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PubMed1990

Effects of phencyclidine on extracellular levels of dopamine, dihydroxyphenylacetic acid and homovanillic acid in conscious and anesthetized rats.

Dose-dependent effects of phencyclidine on extracellular levels of dopamine (DA), dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) in the neostriatum were studied in both urethane-anesthetized and conscious rats. In vivo microdialysis was used to collect 10 min samples that were analyzed for levels of DA, DOPAC and HVA, using high-performance liquid chromatography with electrochemical detection (HPLC-EC). In both the anesthetized and conscious preparations, 20 mg/kg of phencyclidine produced an increase in extracellular levels of DA, 10 mg/kg resulted in no change, while 1 mg/kg produced a slow decrease. In the anesthetized animals phencyclidine did not have a significant effect on levels of DOPAC or HVA, but in the conscious animals phencyclidine produced a dose-dependent decrease in levels of DOPAC and HVA. The increase in levels of DA could be the result of increased release of DA or inhibition of the uptake of DA. The decrease in levels of DOPAC and HVA, at the 1 mg/kg dose, could result from a decrease in the synthesis of DA that is offset at the 10 and 20 mg/kg doses by opposing mechanisms.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1987

A dissociation of conscious visual imagery and visual short-term memory.

Two people who reported an impaired ability to form conscious visual images were tested. Compared to a control group of college students, these impaired visualizers were not impaired on two tests of visual short-term memory. Furthermore, they retained more digits in visual short-term memory than they could visualize. These results suggests that deficits in the ability to form conscious visual images can arise without visual short-term memory being impaired, and conscious visual imagery should not be equated with visual short-term memory.

Adult↗
PubMed1996

Sympathetic nerve responses elicited by cocaine in anesthetized and conscious rats.

Recent evidence suggests that cocaine decreases rather than increases sympathetic nerve discharge (SND). The purpose of the present study was to provide the first complete characterization of the dose-response relationships of cocaine (0.005-3 mg/kg, IV) for arterial pressure, heart rate, and lumbar, splanchnic, or renal SND in pentobarbital-anesthetized rats. Cocaine was also tested in conscious rats. In pentobarbital-anesthetized rats cocaine elicited prolonged (lasting up to 56 min), dose-dependent decreases in SND on all three nerves. The splanchnic nerve was significantly more sensitive to the inhibitory actions of cocaine than was the lumbar nerve. Cocaine increased arterial pressure and elicited bradycardia at doses above 0.5 mg/kg. Comparison of the dose-response curves of cocaine for splanchnic SND in sham-operated and sinoaortically deafferentated (SAD) rats showed that the baroreceptor reflex made only a minor contribution to the magnitude of sympathoinhibitory response. However, the duration of the sympathoinhibitory response was significantly shorter in SAD than in sham animals. In conscious rats, cocaine (0.1 and 1.0 mg/kg) elicited a pattern of neural and cardiovascular responses similar to that seen in anesthetized rats, except that the prolonged sympathoinhibitory responses were preceded by a brief (lasting < 10 s) increase in SND. From these data we conclude that cocaine produces prolonged decreases in SND in conscious and anesthetized rats. These sympathoinhibitory responses do not appear to result from baroreceptor reflex activation and may involve a central mechanism of action.

Anesthesia↗
PubMed1986

Ventilatory response of the conscious or anesthetized cat to oxygen breathing.

In conscious intact cats, oxygen breathing for up to 1 h does not modify ventilation, and the ventilatory response to CO2 in hyperoxia is not consistently decreased. However, oxygen breathing induces sustained hyperventilation in conscious cats after carotid body denervation. In anesthetized cats, oxygen breathing provokes a hypoventilation which is transient under light anesthesia but more sustained under deeper levels of anesthesia. At all levels of anesthesia, the ventilatory response to CO2 is decreased in hyperoxia as compared with normoxia. These results suggest that: the effects of hyperoxia include a central stimulating component, seen only in conscious animals, which offsets the decreased ventilatory drive from peripheral chemoreceptors; this central component is sensitive to anesthesia, thus allowing an explanation for the permanent decrease in ventilation and decrease in ventilatory response to CO2 observed when oxygen is given during deep anesthesia; and anesthesia may help to purposefully unmask factors involved in the control of breathing, but it markedly alters the normal functioning of the respiratory network.

Anesthesia↗
PubMed1994

Distribution of pulmonary blood flow in conscious resting rats.

The pattern of pulmonary blood flow (PBF) distribution was determined in the rat, in which lung gravitational forces are minimal. Microspheres were infused into the inferior vena cava of 15 conscious, and 5 anesthetized rats. Relative scatter of specific PBF [(sample activity/sample weight)/(total activity/total weight)] in 28 lung samples was calculated. In 5 of the conscious rats, consecutive determinations were made 30 min apart. In 5 anesthetized rats, PBF was determined in prone and supine positions. Relative scatter of specific PBF varied from 0.84 to 1.12, with PBF being distributed preferentially to the hilar, central regions. There was a high correlation between consecutive measurements: y = 0.88 x +0.11 (n = 140, r = 0.92). By changing from prone to supine position, PBF to the topmost regions increased, and that to the lowermost regions decreased, by only 3 percent. The results indicate that in the conscious resting rat, PBF has a small but significant preferential distribution to the hilar, central regions, with lower blood flow to the peripheral regions of the lung.

Animals↗
PubMed1982

MIF-1 does not act like naloxone in antagonizing the cardiovascular activity of leucine-enkephalin in the conscious dog.

MIF-1 (Pro-Leu-Gly-NH2), a hypothalamic tripeptide, has been demonstrated to stimulate naloxone in antagonizing the effects of opioid peptides in a number of experimental systems including enkephalin-induced analgesia in the tail-flick assay, beta-endorphin induced hypothermia and hypomotility, deprivation-induced drinking, and analgesia in goldfish. MIF-1, however, has no effect upon the activity of enkephalins in the mouse vas deferens or enkephalin binding in the rat striatum. We have studied the interactions of MIF-1 with Leu5-enkephalin (Leu5-ENK) in the conscious, chronically instrumented dog. Although naloxone inhibits both the elevations of heart rate and blood pressure produced by IV Leu5-ENK in the conscious state and the depressions in these variables produced by Leu5-ENK after pentobarbital anesthesia, MIF-1 has no effect upon the Leu5-ENK response in either state. However, both naloxone and MIF-1 seem to raise mean arterial pressure in the conscious dog. These results indicate that MIF-1 does not act like naloxone in antagonizing the peripheral effects of Leu5-ENK and lend further support to the existence of mechanistic differences among opiate-mediated behavior, analgesia, and cardiovascular activity.

Animals↗
PubMed1980

Cardiac output by dye dilution using a left carotid loop in conscious rats.

By a modified dye dilution method using a simple dichromatic densitometer, cardiac output (CO) in conscious rats was determined. Under anesthesia, a carotid loop was made in the left carotid artery with a polyethylene tube (PE50) and exteriorized. A sensor of the densitometer was set at the center of the carotid loop. Indocyanine green dye solution was injected into the right atrium via the jugular vein. CO was calculated from the dye dilution curve obtained. In the conscious state (6 hours after ether anesthesia),CO in normotensive, spontaneously and DOC/saline hypertensive rats was determined without affecting blood pressure and heart rate. However, CO in the pentobarbital or urethane anesthetized rats was decreased with other hemodynamic changes. The validity of this method was confirmed with a hydraulic model system and in anesthetized open-chest cats using an electromagnetic flowmetry. From these studies, it was concluded that the modifed dye dilution method for measuring CO in conscious rats was reliable and useful for hemodynamic studies in hypertensive rats.

Animals↗
PubMed1980

Drug administration into the third ventricle of the brain of anesthetized and conscious cats.

A method is described for the administration of drugs into the third ventricle of the brain of conscious and anesthetized cats. Noradrenaline administered by this route produced cardiovascular stimulant effects as against depressor effects when administered into a lateral cerebral ventricle. The pressor responses evoked by third ventricular administration of noradrenaline were antagonized by spinal section in anesthetized cats and by hexamethonium in conscious animals. Conscious cats were more sensitive to the pressor effects of third ventricular noradrenaline than chloralose-anesthetized animals.

Anesthesia↗
PubMed1983

Coronary artery ligation, early arrhythmias, and determination of the ischemic area in conscious rats.

A method for studying the acute phase of myocardial infarction in conscious rats has been developed. In preliminary surgery, a loose ligature of atraumatic silk was understitched around the left coronary artery. Its ends were pulled through a polyethylene tube placed within the thorax and fixed under the skin. Seven days later, coronary occlusion was performed by tightening the ligature in conscious animal. Lidocaine and pindolol pretreatment increased the survival rate and attenuated the life-threatening arrhythmias during the first 20 min, but did not influence the infarct size 16 hrs later. An ex vivo perfusion technique for determining the ischemic area has also been developed. 3, 6, and 20 min after coronary ligation, the hearts were excised and perfused with 4% formaldehyde. The ischemic area could not be perfused and remained dark red with a sharp border-line. At the 3rd and 20th min its size was as same as that of the 16-hr infarcted area; however at the 6th min it increased by 50%. Lidocaine and pindolol eliminated this transitory increase. These methods appear to be valuable for large-scale determination of drug effects on the acute phase of experimental myocardial infarction in conscious rats, and for estimating their action on the size of ischemic area very early after coronary occlusion.

Animals↗
PubMed1987

A new blood pressure measuring apparatus equipped with a microcomputer system for conscious rats.

In order to measure the systolic blood pressure of conscious rats without thermal stress, a highly sensitive pulse sensor was developed using a light-emitting diode-photo diode system. The combination of this pulse sensor and microcomputer system led to the development of a six-channel automatic blood pressure measuring apparatus for rats. It can measure the systolic tail arterial pressure of conscious rats at 28-30 degrees C. The relationship between direct carotid arterial pressure (Y) and indirect tail arterial pressure (X) in conscious spontaneously hypertensive rats can be expressed as follows: Y = 0.95X + 19.9 (mm Hg, r = 0.988, 28 degrees C). The new apparatus was also used to confirm the acute hypotensive effects of hydralazine, nifedipine, and pindolol in spontaneously hypertensive rats and the subacute antihypertensive effect of trichlormethiazide in desoxycorticosterone/saline hypertensive rats.

Animals↗
PubMed1989

Holter monitoring in conscious dogs. Assessment of arrhythmias occurring during ischemia and in the early reperfusion phase.

Myocardial ischemic episodes of 5 min, 15 min, and 4 hr duration, with interposed reperfusion periods, were induced in the same conscious, chronically instrumented dogs. A drop in systolic blood pressure and an increase in heart rate and in the arrhythmic ratio (AR% = number of ectopic beats x 100/total number of beats, as assessed by Holter monitoring) was registered in response to the induction of myocardial ischemia. Reperfusion-induced salvage after coronary occlusion of 5 and 15 min duration was documented by an immediate return of systolic blood pressure, heart rate, and AR to the preocclusion control level. However, after coronary occlusion lasting for 4 hr, reperfusion induced a further drop in blood pressure and an increase in heart rate and in AR. We conclude that in conscious dogs, reperfusion-induced arrhythmias do not occur after short-lasting myocardial ischemic episodes. Reperfusion after long-lasting ischemia induces marked ventricular ectopic activity, yielding an arrhythmic ratio of more than 80%. Although these reperfusion-induced arrhythmias impair the hemodynamic state, they are well tolerated in the conscious dog and can be assessed by the Holter monitoring technique. This new experimental approach promises to be of clinical relevance for investigations on the therapeutic efficacy of new antiarrhythmic drugs.

Animals↗
PubMed1989

Holter monitoring in conscious dogs. Assessment of arrhythmias occurring in the late reperfusion phase after coronary occlusion.

Arrhythmias occurring in the late reperfusion phase, i.e., up to 3 days after episodes of 5 min, 15 min, and 4 hr of coronary occlusion (CAO), were investigated in six conscious, chronically instrumented dogs using the Holter monitoring technique. The arrhythmic ratio (AR% = number of premature ventricular complexes x 100/total number of beats) of a 24-hr preocclusion control record was 0.004% and did not differ from the values assessed for day 1 (0.004%) and 2 (0.001%) of the late reperfusion phase after 5 min CAO. After 15 min, CAO increased, but insignificantly elevated AR values were registered on days 1 (2.5%), 2 (0.26%), and 3 (0.1%) of the late reperfusion phase. On day 1 of the late reperfusion phase after 4 hr CAO, the AR increased markedly to 75%. On day 2 of this phase, the AR was lower (20%) but still significantly elevated. On day 3, the AR was 3.5%, a value still markedly, although not significantly, above the preocclusion control level. We conclude that in conscious dogs, arrhythmias in the late reperfusion phase do not occur after 5 min CAO. However, after 15 min CAO and, especially, after 4 hr CAO, an increase in arrhythmic activity occurs in the late reperfusion phase and gradually declines towards the preocclusion control level over a period of 3 days. Thus, it could be demonstrated that the long-term assessment of reperfusion arrhythmias by ECG monitoring using the Holter technique is feasible in conscious dogs. This method represents a promising approach to clinically relevant experimental investigations on the therapeutic efficacy of a new antiarrhythmic drugs.

Animals↗
PubMed1991

A method for maintaining and protecting chronic arterial and venous catheters in conscious rats.

The ability to monitor arterial blood pressure and heart rate directly, as well as to sample venous blood, or inject pharmaceutical agents intravenously is important in pharmacological studies of the cardiovascular system. The rat is a frequently used and accepted animal model for cardiovascular investigations, especially those relating to hypertension. Even though the rat is a major model for these studies, the size of the rat has made it difficult to maintain catheters for a long period of time. Although there have been previous methods available, the authors report on an improved method to implant, maintain, and protect arterial and venous catheters in conscious rats for extended periods of time. A Silastic/Tygon catheter is implanted intraarterially and intravenously, exteriorized, and protected with a spring device. Catheters remained patent throughout a 5-week period during which time direct blood pressure recordings were obtained and baroreflexes were evaluated in conscious, unrestrained rats. The described design and methods provide an inexpensive means to maintain chronically implanted venous and arterial catheters in the conscious rat. Furthermore, rats may be gang housed.

Animals↗
PubMed1986

Effects of acute myocardial infarction on the circulation of the conscious rat.

This study was conducted to determine if experimental left coronary artery ligation resulting in a small myocardial infarction (MI, 15% of the left ventricle) affects the peripheral circulation in conscious rat during the first 48 h of recovery. At 24 or 48 h post-MI or sham surgery, animals were instrumented and evaluated using the radioactive microsphere technique. There were no overt central hemodynamic changes 24 h post-MI but at 48 h, left ventricular end diastolic pressure was significantly increased compared to the parallel control (MI: 5.9 +/- 0.6, sham 2.0 +/- 0.5 mm Hg, P less than 0.005). At 24 h post-MI, renal vascular resistance was increased and similar but non-significant changes occurred in the gut. At 48 h post-MI, vascular resistance in the skeletal muscle, spleen, gut and cutaneous circulations were significantly reduced compared to sham-operated rats. Similar changes at 24 h were seen in a separate group of conscious rats with MI which had previously undergone cardiac denervation suggesting that cardiac afferent activity was not directly responsible for the peripheral response to MI at 24 h. Denervation did eliminate the 48 h peripheral vasodilator response. In denervated animals, circulating renin levels were similar in MI and sham-operated rats and were unchanged between 24 and 48 h. Thus, small MI in conscious rat induces a sequela of effects on the peripheral circulation over 48 h. These changes are associated with cardiac afferent nerve activity but appear to be unrelated to plasma renin levels.

Animals↗
PubMed1993

Power spectrum analysis of cardiovascular variability monitored by telemetry in conscious unrestrained rats.

Beat-to-beat variability of arterial pressure and heart period (R-R) was studied in eight conscious freely-moving adult male rats in which telemetric recordings of arterial pressure, ECG and respiratory movements were obtained under unrestrained and unstressed conditions. The beat-to-beat time series of these signals (systolic arterial pressure, diastolic arterial pressure and R-R) were analyzed, in the frequency domain, using autoregressive spectral analysis in order to detect and quantify the rhythmic components. In basal conditions, the systolic arterial pressure variability spectrum was characterized by three major spectral components which had central frequencies respectively of 0.08 +/- 0.03 Hz (very low frequency), 0.43 +/- 0.02 Hz (low frequency) and 1.36 +/- 0.19 Hz (high frequency). Similar rhythmic components were found in R-R signal variability. The very low frequency component included a higher percentage of total power in R-R variability spectrum (75.3%) than in systolic arterial pressure variability spectrum (58.4%). The low frequency component was more pronounced in both systolic and diastolic arterial pressure variability spectra. The high frequency component of R-R, systolic and diastolic arterial pressure was synchronous with respiration. Cross-spectral analysis revealed a high statistical coherence between R-R and arterial pressure variabilities in all the three frequency bands. An alpha-adrenergic blocker (phentolamine) specifically abolished the low frequency components of systolic and diastolic arterial pressure variability spectra, thus suggesting that low frequency is a marker of sympathetic modulation of vasomotor activity. The low frequency component of R-R variability spectrum was also markedly blunted. We suggest that cardiovascular variability signals, (R-R, systolic and diastolic arterial pressure) are composed almost of two main rhythms linked to respiration and vasomotor activity. These rhythms can be quantified in conscious unrestrained rats by using telemetry and spectral analysis. This approach seems to offer a new powerful tool for pharmacological studies in conscious small animals.

Animals↗
PubMed1991

Divergent circulatory effects of betaxolol in conscious and anesthetized normal and portal hypertensive rats.

We aimed to define the circulatory effects of beta 1-blockade in conscious normal and portal hypertensive rats and determine if pentobarbital anesthesia affected these responses. A selective beta 1-antagonist, betaxolol, was given to four groups: conscious and anesthetized sham-operated and portal hypertensive rats. Cardiac output and splanchnic organ blood flows were measured by radioactive microspheres twice in each rat, before and 15 min after betaxolol. Both groups of conscious rats maintained mean arterial pressure despite significant decreases in cardiac output and heart rate, by increasing total peripheral resistance. Anesthetized rats were unable to do this and thus also diminished arterial pressure significantly, with portal hypertensive rats showing greater decreases than sham-operated rats. Portal tributary flow and portal pressure decreased only in the anesthetized rats. Autoregulation of splanchnic blood flow was not uniform between groups or organs: although splenic flow decreased in all four groups, intestinal blood flow decreased only in anesthetized portal hypertensive rats. The greatest decreases in several splanchnic organ blood flows were seen in this latter group. These results indicate that: (i) pentobarbital markedly changes systemic and splanchnic responses to beta 1-blockade; (ii) splanchnic autoregulation is not uniform--the intestinal circulation enjoys more protection than the splenic; and (iii) portal hypertensive rats seem to be more vulnerable to the circulatory effects of beta 1-blockade.

Animals↗
PubMedDate not supplied

Pressor, tachycardic and behavioral excitatory responses in conscious rats following ICV administration of ACTH and CRF are blocked by naloxone pretreatment.

Experiments were conducted to compare the blood pressure and heart rate responses of conscious rats given intracerebroventricular (ICV) injections of adrenocorticotropin (ACTH 1-24) and corticotropin releasing factor (CRF). Under sodium pentobarbital anaesthesia, rats were implanted with a stainless-steel cannula into the lateral cerebral ventricle and had their right femoral artery and vein cannulated. Upon recovery (24-48 hr later) conscious, unrestrained rats were given ICV injections (total volume 5 microliter by gravity flow) of sterile saline, ACTH (1-24) (0.85 and 1.7 nmoles) or CRF (0.55 and 1.1 nmoles) and blood pressure and heart rate were monitored over the next 2 hr (from the abdominal aorta via the femoral arterial catheter). Both ACTH and CRF caused mean arterial pressure (MAP) to increase, which was paralleled with increases in mean heart rate (MHR). Moreover, these elevations in MAP and MHR were temporally associated with excessive grooming (for ACTH) and locomotor activity (for CRF), which occurred before and lasted as long as MAP and MHR were enhanced. Intravenous (IV) pretreatment whereby naloxone was given 10 min before ICV administration of ACTH (1.7 nmoles) or CRF (1.1 nmoles), showed that naloxone blocked the behavioral, pressor and tachycardic effects of both ACTH and CRF. The results demonstrate that the pressor, tachycardic and locomotor effects evoked in conscious rats by ICV administration of ACTH or CRF are antagonized by naloxone and that their hemodynamic changes may, in part, be mediated by prior behavioral activation.

Adrenocorticotropic Hormone↗
PubMed1990

Noradrenaline thermogenesis in conscious and anaesthetised pouched mice (Saccostomus campestris).

1. The metabolic response to injections of noradrenaline (NA) and saline (control) was investigated in conscious and anaesthetised (sodium pentobarbitone) pouched mice, Saccostomus campestris. 2. NA injection produced a calorigenic response which was significantly greater than that elicited by saline injection in both conscious and anaesthetised animals. 3. This calorigenic response was enhanced by motor activity in conscious pouched mice, but the exclusion of measurements recorded during visible activity eliminated the influence of movement. 4. Anaesthetised pouched mice underwent mild Hypothermia and displayed a retarded metabolic response to NA injection which suggests that anaesthesia affects the expression of NA-induced thermogenesis. 5. The validity of proposed techniques for the measurement of NA thermogenesis is further discussed.

Anesthesia↗