scholarly journals The cardiovascular and endocrine responses to voluntary and forced diving in trained and untrained rats

2010 ◽  
Vol 298 (1) ◽  
pp. R224-R234 ◽  
Author(s):  
Paul F. McCulloch ◽  
Karyn. M. DiNovo ◽  
Tiffanny M. Connolly
Keyword(s):  
Heart Rate ◽  
Sympathetic Activity ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Conscious Awareness ◽  
Sprague Dawley ◽  
Diving Response ◽  
Laboratory Rats ◽  
Cardiorespiratory Response ◽  
Sprague Dawley Rats

The mammalian diving response, consisting of apnea, bradycardia, and increased total peripheral resistance, can be modified by conscious awareness, fear, and anticipation. We wondered whether swim and dive training in rats would 1) affect the magnitude of the cardiovascular responses during voluntary and forced diving, and 2) whether this training would reduce or eliminate any stress due to diving. Results indicate Sprague-Dawley rats have a substantial diving response. Immediately upon submersion, heart rate (HR) decreased by 78%, from 453 ± 12 to 101 ± 8 beats per minute (bpm), and mean arterial pressure (MAP) decreased 25%, from 143 ± 1 to 107 ± 5 mmHg. Approximately 4.5 s after submergence, MAP had increased to a maximum 174 ± 3 mmHg. Blood corticosterone levels indicate trained rats find diving no more stressful than being held by a human, while untrained rats find swimming and diving very stressful. Forced diving is stressful to both trained and untrained rats. The magnitude of bradycardia was similar during both voluntary and forced diving, while the increase in MAP was greater during forced diving. The diving response of laboratory rats, therefore, appears to be dissimilar from that of other animals, as most birds and mammals show intensification of diving bradycardia during forced diving compared with voluntary diving. Rats may exhibit an accentuated antagonism between the parasympathetic and sympathetic branches of the autonomic nervous system, such that in the autonomic control of HR, parasympathetic activity overpowers sympathetic activity. Additionally, laboratory rats may lack the ability to modify the degree of parasympathetic outflow to the heart during an intense cardiorespiratory response (i.e., the diving response).

Cardiovascular responses to nasal water flow in rats are unaffected by chemoreceptor drive

1992 ◽  
Vol 263 (5) ◽  
pp. R1049-R1056 ◽  
Author(s):  
P. F. McCulloch ◽  
N. H. West
Keyword(s):  
Water Flow ◽  
Cardiovascular Responses ◽  
Sprague Dawley ◽  
Diving Response ◽  
Peripheral Chemoreceptors ◽  
Initial Development ◽  
Cardiovascular Changes ◽  
Conscious Rats ◽  
Limited Role ◽  
Sprague Dawley Rats

Peripheral chemoreceptors generally play a limited role in the initial development of diving bradycardia in mammals. However, T.F. Huang and Y.I. Peng (Jpn. J. Physiol. 26: 395-401, 1976) reported that peripheral chemoreceptors are very important for manifestation of the diving response in conscious rats. The objectives of this study were to reinvestigate those findings and determine whether the cardiovascular responses to simulated diving in the rat were potentiated during preexisting hypoxia or hypercapnia. Responses to simulated diving were elicited by nasal water flow with concurrent apnea in paralyzed, artificially ventilated Sprague-Dawley rats anesthetized with Innovar. The experiments show that nasal stimulation in the rat results in rapid bradycardia and hypotension and that these responses are not due to laryngeal stimulation. The data also suggest that chemoreceptors do not play a role in the initiation of the responses to simulated diving in rats and that preexisting chemoreceptor drive does not alter the cardiovascular responses. Additionally, we found that concomitant expiratory apnea is necessary to sustain the profound initial cardiovascular changes induced by nasal water flow.

Effect of pharmacological blockade on cardiovascular responses to voluntary and forced diving in muskrats.

1995 ◽  
Vol 198 (11) ◽  
pp. 2307-2315 ◽  
Author(s):  
P E Signore ◽  
D R Jones
Keyword(s):  
Heart Rate ◽  
Neural Control ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Adrenergic Blocker ◽  
Adrenergic Blockers ◽  
Pharmacological Blockade ◽  
Parasympathetic Influences ◽  
Neural Effect

Neural control of free and forced diving bradycardia and peripheral resistance was studied in the muskrat (Ondatra zibethicus) by means of acute pharmacological blockade with the muscarinic blocker atropine, the alpha-adrenergic blocker phentolamine and the beta-adrenergic blockers nadolol and propranolol. Saline injection was used as a control. Heart rate in control animals increased before voluntary dives and dropped markedly as soon as the animals submerged. Heart rate started increasing towards the end of voluntary dives and reached pre-dive values within the first 5 s of recovery. Pre-dive and post-dive tachycardia were reduced in beta-blocked animals, emphasizing the role of the sympathetic system during the preparatory and recovery periods of voluntary dives. Diving bradycardia and the acceleration in heart rate before surfacing were abolished by atropine and unaffected by nadolol, demonstrating the importance of vagal efferent activity during diving. The results after blockade with nadolol suggest that there is an accentuated antagonism between the two branches of the autonomic nervous system during diving, so that parasympathetic influences on the heart predominate. Propranolol-treated muskrats had a higher diving heart rate than saline- and nadolol-treated animals, which may be due to a sedative effect caused by propranolol crossing the blood-brain barrier, a blockade of central catecholaminergic pathways or a peripheral neural effect, due to the anaesthetic properties of propranolol. Phentolamine did not affect diving bradycardia, indicating that diving bradycardia occurs independently of peripheral vasoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)

Androgen-mediated sex differences of cardiovascular responses in rats

1978 ◽  
Vol 235 (2) ◽  
pp. H242-H246 ◽  
Author(s):  
P. J. Baker ◽  
E. R. Ramey ◽  
P. W. Ramwell
Keyword(s):  
Sex Differences ◽  
Arachidonic Acid ◽  
Rank Order ◽  
Cardiovascular Responses ◽  
Sprague Dawley ◽  
Similar Treatment ◽  
Depressor Response ◽  
Sprague Dawley Rats ◽  
Significant Change ◽  
Dose Levels

Sex differences in the systemic depressor response to arachidonic acid (50 or 150 microgram/kg iv) were observed in intact and castrated anesthetized Sprague-Dawley rats. The rank order of responsiveness was: castrate males, castrate females, females, males; all four groups were significantly different (P less than 0.05) at the higher dose. Castrated males pretreated with testosterone (1 mg/kg sc) 5 or 7 days previously gave a response at the higher arachidonate dose levels that was of the same order as that obtained with intact males. Similar treatment of castrate males with androgen potentiated (P less than 0.05) the vasopressor action of norepinephrine (0.25 microgram/kg) on day 7 after the testosterone pretreatment. In contrast, treatment with depot estradiol (100 microgram/kg sc) in castrate males produced no significant change in the response to either of the vasoactive compounds on both days 5 and 7 after pretreatment. These data suggest that testosterone may be a significant factor in the development of sex differences in the cardiovascular systems of rats.

Adrenomedullin microinjection into the area postrema increases blood pressure

1997 ◽  
Vol 272 (6) ◽  
pp. R1698-R1703 ◽  
Author(s):  
M. A. Allen ◽  
P. M. Smith ◽  
A. V. Ferguson
Keyword(s):  
Blood Pressure ◽  
Area Postrema ◽  
Area Under The Curve ◽  
Physiological Role ◽  
Cardiovascular Responses ◽  
Hypotensive Effect ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Brain Site

Adrenomedullin (ADM) circulates in the blood at concentrations comparable to other vasoactive peptides with established roles in cardiovascular regulation. Intravenously administered ADM produces a clear hypotensive effect, whereas intracerebroventricular microinjections result in increases in blood pressure (BP). Recently, we demonstrated that ADM influences neurons of the area postrema (AP), a central nervous system site implicated in cardiovascular control. However, to address directly the physiological significance of the actions of ADM at the AP, an in vivo microinjection study was undertaken. ADM, at two concentrations (1 and 10 microM), in volumes of 50, 100, and 200 nl, was microinjected into the AP or NTS of 21 urethan-anesthetized male Sprague-Dawley rats. Microinjection of 10 microM ADM (100 nl) resulted in significant transient (2-5 min) increases in BP [120 s area under the curve (AUC): 684.3 +/- 268.6 mmHg/s (P < 0.05)], and heart rate (HR) [AUC: 12.5 +/- 4.5 beats/min (P < 0.05)]. The lower concentration of ADM (1 microM) had no effect on either BP (179.1 +/- 143.6 mmHg/s) or HR (0.8 +/- 2.6 beats/min). ADM was also microinjected into the immediately adjacent nucleus of the solitary tract, where it was found to be without effect on either BP or HR. This study demonstrates, for the first time, a physiological role for ADM acting at a specific brain site, the AP, to produce significant cardiovascular responses.

A STANDARDIZED METHOD FOR THE PRODUCTION OF HEMORRHAGIC SHOCK IN THE RAT

1955 ◽  
Vol 33 (3) ◽  
pp. 436-447 ◽  
Author(s):  
H. G. Downie ◽  
J. A. F. Stevenson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Mortality Rate ◽  
Hemorrhagic Shock ◽  
Respiratory Rate ◽  
Rectal Temperature ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Standardized Method

Although the blood pressure is one of the important criteria in the standardization of hemorrhagic shock in the dog, it has rarely been used for this purpose in the rat. A method resembling the reservoir technique developed by Wiggers and Werle (1942) for the dog using blood pressure as the criterion has been modified for use with the rat. Male Sprague-Dawley rats weighing approximately 400 gm. were used. In the standardization of this technique the blood pressure was reduced to 30 mm. Hg in a 10-min. period of hemorrhage and then maintained at this level by subsequent small hemorrhages into the reservoir until reinfusion indicated the beginning of vascular collapse, at which time all the blood in the reservoir was returned. Considering that those animals which lived longer than 48 hr. were survivors, in a series of 27 animals, 21 died and 6 survived—a mortality rate of 78%.During the hypotensive period there was a consistent and steady drop in the respiratory rate and rectal temperature. The heart rate declined initially and tended to recover as the hypotensive period progressed. After reinfusion the blood pressure rose but. did not reach prehemorrhage levels. Hemorrhage into the bowel and convulsions were significant postreinfusion findings.

Compensation to exsanguination hypotension in healthy conscious dogs

1963 ◽  
Vol 205 (5) ◽  
pp. 1000-1004 ◽  
Author(s):  
Robert F. Rushmer ◽  
Nolan Watson ◽  
Donald Harding ◽  
Donald Baker
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Human Subjects ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Systemic Arterial Pressure ◽  
Conscious Dogs ◽  
Series Of Experiments ◽  
The Mean ◽  
The Right

In some earlier studies on exsanguination hypotension in conscious dogs, reduction in systemic arterial pressure to shock levels was accompanied by a transient tachycardia during the removal of blood, but the heart rate returned to level, at or near control values during extended periods with the mean arterial pressure between 40 and 60 mm Hg. This observation stimulated a series of experiments on five healthy conscious dogs in which transient hypotension was induced by withdrawing blood from the region of the right atrium to determine which mechanisms were dominant in the compensatory reaction. A surprising degree of variability in response was encountered, such that tachycardia was the main response on some occasions, increased peripheral resistance on others, and in still others, several mechanisms appeared to play a role. Similar variability in the response to exsanguination have been reported in human subjects. These observations suggest that the baroceptor reflexes are not simple servo controls and their role in everyday cardiovascular responses should be re-examined.

Role of vasopressin in the cardiovascular response to hypoxia in the conscious rat

1986 ◽  
Vol 251 (6) ◽  
pp. H1316-H1323 ◽  
Author(s):  
B. R. Walker
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Cardiovascular Response ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Hypoxic Exposure ◽  
Conscious Rat ◽  
Time Control ◽  
Hemodynamic Variables

Previous experiments have demonstrated that hypoxia stimulates the release of arginine vasopressin in conscious animals including the rat. The present study was designed to test whether AVP may exert a vasoconstrictor influence during hypoxia at varying levels of CO2. Systemic hemodynamics were assessed in conscious rats for 30 min under hypocapnic hypoxic, isocapnic hypoxic, hypercapnic hypoxic, and room air conditions. Progressive effects on heart rate (HR), cardiac output (CO), and total peripheral resistance (TPR) were observed with varying CO2 under hypoxic conditions. Hypocapnic hypoxia [arterial PO2 (PaO2) = 32 Torr; arterial PCO2 (PaCO2) = 22 Torr] caused HR and CO to rise and TPR to fall. Isocapnic hypoxia (PaO2 = 36 Torr; PaCO2 = 35 Torr) was associated with no significant changes in HR and CO or TPR, whereas hypercapnic hypoxia (PaO2 = 35 Torr; PaCO2 = 51 Torr) caused HR and CO to fall and TPR to rise. Room air time control experiments were associated with no change in measured hemodynamic variables. To determine the possible role of circulating AVP on these cardiovascular responses, additional experiments were performed where the specific V1-vasopressinergic antagonist d(CH2)5Tyr(Me)AVP (10 micrograms/kg iv) was administered at the midpoint of hypoxic exposure. Antagonist administration had no effect on hypocapnic hypoxic animals or animals breathing room air; however, blood pressure and TPR were significantly reduced by d(CH2)5Tyr(Me)AVP in both isocapnic and hypercapnic hypoxic animals. The heart rate response to hypoxia at the various CO2 levels was unaffected; however, cardiac output and stroke volume were increased after V1-antagonism in the isocapnic and hypercapnic hypoxic animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Dietary obesity and weight cycling in rats: a model of stress-induced hypertension?

1991 ◽  
Vol 261 (4) ◽  
pp. R848-R857 ◽  
Author(s):  
R. J. Contreras ◽  
S. King ◽  
L. Rives ◽  
A. Williams ◽  
T. Wattleton
Keyword(s):  
Heart Rate ◽  
Sodium Excretion ◽  
Mild Hypertension ◽  
Weight Cycling ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Sweetened Condensed Milk ◽  
Condensed Milk ◽  
Sprague Dawley Rats ◽  
Dietary Obesity

The present study was designed to reproduce the mild hypertension seen in dietary obese weight-cycled rats [P. Ernsberger and D. O. Nelson. Am. J. Physiol. 254 (Regulatory Integrative Comp. Physiol. 23): R47-R55, 1988] and determine whether this mild hypertension was associated with changes in sodium excretion and pressor responsiveness to angiotensin II (ANG II). Male Sprague-Dawley rats were fed pelleted chow (Pellet group) or chow plus sweetened condensed milk (Milk group) or were exposed to four cycles of a 4-day fast alternated with 2 wk of refeeding of pelleted chow and sweetened condensed milk (Cycled group). Blood pressure and heart rate were measured by tail cuff at the onset and last day of each fast and after 3 days of refeeding. During fasting, urine sodium excretion was measured. Mean arterial pressure and heart rate responses to intravenous administration of ANG II (40, 80, and 120 ng/kg), metoprolol (1 mg/kg), and methyl scopolamine (2 mg/kg) were obtained from the femoral artery in awake unrestrained rats. Weight cycling did not lead to mild hypertension or increased bradycardic response to sympathetic blockade with metoprolol. ANG II-elicited pressor responses were similar for Pellet, Milk, and Cycled groups. Sodium excretion did not change with fasting. Mild hypertension developed when obese weight-cycled rats were housed together in groups and not when housed individually. Our preliminary data are consistent with the notion that stress associated with group housing may be a factor in the mild hypertension of obese weight-cycled rats.

Identification of spontaneous cardiac baroreflex episodes at different timescales in rats

1998 ◽  
Vol 274 (2) ◽  
pp. H488-H493 ◽  
Author(s):  
Marie-Paule Gustin ◽  
Catherine Cerutti ◽  
Robert Unterreiner ◽  
Christian Paultre
Keyword(s):  
Heart Rate ◽  
Sampling Interval ◽  
Statistical Relationship ◽  
Sprague Dawley ◽  
Time Intervals ◽  
Sprague Dawley Rats ◽  
Low Pass ◽  
Freely Moving ◽  
Spontaneous Baroreflex ◽  
Long Timescales

To study spontaneous cardiac baroreflex at different timescales, a new method has been developed that identifies such episodes. Mean arterial pressure (MAP) and heart rate (HR) were recorded beat to beat over 1 h in freely moving control ( n = 10) and acutely (1 day before study, n = 7) and chronically (2 wk before study, n = 10) sinoaortic-denervated (SAD) 12- to 14-wk-old male Sprague-Dawley rats. These beat-to-beat time series were successively low-pass filtered seven times and resampled at different time intervals from 0.1 to 6.4 s, allowing different timescales to be scanned. With the use of the Z coefficient, the statistical relationship was estimated for the associations of inverse MAP and HR variations when these inverse MAP and HR variations occurred simultaneously or were time shifted. In control rats and for timescales ≥0.4 s, the highest Zcoefficient(0.38) was obtained when MAP variations preceded inverse HR variations by one sampling interval. The baroreflex origin of this link was demonstrated by its disappearance after acute SAD. In conclusion, this method enabled spontaneous baroreflex episodes to be identified for unusually long timescales without limiting the study to fast, linear, stationary, or oscillating phenomena.

Spinal cord regulation of sympathetic activity in intact and spinal rats

1994 ◽  
Vol 266 (4) ◽  
pp. H1485-H1493 ◽  
Author(s):  
Y. Hong ◽  
D. F. Cechetto ◽  
L. C. Weaver
Keyword(s):  
Spinal Cord ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Activity ◽  
Excitatory Amino Acid ◽  
Intrathecal Injection ◽  
Cardiovascular Responses ◽  
Homocysteic Acid ◽  
Arterial Blood ◽  
Cord Injury

Excitatory amino acid (EAA) and cholinergic neurotransmission in the spinal cord of urethan-anesthetized rats was investigated to assess mechanisms regulating sympathetic activity after spinal cord injury. Blockade of EAA transmission by intrathecal injection of kynurenic acid decreased arterial blood pressure by 24 +/- 4 mmHg, heart rate by 15 +/- 10 beats/min, and renal sympathetic nerve activity (RSNA) by 85 +/- 4% in intact rats. In rats with cervical spinal transections, this blockade decreased RSNA by 51 +/- 5% and had no effect on arterial pressure and heart rate. Muscarinic blockade by intrathecal atropine decreased RSNA by 12 +/- 3 and 32 +/- 6% in intact and spinal rats, respectively, and caused no cardiovascular responses in either group. Combined blockade of EAA and muscarinic receptors in spinal rats decreased RSNA by 77 +/- 1%. Intrathecal injections of the EAA agonist D,L-homocysteic acid in spinal rats caused initial increases (335 +/- 28%) in RSNA lasting approximately 3 min and later sustained increases (157 +/- 19%) lasting 36 +/- 8 min. Only the early excitation increased arterial pressure by 17 +/- 3 mmHg, and then pressure returned to baseline values. The EAA agonist kainic acid increased RSNA by 402 +/- 90% in spinal rats, an effect lasting 70 +/- 5 min, and increased arterial pressure by only 8 +/- 2 mmHg for 12 +/- 5 min. These findings suggest that tonic activity of spinal neurons with EAA and cholinergic receptors maintains tonic RSNA after spinal cord transection. However, this activity does not play a major role in maintaining arterial pressure, even if it is increased substantially by EAA receptor stimulation.

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