Peripheral vascular responses to hyperthermia in the rat

1988 ◽  
Vol 64 (6) ◽  
pp. 2582-2588 ◽  
Author(s):  
K. C. Kregel ◽  
P. T. Wall ◽  
C. V. Gisolfi
Keyword(s):  
Elevated Level ◽  
Heat Stroke ◽  
Vascular Response ◽  
Peripheral Vascular ◽  
Sharp Decline ◽  
Vascular Responses ◽  
Doppler Flow ◽  
Arterial Blood ◽  
Unanesthetized Animals ◽  
Skin Temperatures

To investigate the sequence and nature of the peripheral vascular responses during the prodromal period of heat stroke, rats were implanted with Doppler flow probes on the superior mesenteric (SMA), left iliac (LIA) or left renal (LRA), and external caudal (ECA) arteries. Studies were performed in unanesthetized rats (n = 6) exposed to 46 degrees C and in chloralose-anesthetized animals (n = 11) at 40 degrees C. Core (Tc) and tail-skin temperatures, heart rate, and mean arterial blood pressure (MAP) were also monitored. In both groups, prolonged (70–150 min) exposure progressively elevated Tc from 37.0 to 44.0 degrees C. MAP rose to a plateau then fell precipitously as Tc exceeded 41.5 degrees C. SMA resistance increased throughout the early stages of heating, with a sharp decline from this elevated level 10–15 min before the precipitous fall in MAP. ECA resistance fell initially but increased in the terminal stage of heating. In unanesthetized animals, LIA resistance progressively declined. In chloralose-anesthetized animals LRA resistance rose progressively, then increased markedly as Tc exceeded 41.5 degrees C. These data support the hypothesis that a selective loss of compensatory splanchnic vasoconstriction may trigger the cascade of events that characterize heat stroke. This differential vascular response was similar in both unanesthetized and anesthetized animals.

Hemodynamics of hemorrhage in the conscious rat and chicken

1986 ◽  
Vol 251 (5) ◽  
pp. R846-R850 ◽  
Author(s):  
J. M. Ploucha ◽  
G. D. Fink
Keyword(s):  
Vascular Tone ◽  
Peripheral Resistance ◽  
Fluid Loss ◽  
Pulsed Doppler ◽  
Vascular Response ◽  
Peripheral Vascular ◽  
Conscious Rat ◽  
Vascular Responses ◽  
Anesthetic Agents ◽  
On Line

Hemodynamic responses to hemorrhage in conscious chicks (n = 10, 233 g) and rats (n = 10, 309 g) were compared. The animals were fitted with miniature pulsed Doppler aortic flow probes 2 days (chickens) or 5 days (rats) before catheterization, and the experiment began 1 (chickens) or 2 (rats) days later. Mean arterial pressure (MAP) and cardiac output (CO) were recorded continuously and simultaneously digitized to compute total peripheral resistance (TPR). MAP, CO, and TPR values were graphed on-line by a microcomputer and stored for later analysis. A 4-ml hemorrhage reduced MAP and CO by 25 and 43% in the rat, and 15 and 4% in the chickens, respectively. The fall in CO in the rat was due to reduction of stroke volume (SV) unlike the birds where SV was well maintained. TPR was elevated 65% in the rats and fell 13% in the chickens. The minimal fall in CO and SV in these conscious birds suggests that anesthetic agents used previously (i.e., urethane, paraldehyde, phenobarbital, and pentobarbital sodium) suppressed cardiac function. However, they do not account for the lack of a peripheral vascular response during hemorrhage. The chicken apparently maintains MAP by a volume regulating mechanism operating independently of peripheral vascular tone inasmuch as circulating fluid volume restitution is rapid and occurs without vasoconstriction. The rat maintains MAP through reflex cardiac and peripheral vascular responses which eventually may contribute to transvascular fluid loss and the ultimate collapse after prolonged hemorrhagic hypotension.

Gender Differences in Temperature and Vascular Characteristics During Exercise Recovery

2001 ◽  
Vol 26 (5) ◽  
pp. 425-441 ◽  
Author(s):  
Ingrid Marchand ◽  
Dominique Johnson ◽  
David Montgomery ◽  
Guy R. Brisson ◽  
Hélène Perrault
Keyword(s):  
Forearm Blood Flow ◽  
Venous Occlusion ◽  
Fat Free Mass ◽  
Exercise Recovery ◽  
Peripheral Vascular ◽  
Post Exercise ◽  
Men And Women ◽  
Vascular Responses ◽  
Forearm Skin ◽  
Skin Temperatures

Temperature and vascular responses during exercise recovery were examined in men and women of similar age and fitness status ([Formula: see text] 76 ± 5 vs 73 ± 5 mL O2/kg Fat Free Mass • min). Forearm blood flow (venous occlusion plethysmography: FBF), rectal (Trectal) and forearm skin (Tskin) temperatures (°C) were measured before and every 15 min up to 105 min (t105) during recovery from a 45-min run at 75% of [Formula: see text]. Results indicate Trectal decreased to pre-exercise levels within 25 min in men but reached and remained at values lower than baseline between 60 and 105 min of recovery in women. From 90 to 105 min of recovery. Tskin was lower in women than men (t105: 29.0 ± 1.3 vs 30.7 ± 1.5; p < .05). Recovery FBF (mL/100mL • min) was higher in men than women from the start (6.2 ± 1.9 vs 4.9 ± 1.9) to the end of recovery (t105 = 1.7 ± 0.6 vs 2.6 ± 1.1) (p < .05). Heat flux calculated at the forearm was higher in women and increased throughout the last hour of recovery (p < .05). Further investigations are needed to examine mechanisms underlying failure of post-exercise core and skin temperatures in women to stabilize at pre-exeivise levels. Key words: exercise recovery, peripheral vascular resistance, thermoregulation

Vascular responses to catecholamines during respiratory changes in pH

1961 ◽  
Vol 200 (4) ◽  
pp. 755-758 ◽  
Author(s):  
C. W. Nash ◽  
C. Heath
Keyword(s):  
Blood Pressure ◽  
Peripheral Resistance ◽  
Artery Blood Flow ◽  
Vascular Response ◽  
Peripheral Vascular ◽  
Vasomotor Tone ◽  
Vascular Responses ◽  
Blood Ph ◽  
Geometric Factors ◽  
Anesthetized Dogs

The influences of hypercapnia and hyperventilation on peripheral vascular responses to adrenaline and noradrenaline were observed in lightly anesthetized dogs. Changes in the carotid artery blood flow and pressure induced by intra-arterial doses of these amines were measured before, during and after the respiratory changes. During hypercapnia and low blood pH there was a reduced peripheral vascular response, while during hyperventilation and a high pH the vascular response to these drugs increased. However, a fall in blood pressure and flow, and a reflex elevation of the peripheral resistance occurred during both the hyperventilation and the posthypercapnic periods. It appeared that the elevated responses to the amines during those periods of high vasomotor tone may have been produced, in part at least, by the geometric factors involved in resistance, and not entirely by an increased response of the vascular smooth muscle.

Involvement of proteinase activated receptor-2in the vascular response to sphingosine 1-phosphate

2013 ◽  
Vol 126 (8) ◽  
pp. 545-556 ◽  
Author(s):  
Fiorentina Roviezzo ◽  
Antonella De Angelis ◽  
Luana De Gruttola ◽  
Antonio Bertolino ◽  
Nikol Sullo ◽  
...  
Keyword(s):  
Vascular Inflammation ◽  
Vascular Response ◽  
Vascular Effect ◽  
Vascular Responses ◽  
Sphingosine 1 Phosphate

S1P exerts a diverse set of vascular responses, and PAR-2 has been shown to be involved in vascular inflammation as well as in other inflammatory-based diseases. In the present study, we demonstrate that S1P-mediated vascular effect involves PAR-2 activation.

HAEMODYNAMIC CHANGES AND ADRENAL FUNCTION IN MAN DURING INDUCED HYPOGLYCAEMIA

1963 ◽  
Vol 44 (3) ◽  
pp. 430-442 ◽  
Author(s):  
B. Arner ◽  
P. Hedner ◽  
T. Karlefors ◽  
H. Westling
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Mean Arterial Blood Pressure ◽  
Peripheral Vascular ◽  
Adrenocortical Activity ◽  
Arterial Blood ◽  
Haemodynamic Changes ◽  
The Mean ◽  
Temporary Rise ◽  
Catechol Amines

ABSTRACT Observations were made on healthy volunteers during insulin induced hypoglycaemia (10 cases) and infusion of adrenaline (3 cases) or cortisol (1 case). In all cases a rise in the cardiac output was registered during insulin hypoglycaemia. The mean arterial blood pressure was relatively unchanged and the calculated peripheral vascular resistance decreased in all cases. A temporary rise in plasma corticosteroids was observed. After infusion of adrenaline similar circulatory changes were observed but no rise in plasma corticosteroids was found. Infusion of cortisol caused an increased plasma corticosteroid level but no circulatory changes. It is concluded that liberation of catechol amines and increased adrenocortical activity following hypoglycaemia are not necessarily interdependent.

Trait anxiety and peripheral vascular response to mental stress — Sex differences

2008 ◽  
Vol 69 (3) ◽  
pp. 268
Author(s):  
M. Marinov ◽  
Z. Stoyanov ◽  
I. Boncheva ◽  
I. Vartanyan ◽  
T. Chernigovskaya
Keyword(s):  
Sex Differences ◽  
Trait Anxiety ◽  
Mental Stress ◽  
Vascular Response ◽  
Peripheral Vascular

Interaction of hypoxia and hypercapnia on cerebral hemodynamics and brain electrical activity in dogs

1987 ◽  
Vol 253 (4) ◽  
pp. H890-H897 ◽  
Author(s):  
R. W. McPherson ◽  
D. Eimerl ◽  
R. J. Traystman
Keyword(s):  
Partial Pressure ◽  
Elevated Level ◽  
Severe Hypoxia ◽  
O2 Uptake ◽  
Animal Group ◽  
Moderate Hypoxia ◽  
Co2 Partial Pressure ◽  
Arterial Blood ◽  
O2 Partial Pressure ◽  
O2 Delivery

The interaction of hypoxic hypoxia, hypercapnia, and mean arterial blood pressure (MABP) was studied in 15 pentobarbital-anesthetized ventilated dogs. In one group of animals (n = 5) hypercapnia [arterial CO2 partial pressure (PaCO2) approximately 50 Torr] was added to both moderate hypoxia and severe hypoxia. Moderate hypoxia [arterial O2 partial pressure (PaO2) = 36 mmHg] increased MABP and cerebral blood flow (CBF) without changes in cerebral O2 uptake (CMRO2). Superimposed hypercapnia increased CBF and MABP further with no change in CMRO2. In another group of animals (n = 5), a MABP increase of approximately 40 mmHg during moderate hypoxia without hypercapnia did not further increase CBF, suggesting intact autoregulation. Thus, during moderate hypoxia, hypercapnia is capable of increasing CBF. Severe hypoxia (PaO2 = 22 mmHg) increased CBF, but MABP and CMRO2 declined. Superimposed hypercapnia further decreased MABP and decreased CBF from its elevated level and further decreased CMRO2. Raising MABP under these circumstances in another animal group (n = 5) increased CBF above the level present during severe hypoxia alone and increased CMRO2. The change in CBF and CMRO2 during severe hypoxia plus hypercapnia with MABP elevation were not different from that severe hypoxia alone. We conclude that, during hypoxia sufficiently severe to impair CMRO2, superimposed hypercapnia has a detrimental influence due to decreased MABP, which causes a decrease in CBF and cerebral O2 delivery.

Postural vascular response in human skin: passive and active reactions to alteration of transmural pressure

1993 ◽  
Vol 265 (3) ◽  
pp. H949-H958 ◽  
Author(s):  
H. Jepsen ◽  
P. Gaehtgens
Keyword(s):  
External Pressure ◽  
Passive Movement ◽  
Transmural Pressure ◽  
Vertical Position ◽  
Vascular Response ◽  
Pressure System ◽  
Arterial Blood ◽  
Actual Movement ◽  
Low Pressure System ◽  
Skin Blood Vessels

Laser-Doppler (LD) fluxmetry was performed in the palmar finger skin of healthy subjects to study the mechanisms contributing to the postural vascular response. Local transmural pressure in the skin blood vessels of the region studied was altered for 1 min in two experimental series either by passive movement of the arm to different vertical hand positions relative to heart level or by application of external pressure (-120-180 mmHg) to the finger. Heart and respiratory rate, arterial blood pressure, and LD flux in the contralateral finger (kept at heart level) were measured. The measurements suggest a compound reaction of local (myogenic) and systemic (neurogenic) mechanisms: the local regulatory component appears as a graded active vascular response elicited by passive vessel distension or compression. A systemic component, associated with a single deep inspiration, is frequently observed during the actual movement of the arm. In addition, prolonged holding of the test hand in a given vertical position also elicits a delayed vascular response in the control hand at heart level, which may be generated by volume receptors in the intrathoracic low-pressure system.

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