Lesions of the anteroventral third ventricle region (AV3V) disrupt cardiovascular responses to an elevation in core temperature

2005 ◽  
Vol 288 (6) ◽  
pp. R1783-R1790 ◽  
Author(s):  
Douglas G. Whyte ◽  
Alan Kim Johnson
Keyword(s):  
Blood Flow ◽  
Heat Stress ◽  
Core Temperature ◽  
Cardiovascular Response ◽  
Third Ventricle ◽  
Cardiovascular Responses ◽  
Hydration Status ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Electrolytic Lesions

Blood flow is redistributed from the viscera to the periphery during periods of heat stress to maximize heat loss. The heat-induced redistribution of blood flow is strongly influenced by nonthermal inputs such as hydration status. At present, little is known about where thermal and nonthermal information is integrated to generate an appropriate effector response. Recently, the periventricular tissue that surrounds the anteroventral third ventricle (AV3V) has been implicated in the integration of thermal and osmotic information. The purpose of the present study was to determine the effects of electrolytic lesions of the AV3V on the cardiovascular response to a passive heat stress in unanesthetized, free-moving male Sprague-Dawley rats. Core temperature was elevated at a constant rate of ∼0.03°C/min in sham- and AV3V-lesion rats using an infrared heat lamp. Changes in mesenteric and hindquarter vascular resistance were determined using Doppler flow probes, and heat-induced salivation was estimated using the spit-print technique. The rise in mean arterial pressure (MAP), heart rate (HR), and mesenteric resistance in response to elevations in core temperature were all attenuated in AV3V-lesion rats; however, hindquarter resistance was unaffected. Heat-induced salivation was also diminished. In addition, AV3V-lesion rats were more affected by the novelty of the experimental environment, resulting in a higher basal core temperature, HR, and MAP. These results indicate that AV3V lesions disrupt the cardiovascular and salivatory response to a passive heat stress in rats and produce an exaggerated stress-induced fever triggered by a novel environment.

Nitric Oxide in the Gracile Nucleus Mediates Depressor Response to Acupuncture (ST36)

2003 ◽  
Vol 90 (2) ◽  
pp. 780-785 ◽  
Author(s):  
Shuang Chen ◽  
Sheng-Xing Ma
Keyword(s):  
Nitric Oxide ◽  
Cardiovascular Response ◽  
Cardiovascular Responses ◽  
Sprague Dawley ◽  
Arterial Blood ◽  
Gracile Nucleus ◽  
Sprague Dawley Rats ◽  
Antisense Oligos ◽  
Stimulation Of

The purpose of these studies was to determine the role of gracile nucleus and the effects of l-arginine-derived nitric oxide (NO) synthesis in the nucleus on the cardiovascular responses to electroacupuncture (EA) stimulation of “Zusanli” (ST36). Arterial blood pressure and heart rate were monitored during EA stimulation of ST36 following microinjections of agents into gracile nucleus. EA ST36 produced depressor and bradycardiac responses in anesthetized Sprague-Dawley rats. The cardiovascular responses to EA ST36 were blocked by bilateral microinjection of lidocaine into gracile nucleus. Microinjection of l-arginine into gracile nucleus facilitated the hypotensive and bradycardiac responses to EA ST36. The cardiovascular responses to EA ST36 were attenuated by bilateral microinjection of neuronal NO synthase (nNOS) antisense oligos into gracile nucleus. Microinjection of nNOS sense oligos into gracile nucleus did not alter the cardiovascular response to EA ST36. The results demonstrate that a blockade of neuronal conduction in the gracile nucleus inhibits the cardiovascular responses to EA ST36. The hypotensive and bradycardiac responses to EA ST36 are modified by influences of l-arginine-derived NO synthesis in the gracile nucleus. We conclude that NO plays an important role in mediating the cardiovascular responses to EA ST36 through gracile nucleus.

Cardiovascular responses to voluntary and treadmill exercise in rats

1993 ◽  
Vol 75 (3) ◽  
pp. 1334-1340 ◽  
Author(s):  
S. L. Yancey ◽  
J. M. Overton
Keyword(s):  
Blood Flow ◽  
Treadmill Exercise ◽  
Exercise Bout ◽  
Cardiovascular Responses ◽  
Voluntary Exercise ◽  
Treadmill Running ◽  
Sprague Dawley ◽  
Mesenteric Blood Flow ◽  
Doppler Flow ◽  
Sprague Dawley Rats

Male Sprague-Dawley rats (n = 12) were housed in activity wheels and familiarized with treadmill running 2 wk before they were instrumented with Doppler flow probes and a carotid catheter. Mean arterial pressure (MAP), heart rate (HR), mesenteric blood flow (BFmes), and iliac blood flow were determined during bouts of voluntary and treadmill exercise. One voluntary exercise bout (speed = 33 +/- 2 m/min, duration = 26 +/- 5 s) from each rat was selected to compare with 30 s of treadmill exercise at 30 m/min. Voluntary exercise produced increases in MAP (7 +/- 3 mmHg) and HR (63 +/- 7 beats/min) that were significantly less than the increases of 21 +/- 5 mmHg and 95 +/- 9 beats/min, respectively, with treadmill exercise. Voluntary exercise caused an immediate reduction in BFmes of 32 +/- 6%, whereas treadmill exercise produced a significantly greater reduction of 57 +/- 4%. Voluntary and treadmill exercise caused similar increases in iliac blood flow of 112 +/- 15 and 169 +/- 31%, respectively. The patterns of cardiovascular adjustments to the initiation of voluntary exercise are similar to those observed at the initiation of treadmill exercise; however, MAP, HR, and BFmes responses were significantly greater with treadmill exercise.

Influence of autonomic blockade on cardiovascular responses to exercise in rats

1993 ◽  
Vol 75 (1) ◽  
pp. 155-161 ◽  
Author(s):  
J. M. Overton
Keyword(s):  
Blood Flow ◽  
Cardiovascular Responses ◽  
Beta Blockade ◽  
Sprague Dawley ◽  
Exercise Tests ◽  
Sprague Dawley Rats ◽  
Autonomic Blockade ◽  
Atropine Methyl Nitrate ◽  
Exercise Induced ◽  
Response To Exercise

The purposes of this study were to determine the role of the sympathetic and parasympathetic nervous systems in producing the heart rate (HR) response to dynamic exercise in rats and to determine the effect of attenuation of the HR response to exercise on blood flow redistribution. Sprague-Dawley rats (n = 10) were instrumented with arterial and venous catheters and Doppler flow probes. Mean arterial pressure (MAP), HR, mesenteric blood flow (MBF), and iliac blood flow (IBF) were determined during four exercise tests. On 4 consecutive days, rats were treated with saline (SAL, 1 mg/kg iv), atropine methyl nitrate (ATR, 2 mg/kg), timolol maleate (TIM, 0.5 mg/kg), and combined timolol and atropine. One minute of mild exercise (10 m/min) produced an increase in HR of 90 +/- 6 beats/min after SAL treatment, which was significantly less than the increment after ATR (56 +/- 5 beats/min) or TIM (4 +/- 3 beats/min). For the remainder of graded exercise, ATR treatment produced a modest attenuation in the increment in HR and no effect on MAP, IBF, and MBF. At 30 m/min, TIM markedly blunted the exercise-induced increment in HR (SAL, 138 +/- 8 beats/min; TIM, 53 +/- 4 beats/min) and IBF (SAL, 324 +/- 33%; TIM, 197 +/- 33%) with no effect on MAP or MBF. The results suggest that 1) the sympathetic nervous system is an important mediator of exercise-induced tachycardia in rats and 2) exercised-induced hyperemia, but not MAP, is attenuated by nonselective beta-blockade during exercise in rats.

Afferent mechanisms underlying stimulation modality-related modulation of acupuncture-related cardiovascular responses

2005 ◽  
Vol 98 (3) ◽  
pp. 872-880 ◽  
Author(s):  
Wei Zhou ◽  
Liang-Wu Fu ◽  
Stephanie C. Tjen-A-Looi ◽  
Peng Li ◽  
John C. Longhurst
Keyword(s):  
Cardiovascular Response ◽  
Heart Diseases ◽  
Pressor Response ◽  
Low Frequency ◽  
Cardiovascular Responses ◽  
Needle Insertion ◽  
Sham Acupuncture ◽  
Gastric Distension ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

Despite the use of acupuncture to treat a number of heart diseases, little is known about the mechanisms that underlie its actions. Therefore, we examined the influence of acupuncture on sympathoexcitatory cardiovascular responses to gastric distension in anesthetized Sprague-Dawley rats. Thirty minutes of low-current, low-frequency, (0.3–0.5 mA, 2 Hz) electroacupuncture (EA), at P 5–6, S 36–37, and H 6–7 overlying the median, deep peroneal, and ulnar nerves significantly decreased reflex pressor responses by 40, 39, and 44%, respectively. In contrast, sham acupuncture involving needle insertion without stimulation at P 5–6 or 30 min of EA at LI 6–7 acupoints overlying the superficial radial nerve did not attenuate the reflex. Similarly, EA at P 5–6 using 40- or 100-Hz stimulation frequencies did not inhibit the reflex. Compared with EA at P 5–6, EA at two sets of acupoints, including P 5–6 and S 36–37, did not lead to larger inhibition of the reflex. Two minutes of manual acupuncture (MA; 2 Hz) at P 5–6 every 10 min for 30 min inhibited the reflex cardiovascular pressor response by 33%, a value not significantly different from 2-Hz EA at P 5–6. Single-unit afferent activity was not different between electrical stimulation (ES) and manual stimulation. However, 2-Hz ES activated more somatic afferents than 10- or 20-Hz ES. These data suggest that, although the location of acupoint stimulation and the frequency of stimulation determine the extent of influence of EA, there is little difference between low-frequency EA and MA at P 5–6. Furthermore, simultaneous stimulation using two acupoints that independently exert strong effects did not lead to an additive or a facilitative interaction. The similarity of the responses to EA and MA and the lack of cardiovascular response to high-frequency EA appear to be largely a function of somatic afferent responses.

Effect of electroacupuncture on pressor reflex during gastric distension

2002 ◽  
Vol 283 (6) ◽  
pp. R1335-R1345 ◽  
Author(s):  
Peng Li ◽  
Kasra Rowshan ◽  
Melissa Crisostomo ◽  
Stephanie C. Tjen-A-Looi ◽  
John C. Longhurst
Keyword(s):  
Peroneal Nerve ◽  
Cardiovascular Response ◽  
Pressor Response ◽  
Gastric Wall ◽  
Ventrolateral Medulla ◽  
Gastric Distension ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Stomach Meridian ◽  
Pressor Reflex

The effect of electroacupuncture (EA) on the reflex cardiovascular response induced by mechanical distension of the stomach was studied in ventilated male Sprague-Dawley rats anesthetized by ketamine and α-chloralose. Repeated balloon inflation of the stomach to produce 20 mmHg tension on the gastric wall induced a consistent rise in mean arterial pressure, while heart rate (372 ± 22 beats/min) was unchanged. This response was reversed by transection of the splanchnic nerves. Bilateral application of EA (1–2 mA, 2 Hz) at Neiguan-Jianshi acupoints (pericardial meridian, Pe 5–6) over the median nerve for 30 min significantly decreased the pressor response from 33 ± 6 to 18 ± 4 mmHg ( n = 7, P < 0.05). This effect began after 10 min of EA and continued for 40 min after termination of EA. EA at Zusanli-Shangquxu acupoints (stomach meridian, St 36–37) over the deep peroneal nerve similarly inhibited the pressor response. The effect lasted for 10 min after EA was stopped ( n = 6, P < 0.05), while EA at Guangming-Xuanzhong acupoints (gallbladder meridian, GB 37–39) over the superficial peroneal nerve did not inhibit the pressor response. Naloxone injected intravenously ( n = 6) immediately after termination of EA or administered by microinjection into the rostral ventrolateral medulla (rVLM) 25 min after initiation of EA ( n = 6) reversed the inhibition by EA, suggesting an opiate mechanism, including the rVLM, was involved.

Blood flow in normal and denervated muscle during exercise in conscious rats

1988 ◽  
Vol 255 (6) ◽  
pp. H1509-H1515 ◽  
Author(s):  
M. D. Delp ◽  
R. B. Armstrong
Keyword(s):  
Blood Flow ◽  
Muscular Activity ◽  
Sprague Dawley ◽  
Blood Flows ◽  
Sprague Dawley Rats ◽  
Mechanical Factors ◽  
Denervated Muscles ◽  
Gastrocnemius Muscles ◽  
Low Intensity Exercise ◽  
Hyperemic Response

The purpose of this study was to test the hypothesis that extrinsic mechanical factors, i.e., the dynamic shortening and lengthening imposed on a muscle during limb movements and the rhythmic compressions as surrounding muscles contract and relax, contribute to the initial muscle hyperemia during locomotion in conscious male Sprague-Dawley rats. Soleus and lateral head of gastrocnemius muscles were surgically denervated in one hindlimb several hours before exercise to remove 1) local metabolic vasodilator effects, 2) vasoconstrictor or vasodilatory influences mediated through sympathetic postganglionic fibers, and 3) intrinsic mechanical pumping. Blood flow was measured with radioactive microspheres during preexercise and at 30 s and 5 min of exercise in rats walking at 15 m/min or a motor-driven treadmill. Glycogen concentrations were also measured as an indicator of muscular activity to verify the denervation. Blood flows to control muscles in the normal limb were similar to previously reported values during preexercise and exercise. Denervation, however, decreased preexercise blood flow (69–88%) to muscle composed predominantly of oxidative fibers and increased flow (53%) to muscle composed predominantly of glycolytic fibers. During exercise, blood flow to denervated muscles either remained unchanged or decreased. These data suggest that extrinsic mechanical factors do not significantly contribute to the initial hyperemic response at the onset of low-intensity exercise in normal muscle.

Corticosterone tissue-specific response in Sprague Dawley rats under acute heat stress

2019 ◽  
Vol 81 ◽  
pp. 12-19 ◽  
Author(s):  
Jinhuan Dou ◽  
Yuri R. Montanholi ◽  
Zezhao Wang ◽  
Zhongshu Li ◽  
Ying Yu ◽  
...  
Keyword(s):  
Heat Stress ◽  
Specific Response ◽  
Sprague Dawley ◽  
Tissue Specific ◽  
Sprague Dawley Rats ◽  
Acute Heat Stress

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.

scholarly journals Cerebral cortex does not modulate “regulated” decrease in core temperature during hypoxemia in rats

1998 ◽  
Vol 274 (4) ◽  
pp. R1158-R1161
Author(s):  
Evvi-Lynn M. Rollins ◽  
James E. Fewell
Keyword(s):  
Cerebral Cortex ◽  
Core Temperature ◽  
Cortical Spreading Depression ◽  
Spreading Depression ◽  
Temperature Response ◽  
Sprague Dawley ◽  
Adult Rats ◽  
The Core ◽  
Sprague Dawley Rats ◽  
Before And After

In newborns and adults of a number of species including humans, exposure to acute hypoxemia produces a “regulated” decease in core temperature, the mechanism of which is unknown. Considering that various cortical areas participate in autonomic regulation including thermoregulation, the present experiments were carried out to test the hypothesis that the cerebral cortex plays a role in modulating the regulated decrease in core temperature during acute hypoxemia. This hypothesis was tested by determining the core temperature response to acute hypoxemia in chronically instrumented adult Sprague-Dawley rats before and after cortical spreading depression (i.e., functional decortication) was produced by the local application of potassium chloride to the dura overlying the cerebral hemispheres. There was no effect of cortical spreading depression on baseline core temperature. Core temperature decreased during acute hypoxemia in a similar fashion when the cerebral cortex was intact as well as during functional decortication. Thus our data do not support the hypothesis that the cerebral cortex modulates the regulated decrease in core temperature that occurs in adult rats during acute hypoxemia.

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