Central control of sympathetic cardiac augmentation in lower brain stem of the cat

1963 ◽  
Vol 205 (4) ◽  
pp. 749-753 ◽  
Author(s):  
C. Y. Chai ◽  
Norman N. Share ◽  
S. C. Wang
Keyword(s):  
Brain Stem ◽  
Carotid Arteries ◽  
Control Mechanism ◽  
Cardiovascular Responses ◽  
Central Control ◽  
Direct Stimulation ◽  
Vasomotor Reaction ◽  
Lower Brain Stem ◽  
Dorsal Medulla ◽  
Stimulation Of

Fifty-three vagotomized cats under chloralose were studied for cardiac augmentation, cardioacceleration, and vasomotor reaction on direct stimulation of the medulla oblongata and via reflex activations. Cardiac augmentation as well as other cardiovascular responses could be induced on stimulation of the dorsal medulla or the central cut end of the sciatic nerves, or on occlusion of the carotid arteries. The augmentation and other responses remained essentially unchanged regardless of the presence or absence of the rostral neural structures, including the hypothalamus. The results confirm and support the concept that a central control mechanism for vasomotor reaction and cardioacceleration as well as augmentation resides in the dorsal region of the lower brain stem.

Central control of sympathetic cardioacceleration in medulla oblongata of the cat

1962 ◽  
Vol 202 (1) ◽  
pp. 31-34 ◽  
Author(s):  
S. C. Wang ◽  
C. Y. Chai
Keyword(s):  
Heart Rate ◽  
Sciatic Nerve ◽  
Medulla Oblongata ◽  
Carotid Arteries ◽  
Regulatory Function ◽  
Central Control ◽  
The Common ◽  
Common Carotid Arteries ◽  
Dorsal Medulla ◽  
Stimulation Of

Under chloralose, as well as under pentobarbital anesthesia, stimulation of the dorsal medulla elicited after decerebration a cardioacceleration comparable to that before decerebration. Similar increases in the heart rate were also obtained after additional ablation of the remaining midbrain and portion of the pons. In addition, it is possible in these decerebrate animals to elicit cardioaccelerator reflexes by occluding the common carotid arteries or by stimulating the central end of the sciatic nerve. Our findings are contrary to those reported by Peiss ( J. Physiol., London 151: 225, 1960) and do not support his contention that the dorsal medulla constitutes only an afferent cardioaccelerator pathway to the hypothalamus. Our results support the concept that an important integrative mechanism for cardioacceleration, as well as for vasomotor reaction, resides in the dorsal medulla, and that higher neural structures such as the hypothalamus serve a regulatory function.

Gastric motor and cardiovascular effects of insulin in dorsal vagal complex of the rat

1998 ◽  
Vol 275 (5) ◽  
pp. G964-G972 ◽  
Author(s):  
Zbigniew K. Krowicki ◽  
Nicole A. Nathan ◽  
Pamela J. Hornby
Keyword(s):  
Blood Pressure ◽  
Brain Stem ◽  
Pancreatic Polypeptide ◽  
Contractile Activity ◽  
Porcine Insulin ◽  
Dorsal Vagal Complex ◽  
Intragastric Pressure ◽  
Lower Brain Stem ◽  
Motor Effects ◽  
Dorsal Medulla

Insulin-binding sites exist in the lower brain stem of the rat, raising the possibility that the circulating hormone may have cardiovascular and gastric effects at this site. Therefore, we investigated the autonomic effects of applying rat insulin to the surface of the dorsal medulla (0.3 and 3 μU/rat) or microinjecting it into the dorsal vagal complex (DVC) (0.1–10 nU/site) in anesthetized rats. Application of rat insulin to the surface (3 μU/rat) and its microinjection into the DVC (1 and 10 nU/site) both evoked marked, albeit transient, increases in intragastric pressure, pyloric and greater curvature contractile activity, and blood pressure. Much higher doses of human (100 mU) and porcine insulin (3 mU) were needed to evoke modest changes in gastric motor and cardiovascular function when applied to the surface of the dorsal medulla. In addition, a 1,000-fold higher dose of porcine insulin (10 μU) in the DVC was not enough to mimic the autonomic effects of rat insulin microinjected into the same site. The excitatory gastric motor effects of rat insulin in the lower brain stem were abolished by vagotomy, whereas spinal cord transection blocked insulin-evoked increases in blood pressure. To test whether the gastric motor effects of rat insulin in the lower brain stem were caused by potential contamination with pancreatic polypeptide, we microinjected rat pancreatic polypeptide into the DVC at a single dose of 2 pmol. Only a modest increase in intragastric pressure in response to the hormone was observed. Thus it is likely that insulin, through its action in the lower brain stem, may be implicated in the pathogenesis of gastrointestinal and cardiovascular complications in hyperinsulinemia. In addition, species variations in the amino acid sequence of insulin may affect its biological activity in the brain of different species.

Effects of insulin on the cardiovascular integrating mechanisms of brain stem in cats

1993 ◽  
Vol 265 (4) ◽  
pp. E609-E616 ◽  
Author(s):  
S. W. Kuo ◽  
J. H. Hsieh ◽  
W. C. Wu ◽  
H. T. Horng ◽  
L. R. Shian ◽  
...  
Keyword(s):  
Brain Stem ◽  
Cardiovascular Responses ◽  
Serum Glucose ◽  
Ventrolateral Medulla ◽  
Reticular Nucleus ◽  
Motor Nucleus ◽  
Renal Nerve ◽  
Pressor Responses ◽  
The Brain ◽  
Stimulation Of

In 65 cats anesthetized with alpha-chloralose and urethane, the effects of insulin on cardiovascular responses to stimulation of various structures in the brain stem were studied. The threshold dose of insulin injected intravenously that produced systemic hypoglycemia was 5-10 U/kg. Subthreshold hypoglycemic doses of insulin were used intracerebroventricularly (0.25 U/kg) or intracerebrally (2 mU in 200 nl). Sixty minutes after intravenous insulin, when serum glucose concentrations decreased from 158 to 43 mg/100 ml, pressor responses to stimulation of the periaqueductal gray of midbrain (PAG), locus coeruleus (LC), dorsal medulla (DM), ventrolateral medulla (VLM), and parvocellular reticular nucleus (PVC) decreased significantly. Depressor and bradycardiac response to stimulation of paramedian reticular nucleus or dorsal motor nucleus of vagus (DMV) decreased significantly as well. Thirty minutes after intracerebroventricular insulin, pressor responses of PAG, DM, and the bradycardiac response of DMV decreased significantly. Thirty minutes after intracerebral insulin, pressor responses and renal nerve activities of LC (but not PAG), VLM, DM, and PVC decreased significantly. A similar but faster onset (5 min) of depression of cardiovascular responses on stimulating the LC, VLM, DM, and PVC was observed in another six acutely midcollicular-decerebrate cats recovered from halothane anesthesia. These findings suggest that insulin directly inhibits the vasomotor structures of the brain stem and decreases the pressor responses to stimulation.

scholarly journals Reflex cardiovascular responses originating in exercising muscles of mice

2001 ◽  
Vol 90 (2) ◽  
pp. 579-585 ◽  
Author(s):  
Jeffery M. Kramer ◽  
Arthur Aragones ◽  
Tony G. Waldrop
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Muscle Contraction ◽  
Cardiovascular Responses ◽  
Muscular Contraction ◽  
Dependent Manner ◽  
Direct Stimulation ◽  
Systemic Hypoxia ◽  
Dose Dependent ◽  
Stimulation Of

The cardiovascular responses induced by exercise are initiated by two primary mechanisms: central command and reflexes originating in exercising muscles. Although our understanding of cardiovascular responses to exercise in mice is progressing, a murine model of cardiovascular responses to muscle contraction has not been developed. Therefore, the purpose of this study was to characterize the cardiovascular responses to muscular contraction in anesthetized mice. The results of this study indicate that mice demonstrate significant increases in blood pressure (13.8 ± 1.9 mmHg) and heart rate (33.5 ± 11.9 beats/min) to muscle contraction in a contraction-intensity-dependent manner. Mice also demonstrate 23.1 ± 3.5, 20.9 ± 4.0, 21.7 ± 2.6, and 25.8 ± 3.0 mmHg increases in blood pressure to direct stimulation of tibial, peroneal, sural, and sciatic hindlimb somatic nerves, respectively. Systemic hypoxia (10% O2-90% N2) elicits increases in blood pressure (11.7 ± 2.6 mmHg) and heart rate (42.7 ± 13.9 beats/min), while increasing arterial pressure with phenylephrine decreases heart rate in a dose-dependent manner. The results from this study demonstrate the feasibility of using mice to study neural regulation of cardiovascular function during a variety of autonomic stimuli, including exercise-related drives such as muscle contraction.

Brain stem mechanisms underlying acupuncture modality-related modulation of cardiovascular responses in rats

2005 ◽  
Vol 99 (3) ◽  
pp. 851-860 ◽  
Author(s):  
Wei Zhou (Yi Syuu) ◽  
Stephanie C. Tjen-A-Looi ◽  
John C. Longhurst
Keyword(s):  
Brain Stem ◽  
Median Nerve ◽  
Sympathetic Neurons ◽  
Low Frequency ◽  
Cardiovascular Responses ◽  
Splanchnic Nerve ◽  
Thoracic Spinal Cord ◽  
Median Nerve Stimulation ◽  
Cardiovascular Neurons ◽  
Stimulation Of

The present study was designed to investigate brain stem responses to manual acupuncture (MA) and electroacupuncture (EA) at different frequencies at pericardial P (5–6) acupoints located over the median nerve. Activity of premotor sympathetic cardiovascular neurons in the rostral ventral lateral medulla (rVLM) was recorded during stimulation of visceral and somatic afferents in ventilated anesthetized rats. We stimulated either the splanchnic nerve at 2 Hz (0.1–0.4 mA, 0.5 ms) or the median nerve for 30 s at 2, 10, 20, 40, or 100 Hz using EA (0.3–0.5 mA, 0.5 ms) or at ∼2 Hz with MA. Twelve of 18 cells responsive to splanchnic and median nerve stimulation could be antidromically driven from the intermediolateral columns of the thoracic spinal cord, T2–T4, indicating that they were premotor sympathetic neurons. All 18 neurons received baroreceptor input, providing evidence of their cardiovascular sympathoexcitatory function. Evoked responses during stimulation of the splanchnic nerve were inhibited by 49 ± 6% ( n = 7) with EA and by 46 ± 4% ( n = 6) with MA, indicating that the extent of inhibitory effects of the two modalities were similar. Inhibition lasted for 20 min after termination of EA or MA. Cardiovascular premotor rVLM neurons responded to 2-Hz electrical stimulation at P 5–6 and to a lesser extent to 10-, 20-, 40-, and 100-Hz stimulation (53 ± 10, 16 ± 2, 8 ± 2, 2 ± 1, and 0 ± 0 impulses/30 stimulations, n = 7). These results indicate that rVLM premotor sympathetic cardiovascular neurons that receive convergent input from the splanchnic and median nerves during low-frequency EA and MA are inhibited similarly for prolonged periods by low-frequency MA and EA.

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