Short-term cardiovascular responses to a step decrease in peripheral conductance in humans

1994 ◽  
Vol 266 (1) ◽  
pp. H199-H211 ◽  
Author(s):  
K. Toska ◽  
M. Eriksen ◽  
L. Walloe
Keyword(s):  
Pressor Response ◽  
Venous Pressure ◽  
Cardiovascular Responses ◽  
Sudden Increase ◽  
Slow Increase ◽  
Cholinergic Blockade ◽  
Healthy Humans ◽  
Arterial Blood ◽  
Parasympathetic Bradycardia ◽  
Cardiac Stroke Volume

A step decrease in total peripheral conductance (TPC) was introduced in 10 healthy volunteers by rapid inflation to suprasystolic pressure of bilateral thigh cuffs. This provoked a sudden statistically significant increase in mean arterial blood pressure (MAP) of 5 mmHg during supine rest and of 8 mmHg during moderate supine exercise by the quadriceps muscles. Central venous pressure was not changed by cuff inflation. The increase in MAP was blunted by a rapid but transient decrease in both heart rate (HR) and cardiac stroke volume. At rest, a gradual increase in TPC, starting after 4 s, nearly fully restored MAP to its original value at 10 s. During exercise, MAP was halfway corrected at 10 s but then started to increase again, probably as a result of an ischaemic muscle pressor response. After cholinergic blockade by atropine, the immediate HR response was eliminated, but HR decreased gradually after a delay of 3 s. The time development of the slow increase in TPC was not changed by atropine. In conclusion, the regulatory correction of a sudden increase in arterial pressure in supine unanesthetized healthy humans is achieved through an immediate transient parasympathetic bradycardia during the first few seconds and a more gradual sympathetic peripheral vasodilation after 4 s. After cholinergic blockade, a slow presumably sympathetic HR response was observed.

Moderate whole-body heating attenuates the exercise pressor reflex responses in older humans

2021 ◽  
Author(s):  
Jian Cui ◽  
Zhaohui Gao ◽  
Cheryl Blaha ◽  
J. Carter Luck ◽  
Kristen Brandt ◽  
...  
Keyword(s):  
Healthy Subjects ◽  
Pressor Response ◽  
Muscle Sympathetic Nerve Activity ◽  
Cardiovascular Responses ◽  
Whole Body ◽  
Isometric Handgrip ◽  
Healthy Humans ◽  
Arterial Blood ◽  
Isometric Handgrip Exercise ◽  
Fatiguing Exercise

Prior reports show that whole-body heat stress attenuates the pressor response to exercise in young healthy subjects. The effects of moderate whole-body heating (WBH, e.g. increase in internal temperature Tcore ~0.4-0.5 °C) or limb heating on sympathetic and cardiovascular responses to exercise in older healthy humans remains unclear. We examined the muscle sympathetic nerve activity (MSNA), mean arterial blood pressure (MAP) and heart rate (HR) in 14 older (62 ± 2 yrs) healthy subjects during fatiguing isometric handgrip exercise and post exercise circulatory occlusion (PECO). The protocol was performed under normothermic, moderate WBH and local limb (i.e. forearm) heating conditions during 3 visits. During the mild WBH stage (increase in Tcore <0.3 °C), HR increased, whereas BP and MSNA decreased from baseline. Under the moderate WBH condition (increase in Tcore ~0.4 °C), BP decreased, HR increased, while MSNA was unchanged from baseline. Compared with the normothermic trial, the absolute MAP during fatiguing exercise and PECO were lower during the WBH trial. Moreover, MSNA and MAP responses (i.e. changes) to fatiguing exercise were also less than those seen during the normothermic trial. Limb heating induced a similar increase in forearm muscle temperature with that seen in the WBH trial (~0.7-1.5 °C). Limb heating did not alter resting MAP, HR or MSNA. The MSNA and hemodynamic responses to exercise in limb heating trial were not different from those in the normothermic trial. These data suggest that moderate WBH attenuates MSNA and BP responses to exercise in older healthy humans.

Intravenous morphine-induced activation of vagal afferents: peripheral, spinal, and CNS substrates mediating inhibition of spinal nociception and cardiovascular responses

1992 ◽  
Vol 68 (4) ◽  
pp. 1027-1045 ◽  
Author(s):  
A. Randich ◽  
C. L. Thurston ◽  
P. S. Ludwig ◽  
J. D. Robertson ◽  
C. Rasmussen
Keyword(s):  
Intravenous Administration ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Ibotenic Acid ◽  
Vagal Afferents ◽  
Spinothalamic Tract ◽  
Depressor Response ◽  
Arterial Blood ◽  
Intravenous Morphine ◽  
Cervical Vagotomy

1. Intravenous administration of 1.0 mg/kg of morphine produces inhibition of the nociceptive tail-flick (TF) reflex, hypotension, and bradycardia in the pentobarbital-anesthetized rat. The present experiments examined peripheral, spinal, and supraspinal relays for inhibition of the TF reflex and cardiovascular responses produced by morphine (1.0 mg/kg iv) in the pentobarbital-anesthetized rat using 1) bilateral cervical vagotomy, 2) spinal cold block or mechanical lesions of the dorsolateral funiculi (DLFs), or 3) nonselective local anesthesia or soma-selective lesions of specific CNS regions. Intravenous morphine-induced inhibition of responses of unidentified, ascending, and spinothalamic tract (STT) lumbosacral spinal dorsal horn neurons to noxious heating of the hindpaw were also examined in intact and bilateral cervical vagotomized rats. 2. Bilateral cervical vagotomy significantly attenuated inhibition of the TF reflex and bradycardia produced by intravenous administration of morphine. Bilateral cervical vagogtomy changed the normal depressor response produced by morphine into a sustained pressor response. Inhibition of the TF reflex in intact rats was not due to changes in tail temperature. 3. Spinal cold block significantly attenuated inhibition of the TF reflex, the depressor response, and the bradycardia produced by intravenous administration of morphine. However, bilateral mechanical transections of the DLFs failed to significantly affect either inhibition of the TF reflex or cardiovascular responses produced by this dose of intravenous morphine. 4. Microinjection of either lidocaine or ibotenic acid into the nuclei tracti solitarii (NTS), rostromedial medulla (RMM), or ventrolateral pontine tegmentum (VLPT) attenuated morphine-induced inhibition of the TF reflex. Similar microinjections into either the periaqueductal gray (PAG) or the dorsolateral pons (DLP) failed to affect morphine-induced inhibition of the TF reflex. 5. Microinjection of either lidocaine or ibotenic acid into the NTS, RMM, VLPT, DLP, or rostral ventrolateral medulla (RVLM) attenuated the depressor response produced by morphine, although baseline arterial blood pressure (ABP) was affected by ibotenic acid microinjections in the DLP. In all these cases, the microinjections failed to reveal a sustained pressor response as was observed with bilateral cervical vagotomy. Similar microinjections into the PAG failed to affect the depressor response produced by morphine. 6. The lidocaine and ibotenic acid microinjection treatments also showed that the bradycardic response produced by morphine depends on the integrity of the NTS, RMM, RVLM, and possibly the DLP, but not the PAG or VLPT.(ABSTRACT TRUNCATED AT 400 WORDS)

Umbilical venous pressure and other cardiovascular responses of fetal lambs to epinephrine

1962 ◽  
Vol 203 (5) ◽  
pp. 955-960 ◽  
Author(s):  
S. R. M. Reynolds ◽  
John D. Mackie
Keyword(s):  
Blood Pressure ◽  
Umbilical Vein ◽  
Venous Pressure ◽  
Cardiovascular Responses ◽  
Ductus Venosus ◽  
Arterial Blood ◽  
Femoral Route ◽  
The Difference ◽  
Pregnant Ewe

Large fetuses in utero are more sensitive to infused epinephrine than smaller ones. The quality of response is the same. Increased arterial blood pressure and heart rate are associated with an increase in umbilical vein pressure. The large fetus is as sensitive as the pregnant ewe and the latter is more sensitive than the nonpregnant ewe. Single injections of epinephrine into umbilical or femoral veins have similar effects, except for the difference that the latent period is about twice as long when epinephrine is given by the femoral route as by the umbilical route. The sphincter of the ductus venosus is believed to constrict in response to epinephrine. It is shown to be adrenergically controlled. The import of the sphincter for maintenance of umbilical vein pressure is considered.

Measurement Of Bradykinin-Induced Venous Dilation By Ultrasound And Correlation With Heart Rate, Arterial And Venous Pressure And Endothelial Damage

1981 ◽  
Author(s):  
G J Stewart ◽  
R G Schaub ◽  
R E Cartee
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Blood Pressure ◽  
Carotid Arteries ◽  
Jugular Vein ◽  
Venous Pressure ◽  
Cardiovascular Responses ◽  
Endothelial Damage ◽  
Whole Body ◽  
Arterial Blood

This study was done to correlate known cardiovascular responses to bradykinin (increased heart rate, lowered arterial blood pressure) with recently demonstrated endothelial damage and proposed venous dilation. Healthy dogs of mixed breed were used. Blood pressures and heart rate were monitored and recorded on a Narco physiograph. The diameter of a jugular vein was monitored with an ADR ultrasound machine using a 10 MHz probe with linear array of crystals and recorded on polaroid prints. Jugular veins and carotid arteries were removed and prepared for scanning electron microscopy after removal of blood and partial in situ fixation by whole body perfusion. The response of arterial pressure was dose dependent with no change at 6 ug/min, variable drop at 12 ug/min and 22-40% drop at 60 ug/min and above. Venous pressure increased in 1 dog but was unchanged in 4 others. The increase of heart rate paralled the drop in arterial blood pressure. The diameter of a jugular vein increased in 3 of 3 monitored dogs by 25, 33, 50% of baseline diameter (average increase 36%) with high (300 ug/min) bradykinin. Endothelial damage (microtears) occurred around 70-80% of branches, at some valves and on the main vessel occassionally. The tears were infiltrated with leukocytes and some red cells and platelets indicating that tearing occurred while blood was still circulating, i.e. before dissection for removal of vessels. Carotid arteries showed no tears. Dilation of arteries would be limited by their elastic layers (missing in veins). These observations show that venous dilation and endothelial tearing around side branches are part of the cardiovascular response to blood born bradykinin. They also show that venous dilation can be measured by ultrasound.

scholarly journals Effects of endothelin-1 and homologous trout endothelin on cardiovascular function in rainbow trout

2000 ◽  
Vol 278 (2) ◽  
pp. R460-R468 ◽  
Author(s):  
Todd M. Hoagland ◽  
Leroy Weaver ◽  
J. Michael Conlon ◽  
Yugi Wang ◽  
Kenneth R. Olson
Keyword(s):  
Pressor Response ◽  
Venous Pressure ◽  
Cardiovascular Function ◽  
Cardiovascular Responses ◽  
Aortic Pressure ◽  
Systemic Resistance ◽  
Central Venous ◽  
Venous Compliance ◽  
Venous Infusion ◽  
Dose Dependent

The cardiovascular effects of endothelin (ET)-1 and the recently sequenced homologous trout ET were examined in unanesthetized trout, and vascular capacitance curves were constructed to evaluate the responsiveness of the venous system to ET-1. A bolus dose of 667 pmol/kg ET-1 doubled ventral aortic pressure; produced a triphasic pressor-depressor-pressor response in dorsal aortic pressure (PDA); increased central venous pressure, gill resistance, and systemic resistance; and decreased cardiac output, heart rate, and stroke volume. These responses were dose dependent. Bolus injection of trout ET (333 or 1,000 pmol/kg) produced essentially identical, dose-dependent cardiovascular responses as ET-1. Dorsal aortic infusion of 1 and 3 pmol ⋅ kg− 1 ⋅ min− 1ET-1 and central venous infusion into the ductus Cuvier of 0.3 and 1 pmol ⋅ kg− 1 ⋅ min− 1produced similar dose-dependent cardiovascular responses, although the increase in PDA became monophasic. The heightened sensitivity to central venous infusion was presumably due to the more immediate exposure of the branchial vasculature to the peptide. Infusion of 1 pmol ⋅ kg− 1 ⋅ min− 1ET-1 decreased vascular compliance but had no effect on unstressed blood volume. These results show that ETs affect a variety of cardiovascular functions in trout and that branchial vascular resistance and venous compliance are especially sensitive. The multiplicity of effectors stimulated by ET suggests that this peptide was extensively integrated into cardiovascular function early on in vertebrate phylogeny.

Differences in the dynamic cerebrovascular response between stepwise up tilt and down tilt in humans

2001 ◽  
Vol 281 (2) ◽  
pp. H774-H783 ◽  
Author(s):  
Jiro Sato ◽  
Masatoshi Tachibana ◽  
Tsutomu Numata ◽  
Takashi Nishino ◽  
Akiyoshi Konno
Keyword(s):  
Doppler Ultrasonography ◽  
Cerebral Blood Flow Velocity ◽  
Cardiovascular Responses ◽  
Second Order ◽  
Order Model ◽  
Healthy Humans ◽  
Arterial Blood ◽  
Critical Closing Pressure ◽  
Closing Pressure ◽  
Second Order Model

We studied dynamic cerebrovascular responses in eight healthy humans during repetitive stepwise upward tilt (SUT) and stepwise downward tilt (SDT) maneuvers between supine and 70° standing at intervals of 60 s. Mean cerebral blood flow velocity (FVMCA) was measured at the middle cerebral artery (MCA) with transcranial Doppler ultrasonography. Mean arterial blood pressure (ABP) was measured via the radial artery and adjusted at the level of the MCA (ABPMCA). Cerebral critical closing pressure (PCC) was estimated from the systolic-diastolic relationship between FVMCA and ABPMCA. ABPMCA minus PCC was considered the cerebral perfusion pressure (CPP). The tilt maneuvers produced stepwise changes in both CPP and FVMCA. The FVMCA response to SUT was well characterized by a linear second-order model. However, that to SDT presented a biphasic behavior that was described significantly better ( P < 0.05) by the addition of a slowly responding component to the second-order model. This difference may reflect both different cardiovascular responses to SUT or SDT and different cerebrovascular autoregulatory behaviors in response to decreases or increases in CPP.

Integrated autonomic and behavioral responses to L/N Ca2(+)-channel blocker omega-conotoxin in conscious rats

1990 ◽  
Vol 259 (3) ◽  
pp. R427-R438
Author(s):  
S. Shapira ◽  
O. M. Adeyemo ◽  
G. Feuerstein
Keyword(s):  
Pressor Response ◽  
Cardiovascular Responses ◽  
Motor Deficits ◽  
Channel Blockers ◽  
Gamma Aminobutyric Acid ◽  
Central Administration ◽  
Arterial Blood ◽  
Behavioral Variables ◽  
Ca2 Channels

omega-Conotoxin (omega-ctx) was used as a probe for studying the putative role of brain L/N-type Ca2+ channels in regulation of autonomic functions. Rats were injected intracerebroventricularly (icv) with omega-ctx, and hemodynamic, biochemical and behavioral variables were monitored. omega-Ctx (0.032-10 nmol/kg) caused a persistent, dose-dependent shaking behavior, complex thermoregulatory changes, and motor deficits lasting up to 48 h. Cardiovascular responses to omega-ctx included tachycardia (+71 +/- 16%, P less than 0.01) and elevated arterial blood pressure (+16 +/- 1%, P less than 0.05) associated with increased circulating levels of norepinephrine and epinephrine. Higher doses, 1 or 10 nmol/kg, resulted in circulatory shock and death. Central administration of 3,4,5-trimethoxybenzoic acid 8-(diethylamino)octyl ester (TMB-8), diltiazem (100 or 1,000 nmol/kg), neomycin (100 nmol/kg, each), nifedipine (10 nmol/kg), and CdCl2 (100 nmol/kg), which represent intracellular, non-specific N-, L-, and L/N-type Ca2(+)-channel blockers, respectively, did not cause any behavioral or hemodynamic effects, whereas the L-channel agonist BAY K 8644 (100 nmol/kg icv) caused a mild transient pressor response. Pretreatment with the gamma-aminobutyric acid (GABA) agonist muscimol (icv) or a combined intravenous pretreatment with propranolol and N-methylatropine blocked the omega-ctx effects. Our data suggest that omega-ctx actions in the brain involve central GABAergic mechanisms modulated by yet a different type of Ca2+ channels not characterized by any of the known voltage-operated Ca2+ channels.

Peripheral vasoconstriction shortly after onset of moderate exercise in humans

1994 ◽  
Vol 77 (3) ◽  
pp. 1519-1525 ◽  
Author(s):  
K. Toska ◽  
M. Eriksen
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Cardiovascular Responses ◽  
Pressure Control ◽  
Set Point ◽  
Peripheral Vasoconstriction ◽  
Cholinergic Blockade ◽  
Healthy Humans ◽  
Exercise Period

The immediate cardiovascular responses at the onset of supine dynamic leg exercise were studied by noninvasive methods in healthy humans. Total peripheral conductance (TPC), heart rate, and cardiac output increased very rapidly at the onset of exercise. Mean arterial pressure (MAP) showed a moderate anticipatory increase during a 10-s countdown to exercise and then decreased (but not below resting level) during the first 10 s of exercise. The TPC response was biphasic, and TPC started to fall from its peak value approximately 12 s after onset of exercise. This peripheral vasoconstriction increased MAP. After 25 s, the cardiovascular variables were stable for the rest of the 2-min exercise period. In the same subjects, cholinergic blockade was induced by atropine sulfate (0.035 mg/kg) and resting cardiac output, MAP, and TPC increased considerably. The exercise protocol was repeated after atropine, and the increase in heart rate at onset of exercise was slower and smaller. MAP decreased and remained depressed throughout the exercise period. A monophasic increase in TPC was seen. We suggest that, in the normal situation, the biphasic response in TPC reflects a baroreflex sympathetic vasoconstriction very shortly after onset of exercise and that this response is due to a rapid increase in set point for arterial pressure control at the onset of exercise. After cholinergic blockade, MAP was probably continuously well above the set point for arterial pressure control both before and during exercise and no reflex vasoconstriction was observed in this situation.

Cardiovascular and sensory responses to forearm ischemia and dynamic hand exercise

1990 ◽  
Vol 259 (6) ◽  
pp. R1156-R1163 ◽  
Author(s):  
W. Maixner ◽  
R. H. Gracely ◽  
J. R. Zuniga ◽  
C. B. Humphrey ◽  
G. R. Bloodworth
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Cardiovascular Responses ◽  
Ischemic Pain ◽  
Adaptive Responses ◽  
Healthy Humans ◽  
Arterial Blood ◽  
Tightly Coupled ◽  
Sensory Responses ◽  
The Relationship

The relationship between cardiovascular responses and pain produced by the submaximal-effort tourniquet procedure was evaluated in healthy humans. Graded increases in ischemic pain were associated with graded elevations in arterial blood pressure, forearm vascular resistance, and venous tone. Many of the vascular responses to muscle ischemia were typical of the cardiovascular components of the defense reaction and correlated with both the sensory and affective aspects of ischemic pain. The cardiovascular responses to arm ischemia were distinguishable from those produced by rhythmic hand exercise used to produce ischemia. Dynamic hand exercise produced a transient increase in arterial blood pressure, heart rate, and measures of hand discomfort. These responses were enhanced when dynamic hand exercise was conducted under ischemic conditions. The tightly coupled and coordinated cardiovascular responses elicited by ischemic pain represent integrated adaptive responses to painful stimulation.

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.

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