Cardiovascular responses to insulin in the absence of hypoglycemia

1962 ◽  
Vol 202 (2) ◽  
pp. 249-252 ◽  
Author(s):  
Santiago A. Pereda ◽  
John W. Eckstein ◽  
François M. Abboud
Keyword(s):  
Pressor Response ◽  
Direct Action ◽  
Cardiovascular Responses ◽  
Blocking Agent ◽  
Neuromuscular Blocking ◽  
Right Atrial ◽  
Systemic Vein ◽  
Anesthetized Dogs ◽  
Adrenergic Blocking ◽  
The Brain

Cardiovascular responses to intravenous administration of insulin were studied in lightly anesthetized dogs treated with a neuromuscular blocking agent. An early transient pressor response was observed. This abrupt increase in arterial pressure appeared 2–9 min after insulin was given. It was accompanied by increases in cardiac output and right atrial pressure. It occurred in the presence of hyperglycemia and in the absence of hypoglycemia. It was not altered by glucagon but it could be antagonized by ganglionic and adrenergic blocking drugs and by pentobarbital. The response could be produced when insulin was given in the carotid artery in doses that caused no effect when injected in a systemic vein. The experiments suggest that insulin may have a direct action on the brain.

Inhibition of the cardiovascular response to stress by systemic 5-HT1A activation: sympathoinhibition or anxiolysis?

2009 ◽  
Vol 297 (2) ◽  
pp. R495-R501 ◽  
Author(s):  
Daniel M. L. Vianna ◽  
Pascal Carrive
Keyword(s):  
Restraint Stress ◽  
Systemic Treatment ◽  
Cardiovascular Response ◽  
Direct Action ◽  
Cardiovascular Responses ◽  
Sympathetic Activation ◽  
Sympathetic Response ◽  
Growing Body ◽  
Response To Stress ◽  
The Brain

5-HT1A agonists given systemically are known to produce anxiolytic effects. In addition, a growing body of research is showing that those compounds also have central sympathoinhibitory properties. Since emotional arousal gives rise to sympathetic activation, it is not clear whether systemic treatment with a 5-HT1A agonist reduces the sympathetic response to emotional stress primarily by a direct action on sympathetic-related sites in the brain or indirectly through reducing anxiety. To test this, we compared the effect of intraperitoneal injections of 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT; 0.05 and 0.25 mg/kg), a preferential 5-HT1A agonist, or vehicle on the cardiovascular responses to four stressors known to produce sympathetic activation, three being emotional stressors, and one physiological. In conscious rats, 30-min exposure to either a neutral context, a fear-conditioned context, or to restraint stress led to increases in heart rate and blood pressure, which were attenuated by 8-OH-DPAT. In contrast, the same treatment did not reduce the cardiovascular response to 30-min cold exposure (4°C). The results suggest that 8-OH-DPAT acts preferentially on limbic, rather than central, autonomic sites. Hence, doses of 5-HT1A agonists, which are just sufficient to produce anxiolysis, are not enough to cause true sympathoinhibition.

Increasing gracilis muscle interstitial potassium concentrations stimulate group III and IV afferents

1985 ◽  
Vol 58 (3) ◽  
pp. 936-941 ◽  
Author(s):  
K. J. Rybicki ◽  
T. G. Waldrop ◽  
M. P. Kaufman
Keyword(s):  
Pressor Response ◽  
Cardiovascular Responses ◽  
Muscular Contraction ◽  
Muscle Afferents ◽  
Group Iv ◽  
Gracilis Muscle ◽  
Group Iii ◽  
Arterial Blood ◽  
Static Contraction ◽  
Anesthetized Dogs

Static muscular contraction reflexly increases arterial blood pressure and heart rate. One possible mechanism evoking this reflex is that potassium accumulates in the interstitial space of a working muscle to stimulate group III and IV afferents whose activation in turn evokes a pressor response. The responses of group III and IV muscle afferents to increases in interstitial potassium concentrations within the range evoked by static contraction are unknown. Thus we injected potassium chloride into the gracilis artery of anesthetized dogs while we measured both gracilis muscle interstitial potassium concentrations with potassium-selective electrodes and the impulse activity of afferents in the gracilis nerve. We found that increasing interstitial potassium concentrations to levels similar to those seen during static contraction stimulated 14 of 16 group III and 29 of 31 group IV afferents. The responses of the afferents to potassium were concentration dependent. The typical response to potassium consisted of a burst of impulses, an effect that returned to control firing rates within 26 s, even though interstitial potassium concentrations remained elevated for several minutes. Although our results suggest that potassium may play a role in initiating the reflex cardiovascular responses to static muscular contraction, the accumulation of this ion does not appear to be solely responsible for maintaining the pressor response for the duration of the contraction.

Cardiac output and peripheral blood flow during occlusion of carotid arteries

1961 ◽  
Vol 200 (6) ◽  
pp. 1185-1190 ◽  
Author(s):  
C. Polosa ◽  
G. Rossi
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Pressure Rise ◽  
Blocking Agent ◽  
Carotid Occlusion ◽  
Peripheral Blood Flow ◽  
Cardiac Work ◽  
Anesthetized Dogs

Cardiac output and blood flow to the kidney, hind limb, and splanchnic area were studied in anesthetized dogs during the arterial pressure rise due to carotid occlusion. All the vascular beds studied exhibited an increased resistance to flow. Cardiac output was maintained constant through an increased cardiac work in spite of the increased arterial pressure. This increased cardiac work was reflexly produced as evidenced by the action of the adrenergic blocking agent dichloroisoproterenol (DCI). This drug allowed the reflex vasoconstriction and the consequent pressure rise, but preventing the reflex chronotropic and inotropic sympathetic effects on the heart resulted in a fall of cardiac output during carotid occlusion. It is concluded a) that the reflex increase in vasomotor tone is the main factor in the pressor response to carotid occlusion and b) that the reflex effect on the myocardium is an important factor in regulating cardiac output in this situation.

EFFECT OF ADRENERGIC BLOCKADE AND DEXAMETHASONE ON THE ALDOSTERONE RESPONSE TO BRAIN STIMULATION IN THE RHESUS MONKEY

1976 ◽  
Vol 71 (3) ◽  
pp. 393-397 ◽  
Author(s):  
J. S. JENKINS ◽  
R. J. FRANKEL ◽  
J. J. WRIGHT ◽  
M. U. A. KHAN
Keyword(s):  
Rhesus Monkey ◽  
Plasma Renin ◽  
Blocking Agent ◽  
Hypothalamic Stimulation ◽  
Contributory Factor ◽  
Adrenergic Blockade ◽  
Adrenergic Blocking ◽  
The Brain ◽  
Prior Administration ◽  
Stimulation Of

SUMMARY The increase in aldosterone and plasma renin activity (PRA) observed after stimulation of extrahypothalamic sites within the brain of the rhesus monkey was prevented by the prior administration of the β-adrenergic blocking agent propranolol. α-Adrenergic blockade by phentolamine had no inhibiting effect. Propranolol only partially reduced the response of aldosterone to lateral hypothalamic stimulation in spite of inhibition of PRA; a partial reduction in aldosterone was also obtained from this site after dexamethasone treatment without any effect on PRA. It was concluded that the increase in aldosterone observed after extra-hypothalamic stimulation was mediated mainly through the renin-angiotensin mechanism whereas in the case of the hypothalamus, release of ACTH was also a contributory factor.

Medullary lateral tegmental field mediates the cardiovascular but not respiratory component of the Bezold-Jarisch reflex in the cat

2005 ◽  
Vol 289 (6) ◽  
pp. R1693-R1702 ◽  
Author(s):  
Susan M. Barman ◽  
Shaun W. Phillips ◽  
Gerard L. Gebber
Keyword(s):  
Excitatory Amino Acid ◽  
Pressor Response ◽  
Sympathetic Neurons ◽  
Critical Role ◽  
Cardiovascular Responses ◽  
Nmda Receptor Antagonist ◽  
Right Atrial ◽  
Excitatory Amino Acid Receptor ◽  
Spontaneously Breathing ◽  
Nerve Discharge

We determined the effects of bilateral microinjection of muscimol and excitatory amino acid receptor antagonists into the medullary lateral tegmental field (LTF) on changes in sympathetic nerve discharge (SND), mean arterial pressure (MAP), and phrenic nerve activity (PNA; artificially ventilated cats) or intratracheal pressure (spontaneously breathing cats) elicited by right atrial administration of phenylbiguanide (PBG; i.e., the Bezold-Jarisch reflex) in dial-urethane anesthetized cats. The PBG-induced depressor response (−66 ± 8 mmHg; mean ± SE) was converted to a pressor response after muscimol microinjection in two of three spontaneously breathing cats and was markedly reduced in the other cat; however, the duration of apnea (20 ± 3 vs. 17 ± 7 s) was essentially unchanged. In seven paralyzed, artificially ventilated cats, muscimol microinjection significantly ( P < 0.05) attenuated the PBG-induced fall in MAP (−39 ± 7 vs. −4 ± 4 mmHg) and the magnitude (−98 ± 1 vs. −35 ± 13%) and duration (15 ± 2 vs. 3 ± 2 s) of the sympathoinhibitory response. In contrast, the PBG-induced inhibition of PNA was unaffected (3 cats). Similar results were obtained by microinjection of an N-methyl-d-aspartate (NMDA) receptor antagonist, d(-)-2-amino-5-phosphonopentanoic acid, into the LTF. In contrast, neither the cardiovascular nor respiratory responses to PBG were altered by blockade of non-NMDA receptors with 1,2,3,4-tetrahydro-6-nitro-2,3-dioxobenzo[ f]quinoxaline-7-sulfonamide. We conclude that the LTF subserves a critical role in mediating the sympathetic and cardiovascular components of the Bezold-Jarisch reflex. Moreover, these data show separation of the pathways mediating the respiratory and cardiovascular responses of this reflex at a level central to bulbospinal outflows to phrenic motoneurons and preganglionic sympathetic neurons.

An integrated model for the interaction of muscle relaxants with their antagonists

1986 ◽  
Vol 61 (4) ◽  
pp. 1593-1598 ◽  
Author(s):  
J. D. Unadkat ◽  
L. B. Sheiner ◽  
P. J. Hennis ◽  
R. Cronnelly ◽  
R. D. Miller ◽  
...  
Keyword(s):  
Blocking Agent ◽  
Integrated Model ◽  
Neuromuscular Blocking ◽  
Effect Compartment ◽  
Tibialis Muscle ◽  
Anticholinesterase Agent ◽  
Anesthetized Dogs ◽  
Anterior Tibialis ◽  
Better Than ◽  
Naive Model

An integrated model describing the interaction of nondepolarizing neuromuscular blocking agents with reversible anticholinesterase agents is derived and compared with a naive model using experimental data obtained from four anesthetized dogs. Three consecutive but separate steady-state d-tubocurarine blocks (approximately 50, 70, and 90%) were induced in each of the four dogs and reversed by short edrophonium infusions. Edrophonium arterial concentrations and twitch tension of the anterior tibialis muscle were measured. Both the integrated and the naive model were fit to the twitch tension data using a model with a hypothetical “effect” compartment. The integrated model consistently fit the twitch tension data better than the naive model; the sum of squared deviations was lower by 46, 45, 87, and 69%, respectively, with the integrated model than with the naive model. Also, in contrast to the naive model, the integrated model is capable of describing the interaction of the anticholinesterase agent and the neuromuscular blocking agent when the concentration of either varies with time.

Failure of histamine antagonists to prevent hypoxic pulmonary vasoconstriction in dogs

1976 ◽  
Vol 40 (4) ◽  
pp. 496-500 ◽  
Author(s):  
A. Tucker ◽  
E. K. Weir ◽  
J. T. Reeves ◽  
R. F. Grover
Keyword(s):  
Heart Rate ◽  
Pressor Response ◽  
Hypoxic Pulmonary Vasoconstriction ◽  
Blocking Agent ◽  
Vascular Responses ◽  
Pulmonary Vasoconstriction ◽  
Anesthetized Dogs ◽  
Normal Increase ◽  
Antihistaminic Drug

The role of histamine as a mediator of hypoxic pulmonary vasoconstriction was examined in intact anesthetized dogs. Antagonism of histamine vasoconstrictor (H1) receptors with a classic antihistaminic drug (chlorpheniramine) failed to prevent or modify the pulmonary vascular responses to hypoxia (10% O2). Blockade of histamine vasodilator (H2) receptors with a newly synthesized blocking agent (metiamide) potentiated the vasoconstriction induced by hypoxia and prevented the normal increase in heart rate. Combined H1- and H2-receptor blockade also did not prevent or reduce the hypoxic pulmonary pressor response, although it did effectively abolish the cardiovascular actions of infused histamine. In other dogs, histamine infused (3.6 mug/kg per min) during hypoxia attenuated the pulmonary vasoconstriction induced by hypoxia. The results imply that, in the dog, histamine does not mediate hypoxic pulmonary vasoconstriction. However, histamine does appear to be released during hypoxia, and it may play a role in modulating the pulmonary vascular responses to hypoxia by opposing the hypoxia induced vasoconstriction. The results also imply that histamine may be responsible for the increase in heart rate during hypoxia.

Pressor effect of electroacupuncture on hemorrhagic hypotension

2003 ◽  
Vol 285 (6) ◽  
pp. R1446-R1452 ◽  
Author(s):  
Yi Syuu ◽  
Hiromi Matsubara ◽  
Shingo Hosogi ◽  
Hiroyuki Suga
Keyword(s):  
Pressor Response ◽  
Plasma Catecholamines ◽  
Systolic Pressure ◽  
Blocking Agent ◽  
Scientific Basis ◽  
Left Ventricular ◽  
Neuromuscular Blocking ◽  
Pressor Effect ◽  
Hemorrhagic Hypotension ◽  
End Diastolic Volume

Neiguan (PC-6) is a traditional acupoint in each forearm and overlies the trunk of the median nerve. Previous studies show that electroacupuncture (EA) at the Neiguan acupoint could improve not only myocardial ischemic dysfunction by inducing a depressor response but also recover hemorrhagic hypotension by inducing a pressor response. However, their physiological mechanisms are not yet elucidated. We investigated the pressor effect of Neiguan EA and its mechanism by focusing on left ventricular (LV) performance in a canine hemorrhagic hypotension model. We hemorrhaged 36 anesthetized and thoracotomized mongrel dogs and decreased LV end-systolic pressure (ESP) to ∼70 mmHg (35% decrease). We obtained LV pressure-volume (P-V) data with a micromanometer catheter and a conductance catheter. One-hour Neiguan EA significantly recovered the decreased ESP, end-diastolic volume, and stroke volume by 32 ± 13%, 27 ± 13%, and 39 ± 17%, respectively ( P < 0.05), without changing heart rate and the slope of the end-systolic P-V relation. Neiguan EA inhibited a hemorrhage-induced increase in plasma catecholamines. However, vecuronium (neuromuscular blocking agent) administration abolished the antihypotension effect of Neiguan EA. Furthermore, Neiguan EA was much more effective than a nonacupoint thigh EA. We conclude that Neiguan EA achieved the antihypotension effect by improving LV filling of the hemorrhage-depressed LV performance despite the inhibition of the hemorrhage-increased plasma catecholamines. This pressor effect seemed to accompany an increased venous return by Neiguan EA-increased vasomotor tone and muscle pump. This study demonstrated a scientific basis for the therapeutic efficacy of acupuncture in the treatment of hemorrhagic hypotension and shock.

Haemodynamic Effects of Ketanserin, a Selective 5-Hydroxytryptamine (Serotonin) Receptor Antagonist, in Essential Hypertension

1982 ◽  
Vol 63 (s8) ◽  
pp. 435s-438s ◽  
Author(s):  
G. J. Wenting ◽  
A. J. Man In 'T Veld ◽  
A. J. Woittiez ◽  
F. Boomsma ◽  
M. A. D. H. Schalekamp
Keyword(s):  
Essential Hypertension ◽  
Arterial Pressure ◽  
Serotonin Receptor ◽  
Pressor Response ◽  
Systolic Arterial Pressure ◽  
Blocking Agent ◽  
Systemic Arterial Pressure ◽  
Right Atrial ◽  
Response Curves ◽  
Adrenoceptor Antagonist

1. The new peripherally acting selective 5-hydroxytryptamine receptor blocking agent ketanserin was given (10 mg intravenously) to 17 patients with essential hypertension. 2. Systemic mean systolic arterial pressure fell from 192 ± 6 to 146 ± sem 10 mmHg and mean diastolic arterial pressure fell from 90 ± 4 to 68 ± 5 mmHg. Right atrial pressure, pulmonary arterial pressure and pulmonary capillary ‘wedge’ pressure, measured in 12 patients, were also significantly lowered. Heart rate, cardiac output and plasma noradrenaline rose after ketanserin, probably due to baroreflex-mediated sympathetic stimulation, but the changes were small compared with the fall in systemic arterial pressure. 3. Phenylephrine (50, 100 and 200 μg intravenously) was given to five patients before ketanserin and during continuous infusion of ketanserin (2 mg/h after a loading dose of 10 mg) and dose-response curves for mean systemic arterial pressure were constructed. The pressor response to phenylephrine was not shifted by ketanserin. Thus ketanserin, in a dose capable of lowering systemic arterial pressure, does not act as an α-adrenoceptor antagonist. 4. 5-Hydroxytryptamine receptor blockade appears to cause dilatation of resistance vessels and possibly also of capacitance vessels. The data suggest a hitherto unknown role for 5-hydroxytryptamine in the maintenance of high blood pressure.

Ion channel modifying agents influence the electrical activity generated by canine intrinsic cardiac neurons in situ

2000 ◽  
Vol 78 (4) ◽  
pp. 293-300 ◽  
Author(s):  
Gregory W Thompson ◽  
Magda Horackova ◽  
J Andrew Armour
Keyword(s):  
Ion Channels ◽  
Ion Channel ◽  
Neuronal Activity ◽  
Barium Chloride ◽  
Nickel Chloride ◽  
Blocking Agent ◽  
Right Atrial ◽  
Anesthetized Dogs

This study was designed to establish whether agents known to modify neuronal ion channels influence the behavior of mammalian intrinsic cardiac neurons in situ and, if so, in a manner consistent with that found previously in vitro. The activity generated by right atrial neurons was recorded extracellularly in varying numbers of anesthetized dogs before and during continuous local arterial infusion of several neuronal ion channel modifying agents. Veratridine (7.5 µM), the specific modifier of Na+-selective channels, increased neuronal activity (95% above control) in 80% of dogs tested (n = 25). The membrane depolarizing agent potassium chloride (40 mM) reduced neuronal activity (43% below control) in 84% of dogs tested (n = 19). The inhibitor of voltage-sensitive K+ channels, tetraethylammonium (10 mM), decreased neuronal activity (42% below control) in 73% of dogs tested (n = 11). The nonspecific potassium channel inhibitor barium chloride (5 mM) excited neurons (47% above control) in 13 of 19 animals tested. Cadmium chloride (200 µM), which inhibits Ca2+-selective channels and Ca2+-dependent K+ channels, increased neuronal activity (65% above control) in 79% of dogs tested (n = 14). The specific L-type Ca2+ channel blocking agent nifedipine (5 µM) reduced neuronal activity (52% blow control in 72% of 11 dogs tested), as did the nonspecific inhibitor of L-type Ca2+ channels, nickel chloride (5 mM) (36% below control in 69% of 13 dogs tested). Each agent induced either excitatory or inhibitory responses, depending on the agent tested. It is concluded that specific ion channels (INa, ICaL, IKv, and IKCa) that have been associated with intrinsic cardiac neurons in vitro are involved in their capacity to generate action potentials in situ.Key words: calcium channels, intrinsic cardiac neuron, potassium channels, sodium channels.

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