scholarly journals DMSO potentiates the suppressive effect of dronabinol, a cannabinoid, on sleep apnea and REM sleep

2019 ◽  
Author(s):  
Michael W. Calik ◽  
David W. Carley
Keyword(s):  
Sleep Apnea ◽  
Rem Sleep ◽  
Repeated Measures ◽  
Suppressive Effect ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Stainless Steel Screws ◽  
Preclinical And Clinical Studies ◽  
Phosphate Buffered Saline ◽  
Rule Out

AbstractPurposeDimethyl sulfoxide (DMSO) is an amphipathic molecule with innate biological activity that also is used to dissolve both polar and nonpolar compounds in preclinical and clinical studies. Recent investigations of dronabinol, a cannabinoid, dissolved in DMSO demonstrated decreased sleep apnea frequency and time spent in REM sleep in rats. Here, we tested the effects of dronabinol dissolved in 25% DMSO (diluted in phosphate-buffered saline) to rule out potentiating effects of DMSO.MethodsSprague-Dawley rats were anesthetized and implanted with bilateral stainless steel screws into the skull for electroencephalogram recording and bilateral wire electrodes into the nuchal muscles for electromyogram recording. Each animal was recorded by polysomnography. The study was a fully nested, repeated measures crossover design, such that each rat was recorded following each of 8 intraperitoneal injections separated by three days: vehicle (25% DMSO/PBS); vehicle and CB1 antagonist (AM 251); vehicle and CB2 antagonist (AM 630); vehicle and CB1/CB2 antagonist; dronabinol (CB1/CB2 agonist); dronabinol and CB1 antagonist; dronabinol and CB2 antagonist; and dronabinol and CB1/CB2 antagonist. Sleep was manually scored into NREM and REM stages, and apneas were quantified.ResultsDronabinol dissolved in 25% DMSO did not suppress apnea or modify sleep efficiency compared to vehicle controls, in contrast to previously published results. However, dronabinol did suppress REM sleep, which is in line with previously published results.ConclusionsDronabinol in 25% DMSO partially potentiated dronabinol’s effects, suggesting a concomitant biological effect of DMSO on breathing during sleep.

Protoveratrines A and B increase sleep apnea index in Sprague-Dawley rats

1997 ◽  
Vol 83 (5) ◽  
pp. 1602-1606 ◽  
Author(s):  
Sinisa M. Trbovic ◽  
Miodrag Radulovacki ◽  
David W. Carley
Keyword(s):  
Sleep Apnea ◽  
Rem Sleep ◽  
Carotid Sinus ◽  
Minute Ventilation ◽  
Heart Period ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Pharmacological Stimulation ◽  
Freely Moving ◽  
Sensory Endings

Trbovic, Sinisa M., Miodrag Radulovacki, and David W. Carley. Protoveratrines A and B increase sleep apnea index in Sprague-Dawley rats. J. Appl. Physiol. 83(5): 1602–1606, 1997.—The action of protovertarines A and B, which stimulate carotid sinus baroreceptors and vagal sensory endings in the heart as well as pulmonary bed, were assessed on spontaneous and postsigh central sleep apneas in freely moving Sprague-Dawley rats. During the 6-h recording period, animals were simultaneously monitored for sleep by using electroencephalogram and electromyogram recordings, for respiration by single-chamber plethysmography, and for blood pressure and heart period by using radiotelemetry. After administration of 0.2, 0.5, or 1 mg/kg sc of protoveratrines, cardiopulmonary changes lasting at least 6 h were observed in all three behavioral states [heart period increased up to 23% in wakefulness, 21% in non-rapid-eye-movement (non-REM) sleep, and 20% in REM sleep; P < 0.005 for each]. At the same time, there was a substantial increase in the number of spontaneous (375% increase; P = 0.04) and postsigh (268% increase, P = 0.0002) apneas. Minute ventilation decreased by up to 24% in wakefulness, 25% in non-REM, and 35% in REM sleep ( P < 0.05 for each). We conclude that pharmacological stimulation of baroreflexes promotes apnea expression in the sleeping rat.

Effects of remote ischemic preconditioning on the deformability and aggregation of red blood cells in a rat endotoxemia model

2021 ◽  
pp. 1-9
Author(s):  
Yun-Hee Kim ◽  
Sung-Uk Choi ◽  
Jung-Min Youn ◽  
Seung-Ha Cha ◽  
Hyeon-Ju Shin ◽  
...  
Keyword(s):  
Ischemic Preconditioning ◽  
Remote Ischemic Preconditioning ◽  
Sprague Dawley ◽  
Aggregation Index ◽  
Sprague Dawley Rats ◽  
Endotoxemia Model ◽  
Elongation Index ◽  
The Right ◽  
Phosphate Buffered Saline ◽  
Severe Ischemia

BACKGROUND: The prevention of rheologic alterations in erythrocytes may be important for reducing sepsis-associated morbidity and mortality. Remote ischemic preconditioning (RIPC) has been shown to prevent tissue damage caused by severe ischemia and mortality resulting from sepsis. However, the effect of RIPC on erythrocytes in sepsis is yet to be determined. OBJECTIVE: To investigate the effect of RIPC on rheologic alterations in erythrocytes in sepsis. METHODS: Thirty male Sprague-Dawley rats were used in this study. An endotoxin-induced sepsis model was established by intraperitoneally injecting 20 mg/kg LPS (LPS group). RIPC was induced in the right hind limb using a tourniquet, with three 10-minute of ischemia and 10 min of reperfusion cycles immediately before the injection of LPS (RIPC/LPS group) or phosphate-buffered saline (RIPC group). The aggregation index (AI), time to half-maximal aggregation (T1/2), and maximal elongation index (EImax) of the erythrocytes were measured 8 h after injection. RESULTS: The AI, T1/2, and EImax values in the LPS and RIPC/LPS groups differed significantly from those in the RIPC group, but there were no differences between the values in the LPS and RIPC/LPS groups. CONCLUSIONS: RIPC did not prevent rheologic alterations in erythrocytes in the rat model of LPS-induced endotoxemia.

Exercise in the heat is limited by a critical internal temperature

2000 ◽  
Vol 89 (2) ◽  
pp. 799-806 ◽  
Author(s):  
T. J. Walters ◽  
K. L. Ryan ◽  
L. M. Tate ◽  
P. A. Mason
Keyword(s):  
Repeated Measures ◽  
Initial Temperature ◽  
Significant Negative Correlation ◽  
Time To Exhaustion ◽  
Internal Temperature ◽  
Sprague Dawley ◽  
Repeated Measures Design ◽  
Sprague Dawley Rats ◽  
Run Time ◽  
Exertional Heat Stress

We examined whether fatigue during exertional heat stress occurred at a critical internal temperature independent of the initial temperature at the start of exercise. Microwaves (2.1 GHz; 100 mW/cm2) were used to rapidly (3–8 min) heat rats before treadmill exercise to exhaustion. In a repeated-measures design, food-restricted male Sprague-Dawley rats ( n = 11) were preheated to three levels (low, medium, and high). In addition, two sham exposures, Sham 1 and Sham 2, were administered at the beginning and end of the study, respectively. At the initiation of exercise, hypothalamic (Thyp) and rectal (Trec) temperatures ranged from 39.0°C to 42.8°C (Thyp) and 42.1°C (Trec). The treadmill speed was 17 m/min (8° grade), and the ambient temperature during exercise was 35°C. Each treatment was separated by 3 wk. Run time to exhaustion was significantly reduced after preheating. There was a significant negative correlation between run time and initial Thyp and Trec ( r = 0.73 and 0.74, respectively). The temperatures at exhaustion were not significantly different across treatments, with a range of 41.9–42.2°C (Thyp) and 42.2–42.5°C (Trec). There were no significant differences in run time in the sham runs administered at the start and end of the investigation. No rats died as a result of exposure to any of the treatments, and body weight the day after each treatment was unaffected. These results support the concept that a critical temperature exists that limits exercise in the heat.

Impaired NO-mediated vasodilation with increased superoxide but robust EDHF function in right ventricular arterial microvessels of pulmonary hypertensive rats

2007 ◽  
Vol 292 (6) ◽  
pp. H2737-H2744 ◽  
Author(s):  
Masahito Kajiya ◽  
Masanori Hirota ◽  
Yousuke Inai ◽  
Takahiko Kiyooka ◽  
Taro Morimoto ◽  
...  
Keyword(s):  
Right Ventricular ◽  
Pressure Overload ◽  
Suppressive Effect ◽  
Protective Role ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Small Arteries ◽  
Sprague Dawley Rats ◽  
Endothelial Nitric Oxide ◽  
Arteriolar Vasodilation

Pulmonary hypertension (PH) causes right ventricular (RV) hypertrophy and, according to the extent of pressure overload, eventual heart failure. We tested the hypothesis that the mechanical stress in PH-RV impairs the vasoreactivity of the RV coronary microvessels of different sizes with increased superoxide levels. Five-week-old male Sprague-Dawley rats were injected with monocrotaline ( n = 126) to induce PH or with saline as controls ( n = 114). After 3 wk, coronary arterioles (diameter = 30–100 μm) and small arteries (diameter = 100–200 μm) in the RV were visualized using intravital videomicroscopy. We evaluated ACh-induced vasodilation alone, in the presence of Nω-nitro-l-arginine methyl ester (l-NAME), in the presence of tetraethylammonium (TEA) or catalase with or without l-NAME, and in the presence of SOD. The degree of suppression in vasodilation by l-NAME and TEA was used as indexes of the contributions of endothelial nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF), respectively. In PH rats, ACh-induced vasodilation was significantly attenuated in both arterioles and small aretries, especially in arterioles. This decreased vasodilation was largely attributable to reduced NO-mediated vasoreactivity, whereas the EDHF-mediated vasodilation was relatively robust. The suppressive effect on arteriolar vasodilation by catalase was similar to TEA in both groups. Superoxide, as measured by lucigenin chemiluminescence, was significantly elevated in the RV tissues in PH. SOD significantly ameliorated the impairment of ACh-induced vasodilation in PH. Robust EDHF function will play a protective role in preserving coronary microvascular homeostasis in the event of NO dysfunction with increased superoxide levels.

Salty Solutions: Their Effects on Thermal Set Points in Behavioral Repertoires of Albino Rats

1994 ◽  
Vol 79 (1) ◽  
pp. 211-215 ◽  
Author(s):  
William F. Vitulli ◽  
Rwanda Aker ◽  
Stanley W. Howard ◽  
Wendy M. Jones ◽  
Morgan W. Kimball ◽  
...  
Keyword(s):  
Sodium Chloride ◽  
Repeated Measures ◽  
Thermal Environment ◽  
Core Body Temperature ◽  
Behavioral Thermoregulation ◽  
Albino Rats ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Reversal Design ◽  
Post Hoc

Salt (sodium chloride) has been linked to increased blood pressure and a rise in core body temperature. The objective of this study was to investigate the role played by salt in altering behavioral thermoregulation in albino rats. Different doses of sodium chloride were administered (ip) prior to fixed-interval 2-min. schedules of microwave reinforcement in rats tested in a cold Skinner Box. Three Sprague-Dawley rats were conditioned to regulate their thermal environment with 5-sec. exposures of MW reinforcement in a repeated-measures reversal design. Friedman's non-parametric test showed significant differences among sodium chloride doses and physiologically normal saline. Post hoc sign tests showed that all doses of NaCI suppressed operant behavior for heat except 60 mg/kg. The hypothesis that sodium chloride lowers hypothalamic set point for heat was partially supported.

Involvement of AT2 receptors at NRVL in tonic baroreflex suppression by endogenous angiotensins

1997 ◽  
Vol 272 (5) ◽  
pp. H2204-H2210 ◽  
Author(s):  
K. S. Lin ◽  
J. Y. Chan ◽  
S. H. Chan
Keyword(s):  
Suppressive Effect ◽  
Angiotensin Receptors ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Inhibitory Modulation ◽  
Sprague Dawley Rats ◽  
Peptide Antagonist ◽  
Endogenous Activity ◽  
At2 Receptors

We evaluated the role of endogenous angiotensin II and III (ANG II and ANG III) at the rostral nucleus reticularis ventrolateralis (NRVL) in the modulation of baroreceptor reflex (BRR) response and the subtype of angiotensin receptors involved in this process. Adult male Sprague-Dawley rats anesthetized and maintained with pentobarbital sodium were used. Exogenous application of ANG II or ANG III (10, 20, or 40 pmol) by bilateral microinjection into the NRVL significantly suppressed the BRR response to transient hypertension induced by phenylephrine (5 micrograms/kg i.v.). The suppressive effect of ANG II (20 pmol) was reversed by an equimolar dose (1.6 nmol) of its peptide antagonist, [Sar1, Ile8]ANG II, and the nonpeptide antagonists for AT1 and AT2 receptors, losartan and PD-123319, respectively. On the other hand, the inhibitory action of ANG III (20 pmol) was blunted by its peptide antagonist. [Ile7]ANG III or PD-123319, but not by losartan. Blocking the endogenous activity of the angiotensins by microinjection into the bilateral NRVL of [Sar1, Ile8]ANG II, [Ile7]ANG III, or PD-123319 elicited an appreciable enhancement of the BRR response, whereas losartan produced minimal effect. These results suggest that, under physiological conditions, both endogenous ANG II and ANG III may exert a tonic inhibitory modulation on the BRR response by acting selectively on the AT2 receptors at the NRVL.

scholarly journals A Segmental Chronic Pain Syndrome in Rats Associated with Intrathecal Infusion of NMDA: evidence for selective action in the dorsal horn

1994 ◽  
Vol 21 (1) ◽  
pp. 24-28 ◽  
Author(s):  
Douglas W. Zochodne ◽  
Marilyn Murray ◽  
Sukriti Nag ◽  
Richard J. Riopelle
Keyword(s):  
Magnesium Sulfate ◽  
Experimental Pain ◽  
Pain Syndrome ◽  
Sprague Dawley ◽  
Sensory Axons ◽  
Sprague Dawley Rats ◽  
Peripheral Sensory ◽  
Excessive Grooming ◽  
Phosphate Buffered Saline ◽  
Intrathecal Infusion

ABSTRACT:We explored the effects of chronic lumbar intrathecal NMDA infusion (mini-osmotic pumps) in Sprague-Dawley rats on motor and sensory axon integrity. Several different infusion protocols, each given over a 4 week period were examined: 0.15 M NMDA in phosphate buffered saline; phosphate buffered saline without NMDA; and 0.20 M magnesium sulfate plus 0.15 M NMDA; 0.35 M NMDA. In two additional protocols, 0.15 M NMDA or phosphate buffered saline were infused for a total of 8 weeks. Within 1-2 weeks of the onset of NMDA, but not phosphate buffered saline infusions, the rats exhibited irritability, circling, biting and excessive grooming resulting in loss of hair, and skin ulcerations from autotomy localized to lumbar and sacral innervated dermatomes. Co-infusion of NMDA with magnesium sulfate almost completely prevented these findings. The behavioural changes were not associated with abnormalities of sensory or motor conduction. Intrathecal infusion of NMDA induces a chronic “central” experimental pain disorder in rats, localized to the cord segment with the greatest exposure to the infusion, without involvement of peripheral sensory axons and sparing the axonal integrity of anterior horn cells.

scholarly journals Neural Correlates of Wakefulness, Sleep, and General Anesthesia

2016 ◽  
Vol 125 (5) ◽  
pp. 929-942 ◽  
Author(s):  
Dinesh Pal ◽  
Brian H. Silverstein ◽  
Heonsoo Lee ◽  
George A. Mashour
Keyword(s):  
General Anesthesia ◽  
Rem Sleep ◽  
Slow Wave Sleep ◽  
Transfer Entropy ◽  
Sprague Dawley ◽  
Behavioral Arousal ◽  
State Dependent ◽  
Sprague Dawley Rats ◽  
Dependent Change ◽  
Symbolic Transfer Entropy

Abstract Background Significant advances have been made in our understanding of subcortical processes related to anesthetic- and sleep-induced unconsciousness, but the associated changes in cortical connectivity and cortical neurochemistry have yet to be fully clarified. Methods Male Sprague–Dawley rats were instrumented for simultaneous measurement of cortical acetylcholine and electroencephalographic indices of corticocortical connectivity—coherence and symbolic transfer entropy—before, during, and after general anesthesia (propofol, n = 11; sevoflurane, n = 13). In another group of rats (n = 7), these electroencephalographic indices were analyzed during wakefulness, slow wave sleep (SWS), and rapid eye movement (REM) sleep. Results Compared to wakefulness, anesthetic-induced unconsciousness was characterized by a significant decrease in cortical acetylcholine that recovered to preanesthesia levels during recovery wakefulness. Corticocortical coherence and frontal–parietal symbolic transfer entropy in high γ band (85 to 155 Hz) were decreased during anesthetic-induced unconsciousness and returned to preanesthesia levels during recovery wakefulness. Sleep-wake states showed a state-dependent change in coherence and transfer entropy in high γ bandwidth, which correlated with behavioral arousal: high during wakefulness, low during SWS, and lowest during REM sleep. By contrast, frontal–parietal θ connectivity during sleep-wake states was not correlated with behavioral arousal but showed an association with well-established changes in cortical acetylcholine: high during wakefulness and REM sleep and low during SWS. Conclusions Corticocortical coherence and frontal–parietal connectivity in high γ bandwidth correlates with behavioral arousal and is not mediated by cholinergic mechanisms, while θ connectivity correlates with cortical acetylcholine levels.

Cardiopulmonary Interactions Following REM Sleep Deprivation in Sprague–Dawley Rats

1997 ◽  
Vol 145 (2) ◽  
pp. 371-375 ◽  
Author(s):  
Miodrag Radulovacki ◽  
Sinisa M. Trbovic ◽  
David W. Carley
Keyword(s):  
Sleep Deprivation ◽  
Rem Sleep ◽  
Sprague Dawley ◽  
Rem Sleep Deprivation ◽  
Cardiopulmonary Interactions ◽  
Sprague Dawley Rats
Sign in / Sign up

Export Citation Format

Share Document