adjacent to the scleral canal. Average maximum Lagrangian strain across all quadrants for all eyes was 0.013+/-0.005 from 5 mm Hg to 10 mm Hg, 0.014+/-0.004 from 10 mm Hg to 30 mm Hg and 0.004+/-0.001 from 30 mm Hg to 45 mm Hg, demonstrating the nonlinearity in the IOP-strain relationship. For each scleral shell, the observed surface strain mapping implied that the scleral stiffness was relatively low between 5 mm Hg and 10 mm Hg, but dramatically increased for each IOP elevation increment beyond 10 mm Hg. Peripapillary deformation following an acute IOP elevation may be governed by the underlying scleral collagen microstructure and is likely in the high-stiffness region of the scleral stress-strain curve when IOP is above 10 mm Hg.     

Separate hemodynamic roles for chloride and sodium in deoxycorticosterone acetate-salt hypertension

It has been reported that both sodium and chloride ions must be ingested to induce the elevated blood pressure of deoxycorticosterone acetate (DOCA)-salt-sensitive hypertension. This study was designed to determine the separate roles of the sodium and chloride ions in the altered hemodynamics underlying the high blood pressure. DOCA pellets (75 mg) were implanted in uninephrectomized rats and the animals were then fed one of four diets: (i) high sodium chloride, (ii) high sodium-low chloride, (iii) high chloride-low sodium, or (iv) low sodium chloride. Blood pressures were measured weekly by tail-cuff plethysmography for 5 weeks and the animals were then subjected to a terminal experiment to measure cardiac output by thermodilution technique, renal blood flow by electromagnetic flow probe, and direct arterial pressure. Blood pressure in the DOCA-high NaCl group was significantly greater (P less than 0.05) compared with that of the DOCA-low NaCl group (160 +/- 3 mm Hg vs 124 +/- 2 mm Hg, respectively) at 5 weeks after treatment; all other groups were not significantly different from the DOCA-low NaCl group. Cardiac output was significantly greater in DOCA-treated rats consuming diets high in sodium (44 +/- 2 ml/min/100 g) or sodium chloride (40 +/- 2 ml/min/100 g) compared with animals consuming low sodium chloride (31 +/- 2 ml/min/100 g; P less than 0.01 for each comparison). Direct intraarterial blood pressure and renal blood flow were used to calculate renal vascular resistance. Renal vascular resistance was increased in those DOCA-treated rats consuming diets high in chloride (42 +/- 3 mm Hg/ml/min/100 g) and high sodium chloride (54 +/- 3 mm Hg/ml/min/100 g) compared with rats consuming low sodium chloride (30 +/- 3 mm Hg/ml/min/100 g; P less than 0.01 for each). It appears that elevations in cardiac output are associated with increased dietary sodium and act in synergy with the elevations in renal vascular resistance associated with increased dietary chloride. Increases in both cardiac output and renal vascular resistance are involved in the maintenance of elevated blood pressure in the DOCA-salt-sensitive model of hypertension.     

CYCLIC OCULAR HYPERTENSION IN CETACEANS

In the laboratory, intraocular pressure (IOP) was measured in each eye of two adult Tursiops truncatus and one Grampus griseus . Measures were made in alternation between eyes over a time span. Means and standard deviations were calculated. Mean IOP's ranged from 33.4 mm Hg (SD = 2.4) in the male Tursiops to 24.6 (SD = 2.3) in the female Tursiops . IOP in the Grampus was intermediate. Tonograph functions for the Tursiops over periods greater than 25 min had a cyclic character with maxima and minima. These cycles were fitted with a polynomial function with periods of 15 min (female) and 20 to 26 min (male). There was no significant correlation of the IOP variations with time between eyes in either Tursiops . Compared to humans, these cetaceans exhibit clinical ocular hypertension bilaterally. The range of pressures they exhibit, over time, is much greater than reported previously for several terrestrial mammals.     

Seasonal variation of cardiovascular function in the marmot, Marmota flaviventris

Monthly measurements of heart rate, mean arterial pressure, and cardiac output were made on active and hibernating marmots from the time of emergence from hibernation through the next hibernation period. From these measurements cardiac index, stroke index, and total peripheral resistance were calculated on the basis of estimated lean body mass. Heart rate was low after emergence (132 +/- 9.5 beats (B)/min), peaked in August (160 +/- 9.3 B/min), and then fell slightly in September and October. During hibernation heart rate fell to 9 +/- 1.1 B/min. Mean arterial pressure, which was low in early spring (101 +/- 6.9 mm Hg), rose to a peak value in June (131 +/- 7.7 mm Hg) and remained essentially unchanged until hibernation when it fell to 52 +/- 4.0 mm Hg. Cardiac index (61 +/- 4.9 ml/kg min) in March rose to a peak in May (83 +/- 8.5 ml/kg min) and fell linearly until October. There was an additional drop in cardiac index during hibernation (7.6 +/- 0.9 ml/kg min). Total peripheral resistance increased linearly from the time of emergence until October. Most of this change was due to the decrease in cardiac index. Stroke index showed no significant changes in the prehibernation period, but increased by 55% during hibernation. Maintenance of arterial pressure in the months preceding hibernation in the face of diminishing cardiac index indicate that alterations in vasomotor tone or shifts in patterns of blood flow occurred prior to the hibernation period.     

Effect of environment on blood pressure: home versus hospital.

The effect of environment on blood pressure was studied by recording intra-arterial pressure continuously in nine patients with essential hypertension during controlled periods of activity and rest at home and in hospital. Mean systolic pressure was higher at home (152 +/- 16 mm Hg) than in hospital (138 +/- 11 mm Hg, p less than 0.01), the difference being greatest during the period of activity (165 +/- 21 v 142 +/- 13 mm Hg, p less than 0.001); heart rates and diastolic pressures did not differ significantly at these times. Systolic pressure recorded by conventional sphygmomanometry was also higher at home (173 +/- 23 v 159 +/- 23 mm Hg, p less than 0.01), as was diastolic pressure (98 +/- 10 v 89 +/- 11 mm Hg, p less than 0.02). Systolic pressure was consistently higher at home, and this effect was independent of the pressure of an observer. This must be taken into consideration when assessing blood pressure and efficacy of treatment in hospital.     

Respiratory effects of pressor and depressor agents in conscious rats

We hypothesized that the respiratory baroreflex in conscious rats is either more transient, or has a higher pressure threshold than in other species. To characterize the effect of arterial pressure changes on respiration in conscious rats, ventilation (V) was measured by the plethysmographic technique during injections, or infusions, of pressor and depressor agents. Bolus injections of angiotensin II (Ang II) or arginine vasopressin (AVP), transiently increased mean arterial pressure (MAP; mean +/- SE) 43+/-6 and 28+/-5 mm Hg (1 mm Hg = 133.3 Pa), respectively, and immediately reduced tidal volume (Vt) and, in the case of AVP, V. In contrast, by 10 min of a sustained elevation of MAP (40+/-3 mm Hg) with infusion of Ang II, Vt, f, and V were not different from control levels. Bolus injection of sodium nitroprusside (SNP) to lower MAP (-28+/-3 mm Hg) immediately increased breathing frequency (f) and V, whereas sustained infusion of SNP to lower MAP (-21+/-3 mm Hg) did not change for V at 10 and 20 min. In conscious rats, both injection and infusion of the pressor agent PE (+40 to 50 mm Hg) stimulated f and V; this contrasted with anesthetized rats where PE inhibited f and V, as reported by others. In conscious rats, respiratory responses associated with baroreflexes adapt rapidly and, in the case of PE, can be overridden by some other mechanism.     

Effect of indomethacin on modest pressure natriuresis in chloralose-anesthetized, non-laparotomized dogs

To determine if indomethacin (indo) would attenuate the effects of changed renal perfusion pressure on sodium excretion as reported by others, we performed clearance studies in chloralose-anesthetized dogs without the major stress of laparotomy. Mean renal arterial pressure was varied by a balloon-tipped catheter indwelling the aorta suprarenally. With pressure decreases to mean values above 85 mm Hg during isotonic saline infusion, sodium output decreased only by 10.7 +/- 2.4% per 10 mm Hg pressure decrease without indo pre-treatment but decreased by 22.0 +/- 3.8% per 10 mm Hg pressure decrease with indo pre-treatment. The greater, rather than lesser, pressure effect on excretory function after indo in these experiments with chloralose anesthesia suggest that renal prostaglandin (PG) activity does not mediate normally pressure natriuresis. Instead, the data suggest that, in the absence of major stress, the renal pressure effects on excretory function may become more sensitive after indo. In addition, we postulate that the normal acute pressure natriuresis may be modest and may average no more than 20% change for each 10 mm Hg change in mean pressure above 90 mm Hg when stress is minimal and when vasoactive preglomerular autoregulation is nearly perfect. This is a phenomenon which keeps intrarenal tissue pressure and urine output relatively constant with arterial pressure elevations.     

Blood pressure of sinoaortic-denervated dogs is not increased by cardiac denervation

Although blood pressure rises markedly after acute sinoaortic denervation, animals with chronic sinoaortic denervation have normal or only slightly elevated mean arterial pressures. The present study was performed to determine whether reflexes from cardiac receptors exert antihypertensive effects and thereby lower blood pressure in animals with chronic sinoaortic denervation. We made multiple measurements of blood pressures in dogs with chronic sinoaortic denervation before and after their hearts were denervated surgically. Mean arterial pressure after cardiac denervation (100.3 +/- 4.2 mm Hg) was not significantly different from the mean pressures recorded before cardiac denervation in these sinoaortic-denervated dogs (104.8 +/- 3.1 mm Hg). Also, mean heart rate after cardiac denervation (107.4 +/- 5.5 beats/min) did not differ significantly from the mean heart rate recorded before cardiac denervation (107.2 +/- 5.9 beats/min). Cardiac denervation did, however, appear to reduce the lability of both blood pressure and heart rate in sinoaortic-denervated dogs. We conclude that cardiac receptors are not responsible for maintaining arterial pressure within essentially normal limits in animals with chronic sinoaortic denervation.     

Central transmural venous pressure and plasma arginine vasopressin during negative pressure breathing in man

After overnight food and fluid restriction, 8 normal healthy males were examined in the upright sitting position before (prestudy), during and after (recovery) negative pressure breathing (NPB) with a pressure (P = difference between airway pressure and barometric pressure) of -9.6 +/- 0.5 to -10.4 +/- 0.4 mm Hg for 30 min. Plasma arginine vasopressin (pAVP) did not change significantly comparing prestudy with 10 and 30 min of NPB or comparing recovery with NPB at 10, 20 or 30 min. However, at 20 min of NBP, pAVP was slightly lower than at prestudy (p less than 0.05). Central venous pressure (CVP) decreased significantly during NPB, and central transmural venous pressure (CVP-P) increased significantly from -0.9 +/- 0.8 mm Hg to 3.8 +/- 0.7, 4.3 +/- 0.7 and 4.5 +/- 0.6 mm Hg (p less than 0.001) after 10, 20 and 30 min, respectively. Systolic, diastolic and mean arterial pressure and heart rate did not change significantly during NPB. Diuresis, natriuresis, kaliuresis, osmotic excretion and clearance were slightly increased during the recovery hour after NPB compared to prestudy, while urine osmolality decreased during NPB (n = 6). However, none of these changes were significant. There was no significant correlation between CVP-P and pAVP. In conclusion, -10 mm Hg NPB for 30 min in upright sitting subjects did not change pAVP consistently, while CVP-P was significantly increased and HR and arterial pressures were unchanged. This lends support to the concept that arterial baroreceptors and not cardiopulmonary mechanoreceptors are of importance in regulating AVP secretion in man.     

Lack of additional action of oxygen on pulmonary artery pressure at the peak of verapamil or captopril action in pulmonary hypertension secondary to mitral stenosis]

The aim of the study was to investigate whether oxygen causes a further decrease in pulmonary artery pressure after administration of calcium channel blocker-verapamil-or angiotensin converting enzyme inhibitor-captopril-in the secondary pulmonary hypertension. We studied 37 patients with the secondary pulmonary hypertension (mean pulmonary artery systolic pressure = 56.1 mm Hg) due to mitral stenosis. After having completed hemodynamic diagnostic procedures, basal oxygen test was performed and pulmonary artery pressure was recorded at 10 min of oxygen breathing. Then, 10 mg of verapamil was injected into the pulmonary artery of 16 patients and 21 patients received 75 mg of oral captopril. At the peak of vasodilation, 30 min after verapamil and 90 min after captopril administration, pulmonary artery pressure was recorded and oxygen test was repeated. Baseline oxygen test produced a statistically significant decrease in pulmonary artery pressure. Verapamil and captopril also lowered pulmonary artery systolic and diastolic pressures. The second oxygen test did not cause a further decrease in the pulmonary artery pressure; mean pulmonary artery systolic pressure was 52.3 +/- 23.7 mm Hg, pulmonary artery diastolic pressure 22.7 +/- 10.6 mm Hg before and 49.1 +/- 23.8 mm Hg and 23.0 +/- 13.5 mm Hg, respectively after the test in verapamil group, and 47.0 +/- 15.5 mm Hg and 21.7 +/- 8.4 mm Hg before and 46.6 +/- 15.4 mm Hg, respectively in captopril subset. The results may support the thesis that vasodilating effect depends rather on the degree of pulmonary vascular changes than on the vasodilatory mechanism of particular drugs.     

Evaluation of blood pressure changes and heart rate in young health men based on results of a 24-hour monitoring of pressure]

Systolic and diastolic blood pressures and heart rate were monitored in a group of 20 young healthy men for 24 hours. Period of time between 8 o'clock a.m. and 10 o'clock p.m. was treated as waking state whereas period of time from 12 p.m. to 6 a.m. as sleep phase. Mean value of systolic blood pressure for waking state was 124.6 +/- 7.6 mm Hg, and for sleep phase 110.4 +/- 11.5 mm Hg. (p < .001). Mean diastolic blood pressures were also significantly different (76.5 +/- 5.9 mm Hg and 63.8 +/- 7.7 mm Hg, respectively), the same concerns heart rate (79.6 +/- 6.4 and 63.0-7.2 min-1, respectively). In both cases p < .001. To evaluate dependence of heart rate on systolic blood pressure in waking state the following calculation was made: HR = 0.230 x systolic blood pressure +51.4 (r = 0.24; p < .001) whereas for sleep phase r did not reach a level of statistical significance (HR = 0.074 x systolic blood pressure + 53.9; r = 0.094). Single or even multiple measurements of the arterial blood pressure are not sufficient to evaluate circadian changes.     

Effect of prolonged renal dysfunction on intravascular and extravascular pulmonary fluid volumes during left atrial hypertension

To examine the development of pulmonary edema during experimental renal dysfunction, left atrial pressure was altered in 14 mongrel dogs divided into two groups. Group 1 was composed of seven control animals, and Group 2 was composed of seven animals with surgically induced renal failure (1 week of bilateral ureteral ligation). Data were obtained at two levels of matched transmural pulmonary vascular pressure (defined as mean left atrial pressure less serum protein osmotic pressure). In the animals with renal dysfunction, extravascular lung water (EVLW) (thermal-green dye technique) was higher at moderately (-1 to -2 mm Hg) and severely elevated (11 to 12 mm Hg) vascular driving pressures (11.5 +/- 1.2 cc/kg vs 10.6 +/- 0.8 cc/kg and 14.8 +/- 1.3 cc/kg vs 13.0 +/- 1.9 cc/kg, respectively, both P less than 0.05 vs control). Because protein osmotic pressure was lower in the renal failure group (15.0 +/- 1.8 mm Hg vs 18.4 +/- 1.4 mm Hg, P less than 0.05), greater accumulations of extravascular lung water occurred at lower levels of left atrial pressure (14.2 +/- 1.4 mm Hg vs 17.1 +/- 1.2 mm Hg, P less than 0.05; 26.8 +/- 2.6 mm Hg vs 29.5 +/- 2.3 mm Hg, P less than 0.01). In addition, when the ratio of EVLW/PBV (pulmonary blood volume) was examined in both groups at each stage of the experiment, the ratio was greater in the Group 2 animals at each elevated pressure, suggesting increased permeability with renal dysfunction. In conclusion, pulmonary edema formation occurs at lower left atrial pressures in the setting of sustained renal dysfunction, this phenomenon can be partially explained by lower protein osmotic pressure though altered pulmonary microvascular permeability may contribute to edema formation.     

Effectiveness of antagonists for tiletamine-zolazepam/xylazine immobilization in female white-tailed deer

A combination of tiletamine-zolazepam/xylazine (TZ/X) is effective in the chemical immobilization of white-tailed deer (Odocoileus virginianus); however, the lengthy duration of immobilization may limit its usefulness. From October to November 2002, 21 captive female deer were assigned randomly to an alpha(2) antagonist treatment to reverse xylazine-induced sedation (seven does per group). All deer were given 220 mg of TZ (4.5+/-0.4 mg/kg) and 110 mg of X (2.2+/-0.2 mg/kg) intramuscularly (IM). Antagonist treatments were either 200 mg of tolazoline (4.0+/-0.4 mg/kg), 11 mg of atipamezole (0.23+/-0.02 mg/kg), or 15 mg of yohimbine (0.30+/-0.02 mg/kg) injected, half intravenously and half subcutaneously, 45 min after the IM TZ/X injection. In addition, 10 other deer (five per group) were immobilized as before and then given tolazoline (200 mg) after 45 min, with either a carrier (dimethyl sulfoxide [DMSO]) or carrier (DMSO) plus flumazenil (5 mg) to reverse the zolazepam portion of TZ. Mean times from antagonist injection until a deer raised its head were different for alpha(2) antagonist treatments (P=0.02). Times were longer for yohimbine (62.3+/-42.7 min) than for either atipamezole (24.3+/-17.1 min) or tolazoline (21.3+/-14.3 min). Mean times from antagonist injection until standing were not different (P=0.15) among yohimbine (112.0+/-56.4 min), atipamezole (89.7+/-62.8 min), or tolazoline (52.6+/-37.2 min). A sedation score based on behavioral criteria was assigned to each deer every 30 min for 5 hr. On the basis of sedation scores, tolazoline resulted in a faster and more complete reversal of immobilization. Flumazenil treatment did not affect recovery.     

Effects of forskolin on placental vascular resistance in rabbits

Forskolin is a direct stimulant of adenylate cyclase and increases cAMP production. It also acts as a vasodilator. To study the effect of forskolin infusion on rabbit maternal vascular resistance, we instrumented 11 pregnant rabbits with catheters in the left ventricle, jugular vein, and left and right femoral arteries. After a 2-day recovery period, one of two protocols was performed. In the control period of the first protocol (N = 6), 50% ethanol in saline was infused at 0.103 ml.min-1 for 5-min. Forskolin (10(-3) M) in 50% ethanol was then infused for 5 min at 0.103 ml.min-1. After each infusion period, regional blood flows were measured by microsphere injection. Data are expressed as means +/- SEM. Blood pressure decreased from 81 +/- 3 to 79 +/- 3 mm Hg, (P less than 0.05, N = 10) during forskolin infusion. Total placental resistance fell from 180.3 +/- 10.7 to 133.8 +/- 12.0 mm Hg.min.ml-1 per gram, P less than 0.05. Cerebral, coronary, and renal vascular resistance fell significantly. During the second protocol (N = 5), angiotensin II (0.05 microgram.min-1) was infused for 5 min followed by the addition of forskolin (10(-3) M at 0.103 ml.min-1) to the infusate. Regional blood flows, vascular resistances and blood pressures were determined. Blood pressure fell from 99 +/- 6 to 92 +/- 7 mm Hg (P less than 0.05) when forskolin was added to the infusate. Placental resistance fell from 202.5 +/- 21.6 to 158.0 +/- 29.0 mm Hg.min.ml-1 per gram (P less than 0.05). While cerebral vascular resistance did not change, renal and coronary resistances fell in response to forskolin. This study demonstrates that forskolin is able to dilate rabbit placental vessels alone and in the presence of the vasoconstrictive agent angiotensin II.     

The accuracy of the American College of Sports Medicine metabolic equation for walking at altitude and higher-grade conditions

The purpose of this study was to examine the accuracy of the American College of Sports Medicine (ACSM) walking equation at low walking speeds, altitude (1,550 m), and higher grades. Twenty men and women (mean +/- SD, age, 28 +/- 6 years; height, 171 +/- 13 cm; weight, 67.8 +/- 18.1 kg) completed 2 randomized testing sessions under altitude (AL) (P(I)o(2) = 123.1 mm Hg [20.93%]) and sea level control (SLC) (P(I)o(2) = 147.3 mm Hg [25.00%]) conditions. Steady-state oxygen uptake (Vo(2)) was measured while subjects walked at 50 m.min(-1) at 8 separate grades (0, 5, 10, 15, 18, 21, 24, and 27%). Steady-state Vo(2) measurements from the last 2 minutes of each grade in AL and SLC were compared to the predicted Vo(2) of each grade according to the ACSM walking equation. Mean Vo(2) differences between predicted and AL values ranged from -0.5 to 1.4 ml.kg(-1).min(-1), averaged -0.1 ml.kg(-1).min(-1) across all grades, and were significant (p < 0.05) at 0 percent grade. Mean Vo(2) differences between predicted and SLC values ranged from 0.6 to 3.0 ml.kg(-1).min(-1), averaged 1.4 ml.kg(-1).min(-1) across all grades, and were statistically significant (p < 0.05) at 0 and 5 percent. The standard error of the estimate (SEE) for the prediction of Vo(2) under AL and SLC were 2.2 and 2.0 ml.kg(-1).min(-1), respectively. Total errors for the prediction of Vo(2)max under AL and SLC were 2.3 and 2.6 ml.kg(-1).min(-1), respectively. Overall, the findings indicate that the current ACSM prediction equation for walking is appropriate for application at low speeds, moderate altitude, and higher grades.     

Relation between resorption resistance of cerebrospinal fluid and the degree of intracranial pressure]

Changes in the CSF resorption resistance in relation to the value of the intracranial pressure have been assessed in 44 cats. Changes in the intracranial pressure have been produced with fluid infusions. Between 1 to 5 infusion tests with the rate 0.012-1.8 ml/min have been performed in each animal. A relationship between CSF resorption resistance and intracranial pressure has been found. With an increase in the intracranial pressure CSF resorption resistance increased to maximum value of 34 kPa/ml per minute (255.6 mm Hg/ml per minute) at pressure 2.96 +/- 0.69 kPa (22.2 +/- 5.2 mm Hg). At the intracranial pressure about 6.7 kPa (50 mm Hg) CSF resorption resistance rapidly decreased to the value of 13.9 kPa/ml per minute (104 mm Hg/ml per minute). Later, changes have been rather slight. It is possible, that the breaking point at 6.7 kPa corresponds to the mobilisation of all ways of CSF evacuation.     

A comparison of ketamine/xylazine and ketamine/xylazine/acepromazine anesthesia in the rabbit

Parenteral anesthetic combinations such as ketamine and xylazine have become the agents of choice for anesthesia in the rabbit, because they are effective, easily administered and inexpensive. A number of recent reports have recommended including acepromazine in this combination, but a critical evaluation of this combination in the rabbit has not been reported. Five adult New Zealand white rabbits were anesthetized intramuscularly with ketamine (35 mg/kg) and xylazine (5 mg/kg) with or without acepromazine (0.75 mg/kg). The study was conducted in a double blind fashion, where each rabbit was administered both combinations at a minimum of 7 day intervals. Physiologic parameters were evaluated including heart rate, respiratory rate, central arterial blood pressure, pedal, palpebral and postural reflex activity. The duration of general anesthesia, estimated by the time elapsed between the loss and return of the palpebral reflex, was greater (means = 99 +/- 20 minutes) when acepromazine was employed in the combination compared to (means = 77 +/- 5 minutes) when ketamine/xylazine were used alone. Mean central arterial blood pressure reached a lower level when acepromazine was utilized (means = 46 +/- 8 mm/Hg) than when it was not (means = 57 +/- 12 mm/Hg.). The addition of acepromazine in a ketamine/xylazine combination resulted in a 28% longer period of anesthesia, a 19% lower mean central arterial blood pressure and a 32% longer recovery of postural reflexes. The ketamine/xylazine/acepromazine combination is a useful regimen for normovolemic animals when anesthetic duration greater than that produced by ketamine/xylazine alone is required.     

Initial cardiovascular response on change of posture from squatting to standing

The immediate cardiovascular responses on active change from the squatting (control) to the standing position differ from those obtained in the lying-to-standing manoeuvre. Without exception, the first beat after changing from squatting to standing showed a decrease in systolic, diastolic and mean pressure by 2.0 +/- 1.1 kPa (14.6 +/- 8.3 mm Hg), 1.4 +/- 1.7 kPa (10.6 +/- 12.6 mm Hg) and 1.9 +/- 1.0 kPa (13.9 +/- 7.3 mm Hg), respectively. During the 4th or 5th pulse after standing the pulse pressure was significantly higher than when lying (P less than 0.01). Mean pressure reached a minimum of 7.7 +/- 1.9 kPa (57.8 +/- 14.4 mm Hg) after 7.1 +/- 1.1 s. Thereafter the blood pressure increased to a new level within about 15 s. 11 of 16 subjects demonstrated a biphasic heart rate (HR) response. The maximum HR was reached after 11.0 +/- 2.4 s of standing. In all experiments, the peaks in HR were distinctly delayed after the blood pressure dips. We conclude that an arterial baroreflex could be implicated in the immediate HR increase after a squatting-to-standing manoeuvre. The subsequent time course of the initial HR response, however, might be induced by other mechanisms.     

Systemic blood pressure response to the inhibition of two hyperpolarizing pathways: a comparison to NO-synthase inhibition

The impact on blood pressure of two vasodilating mechanisms, underlied by vascular smooth muscle hyperpolarization, was studied and compared to that induced by nitric oxide NO mechanism. Systemic blood pressure, after inhibitory intervention in arachidonic acid metabolism cytochrome P-450 inhibition by miconazole 0.5 mg/100 g b.w. , one of the hyperpolarizing pathways, did not change. After the inhibition of the action voltage-dependent K(+) channels operator by 4-aminopyridine 0.1 mg/100 g b.w. , the other hyperpolarizing pathway, blood pressure declined slightly from 132.3+/-3.2 mm Hg to 116.5+/-5.0 mm Hg, P<0.05 . Inhibition of nitric oxide production L-NAME 5 mg/100 g b.w. increased blood pressure considerably 123.5+/-2.7 mm Hg to 155.4+/-3.1 mm Hg, P<0.001 . After inhibition of the hyperpolarizing pathway by miconazole, hypotension induced by acetylcholine (Ach, 10 microg represented 63.0+/-1.9 mm Hg vs control value 78.6+/-5.2 mm Hg P<0.001 , by bradykinin (BK) 100 microg 59.4+/-3.9 mm Hg vs control value 71.2+/-6.1 mm Hg P<0.05 . After inhibition of the hyperpolarizing pathway by 4-aminopyridine, hypotension induced by ACh 10 microg achieved 64.6+/-2.5 mm Hg vs control value 78.4+/-2.8 mm Hg P<0.001 and that induced by BK 100 microg 56.6+/-5.3 mm Hg vs control value 72.3+/-2.5 mm Hg P<0.001 . ACh or BK hypotension after the inhibition of the above hyperpolarizing pathways was significantly attenuated. On the contrary, after NO-synthase inhibition the hypotension to ACh was significantly enhanced. Blood pressure decrease after ACh 10 microg hypotension was 91.8+/-4.1 mm Hg vs control value 79.3+/-3.3 mm Hg P<0.01 , and after BK 100 microg it was 78.4+/-7.1 mm Hg vs control value 68.3+/-5.2 mm Hg. A different basal BP response, but equally attenuated hypotension to Ach and BK, was detected after the inhibition of two selected hyperpolarizing pathways. In cotrast, the inhibition of NO production elicited an increase in systemic BP and augmentation of ACh and BK hypotension. The effectiveness of further hyperpolarizing mechanisms in relation to systemic BP regulation and nitric oxide level remains open.