Compensation to exsanguination hypotension in healthy conscious dogs

1963 ◽  
Vol 205 (5) ◽  
pp. 1000-1004 ◽  
Author(s):  
Robert F. Rushmer ◽  
Nolan Watson ◽  
Donald Harding ◽  
Donald Baker
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Human Subjects ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Systemic Arterial Pressure ◽  
Conscious Dogs ◽  
Series Of Experiments ◽  
The Mean ◽  
The Right

In some earlier studies on exsanguination hypotension in conscious dogs, reduction in systemic arterial pressure to shock levels was accompanied by a transient tachycardia during the removal of blood, but the heart rate returned to level, at or near control values during extended periods with the mean arterial pressure between 40 and 60 mm Hg. This observation stimulated a series of experiments on five healthy conscious dogs in which transient hypotension was induced by withdrawing blood from the region of the right atrium to determine which mechanisms were dominant in the compensatory reaction. A surprising degree of variability in response was encountered, such that tachycardia was the main response on some occasions, increased peripheral resistance on others, and in still others, several mechanisms appeared to play a role. Similar variability in the response to exsanguination have been reported in human subjects. These observations suggest that the baroceptor reflexes are not simple servo controls and their role in everyday cardiovascular responses should be re-examined.

Baroreceptor-mediated compensation for hemodynamic effects of positive end-expiratory pressure

1999 ◽  
Vol 86 (1) ◽  
pp. 285-293 ◽  
Author(s):  
Stephen S. Blevins ◽  
Martha J. Connolly ◽  
Drew E. Carlson
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Systemic Arterial Pressure ◽  
Baroreceptor Reflex ◽  
Right Atrial ◽  
Positive End Expiratory Pressure ◽  
Carotid Baroreceptor ◽  
The Right

The roles of the carotid arterial baroreceptor reflex and of vagally mediated mechanisms during positive end-expiratory pressure (PEEP) were determined in pentobarbital-anesthetized dogs with isolated carotid sinuses. Spontaneously breathing dogs were placed on PEEP (5–10 cmH2O) with the carotid sinus pressure set to the systemic arterial pressure (with feedback) or to a constant pressure (no feedback). Right atrial volume was measured with a conductance catheter. With carotid baroreceptor feedback before bilateral cervical vagotomy, total peripheral resistance increased ( P < 0.01) and mean arterial pressure decreased (−9.8 ± 4.3 mmHg) in response to PEEP. With no feedback after vagotomy, mean arterial pressure decreased to a greater extent (−45 ± 6 mmHg, P < 0.01), and total peripheral resistance decreased ( P < 0.05) in response to PEEP. In contrast, cardiac index decreased similarly during PEEP ( P < 0.01) for all baroreceptor and vagal inputs. This response comprised a decrease in the passive phase of right ventricular filling ( P< 0.01) that was not matched by the estimated increase in active right atrial output. Although the carotid baroreceptor reflex and vagally mediated mechanisms elicit vasoconstriction to compensate for the effects of PEEP on the arterial pressure, these processes fail to defend cardiac output because of the profound effect of PEEP on the passive filling of the right ventricle.

Reflex control of vascular capacitance during hypoxia, hypercapnia, or hypoxic hypercapnia

1990 ◽  
Vol 68 (3) ◽  
pp. 384-391 ◽  
Author(s):  
Carl F. Rothe ◽  
A. Dean Flanagan ◽  
Roberto Maass-Moreno
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Systemic Arterial Pressure ◽  
Filling Pressure ◽  
Venous Tone ◽  
Mean Circulatory Filling Pressure ◽  
Vascular Capacitance ◽  
The Mean

We tested the hypothesis that the changes in venous tone induced by changes in arterial blood oxygen or carbon dioxide require intact cardiovascular reflexes. Mongrel dogs were anesthetized with sodium pentobarbital and paralyzed with veruronium bromide. Cardiac output and central blood volume were measured by indocyanine green dilution. Mean circulatory filling pressure, an index of venous tone at constant blood volume, was estimated from the central venous pressure during transient electrical fibrillation of the heart. With intact reflexes, hypoxia (arterial Pao2 = 38 mmHg), hypercapnia (Paco2 = 72 mmHg), or hypoxic hypercapnia (Pao2 = 41; Paco2 = 69 mmHg) (1 mmHg = 133.32 Pa) significantly increased the mean circulatory filling pressure and cardiac output. Hypoxia, but not normoxic hypercapnia, increased the mean systemic arterial pressure and maintained the control level of total peripheral resistance. With reflexes blocked with hexamethonium and atropine, systemic arterial pressure supported with a constant infusion of norepinephrine, and the mean circulatory filling pressure restored toward control with 5 mL/kg blood, each experimental gas mixture caused a decrease in total peripheral resistance and arterial pressure, while the mean circulatory filling pressure and cardiac output were unchanged or increased slightly. We conclude that hypoxia, hypercapnia, and hypoxic hypercapnia have little direct influence on vascular capacitance, but with reflexes intact, there is a significant reflex increase in mean circulatory filling pressure.Key words: cardiovascular reflex, vascular capacitance, hypoxia, hypercapnia, mean circulatory filling pressure, venoconstriction.

Control of arterial pressure in conscious, sinoaortic-denervated sheep in normoxia and hypoxia

1987 ◽  
Vol 253 (6) ◽  
pp. H1409-H1417 ◽  
Author(s):  
M. Miki ◽  
K. Miki ◽  
G. Hajduczok ◽  
D. Curran-Everett ◽  
J. A. Krasney
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Sham Group ◽  
Carotid Sinus ◽  
Peripheral Resistance ◽  
Mean Values ◽  
Coefficients Of Variation ◽  
The Mean ◽  
Arterial Po2 ◽  
Lying Down

The contribution of the sinoaortic reflexes to the control of both the mean level and variability of arterial pressure (Pa) and heart rate (HR) was studied in five adult ewes after chronic section of the carotid sinus and aortic depressor nerves (SAD). SAD group responses were compared with a sham-operated group (n = 6). Pa was 15% lower in the SAD group due to a reduction of total peripheral resistance. The standard deviations and coefficients of variation for both Pa and HR obtained by continuous 16-h monitoring (10-s intervals) in the SAD sheep were not significantly different from those of the sham group. Arterial hypoxia (arterial PO2 = 40 mmHg for 96 h) had no significant influence on the mean values or variability for Pa and HR for either group, although both groups spent more time lying down. Ventilation was unchanged in the SAD group. Thus mean Pa is lower after removal of baroreceptor and chemoreceptor inputs, but the variabilities of both HR and Pa are unaltered during both normoxia and hypoxia in this sedentary species.

scholarly journals Abnormal cardiovascular response to nitroglycerin in migraine

Cephalalgia ◽  
2019 ◽  
Vol 40 (3) ◽  
pp. 266-277
Author(s):  
Willebrordus PJ van Oosterhout ◽  
Guus G Schoonman ◽  
Dirk P Saal ◽  
Roland D Thijs ◽  
Michel D Ferrari ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Cardiovascular Response ◽  
Peripheral Resistance ◽  
Cardiovascular Responses ◽  
Initial Increase

Introduction Migraine and vasovagal syncope are comorbid conditions that may share part of their pathophysiology through autonomic control of the systemic circulation. Nitroglycerin can trigger both syncope and migraine attacks, suggesting enhanced systemic sensitivity in migraine. We aimed to determine the cardiovascular responses to nitroglycerin in migraine. Methods In 16 women with migraine without aura and 10 age- and gender-matched controls without headache, intravenous nitroglycerin (0.5 µg·kg−1·min−1) was administered. Finger photoplethysmography continuously assessed cardiovascular parameters (mean arterial pressure, heart rate, cardiac output, stroke volume and total peripheral resistance) before, during and after nitroglycerin infusion. Results Nitroglycerin provoked a migraine-like attack in 13/16 (81.2%) migraineurs but not in controls ( p = .0001). No syncope was provoked. Migraineurs who later developed a migraine-like attack showed different responses in all parameters vs. controls (all p < .001): The decreases in cardiac output and stroke volume were more rapid and longer lasting, heart rate increased, mean arterial pressure and total peripheral resistance were higher and decreased steeply after an initial increase. Discussion Migraineurs who developed a migraine-like attack in response to nitroglycerin showed stronger systemic cardiovascular responses compared to non-headache controls. The stronger systemic cardiovascular responses in migraine suggest increased systemic sensitivity to vasodilators, possibly due to insufficient autonomic compensatory mechanisms.

Effects of phentolamine on hepatic in endotoxemia

1980 ◽  
Vol 58 (3) ◽  
pp. 281-286 ◽  
Author(s):  
C. R. Kaelin ◽  
R. D. Rink
Keyword(s):  
Escherichia Coli ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Plasma Glucose ◽  
Oxygen Supply ◽  
Hepatic Metabolism ◽  
Systemic Arterial Pressure ◽  
Male Rats ◽  
Adrenergic Blocker ◽  
The Mean

The effect of phentolamine, an α-adrenergic blocker, on hepatic oxygen supply, plasma glucose, and lactate, and survival in fasted male rats administered Escherichia coli endotoxin (25 mg/kg, ip) has been studied. Survival at 24 h was 8% in untreated endotoxic rats, 83% in rats receiving phentolamine (5 mg/kg, ip) and endotoxin, and 100% in phentolamine controls. Measurements during the initial 8 h postendotoxin recorded transiently lower systemic arterial pressure in the phentolamine–endotoxic rats. Arterial [Formula: see text] and increases of pH and heart rate were similar in both endotoxic groups. Lactacidemia, present by 4 h in untreated endotoxic rats, did not develop in the phentolamine group and plasma glucose was significantly higher at 8 h (98 ± 2.5 vs. 77 ± 5.6 mg%, mean ± SE). Mean hepatic [Formula: see text] at 6 h in phentolamine–endotoxic rats was 9.6 mmHg with 28% of the values below 5 mmHg. By contrast, the mean in untreated endotoxic rats was 1.9 mmHg with 88% of values below 5 mmHg. Phentolamine controls were stable over 8 h; mean hepatic [Formula: see text] was 17.7 mmHg. The differences in plasma glucose and lactate suggest protection of hepatic metabolism in phentolamine-treated endotoxic rats by prevention of excessive hepatic hypoxia.

Apparent reduction in baroreflex sensitivity to adenosine in conscious dogs

1985 ◽  
Vol 249 (3) ◽  
pp. H554-H559 ◽  
Author(s):  
T. H. Hintze ◽  
F. L. Belloni ◽  
J. E. Harrison ◽  
G. C. Shapiro
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Muscarinic Receptor ◽  
Baroreflex Sensitivity ◽  
Systemic Arterial Pressure ◽  
Conscious Dogs ◽  
Beta Adrenergic ◽  
Apparent Reduction ◽  
Arterial Plasma ◽  
Plasma Adenosine

Relative effects of equihypotensive doses (-35 mmHg) of adenosine (5.0 mumol/kg) and nitroglycerin (25 micrograms/kg) on heart rate and, therefore, baroreflex sensitivity were studied in conscious dogs. Nitroglycerin increased heart rate 133 +/- 24% from 78 +/- 5.5 beats/min, whereas adenosine increased heart rate only 79 +/- 16% from 78 +/- 5.2 beats/min (P less than 0.01). Injection of nitroglycerin during combined beta-adrenergic and muscarinic receptor blockades caused arterial pressure to fall 38 +/- 3.4% from 107 +/- 3.2 mmHg without any significant change in heart rate (3.8 +/- 3.8 from 162 +/- 9.2 beats/min). During combined beta-adrenergic and muscarinic receptor blockades adenosine also reduced arterial pressure 45 +/- 2.7% from 106 +/- 2.9 mmHg but unexpectedly reduced heart rate as well by 37 +/- 1.7% from 160 +/- 9.7 beats/min. This bradycardia reflected an effect on the sinoatrial (SA) node rather than an induction of heart block, since the R-R interval increased by 70 +/- 7.8% from 371 +/- 20 ms (P less than 0.01), while the P-R interval increased only 13 +/- 2.3% from 97 +/- 7.2 ms (P less than 0.05) with no electrocardiographic evidence of nonconducted beats. Arterial plasma adenosine levels were 43 +/- 5 nmol/ml at this time. Adenosine also caused bradycardia during muscarinic blockade alone (-43 +/- 3.4% from 201 +/- 6.4 beats/min) and following bilateral vagal section (-33 +/- 1.9% from 151 +/- 5.9 beats/min). In summary, adenosine appears to alter normal baroreflex function in the conscious dog by reducing the tachycardia that normally follows a fall in systemic arterial pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Analysis of cardiovascular responses to the H2S donors Na2S and NaHS in the rat

2015 ◽  
Vol 309 (4) ◽  
pp. H605-H614 ◽  
Author(s):  
Daniel Yoo ◽  
Ryan C. Jupiter ◽  
Edward A. Pankey ◽  
Vishwaradh G. Reddy ◽  
Justin A. Edward ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Potassium Channels ◽  
Arterial Pressure ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Vascular Tissue ◽  
Sinus Node ◽  
Cardiovascular Responses ◽  
Systemic Arterial Pressure

Hydrogen sulfide (H2S) is an endogenous gaseous molecule formed from L-cysteine in vascular tissue. In the present study, cardiovascular responses to the H2S donors Na2S and NaHS were investigated in the anesthetized rat. The intravenous injections of Na2S and NaHS 0.03–0.5 mg/kg produced dose-related decreases in systemic arterial pressure and heart rate, and at higher doses decreases in cardiac output, pulmonary arterial pressure, and systemic vascular resistance. H2S infusion studies show that decreases in systemic arterial pressure, heart rate, cardiac output, and systemic vascular resistance are well-maintained, and responses to Na2S are reversible. Decreases in heart rate were not blocked by atropine, suggesting that the bradycardia was independent of parasympathetic activation and was mediated by an effect on the sinus node. The decreases in systemic arterial pressure were not attenuated by hexamethonium, glybenclamide, Nw-nitro-l-arginine methyl ester hydrochloride, sodium meclofenamate, ODQ, miconazole, 5-hydroxydecanoate, or tetraethylammonium, suggesting that ATP-sensitive potassium channels, nitric oxide, arachidonic acid metabolites, cyclic GMP, p450 epoxygenase metabolites, or large conductance calcium-activated potassium channels are not involved in mediating hypotensive responses to the H2S donors in the rat and that responses are not centrally mediated. The present data indicate that decreases in systemic arterial pressure in response to the H2S donors can be mediated by decreases in vascular resistance and cardiac output and that the donors have an effect on the sinus node independent of the parasympathetic system. The present data indicate that the mechanism of the peripherally mediated hypotensive response to the H2S donors is uncertain in the intact rat.

Baroreflex mechanisms buffering alpha-adrenergic agonists in conscious dogs

1987 ◽  
Vol 253 (4) ◽  
pp. H728-H736
Author(s):  
A. M. Fujii ◽  
S. F. Vatner
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Adrenergic Receptor ◽  
Peripheral Resistance ◽  
Conscious Dogs ◽  
Receptor Blockade ◽  
Receptor Agonists ◽  
Alpha Adrenergic Receptor

To determine the relative importance of the mechanisms utilized by the arterial baroreflex in buffering the pressor and vasoconstrictor responses to alpha-adrenergic receptor agonists, we studied responses to norepinephrine and phenylephrine in conscious dogs. The dogs were studied 2-8 wk after instrumentation with aortic catheters and aortic electromagnetic flow probes to measure arterial pressure and cardiac output. Total peripheral resistance was calculated on-line by a digital computer. The dogs were studied after beta-adrenergic receptor blockade (propranolol 1.0 mg/kg) to eliminate the complicating inotropic effects of the agonists studied. Norepinephrine (0.2 microgram/kg bolus) increased mean arterial pressure by 30 +/- 3 mmHg, total peripheral resistance by 51 +/- 4 mmHg . l-1 . min-1, and decreased heart rate by 26 +/- 3 beats/min. After arterial baroreceptor denervation, norepinephrine increased mean arterial pressure by 69 +/- 8 mmHg, total peripheral resistance by 48 +/- 6 mmHg . l-1 . min-1, and heart rate did not change. After ganglionic blockade (hexamethonium 40 mg/kg), norepinephrine increased mean arterial pressure by 76 +/- 3 mmHg, total peripheral resistance by 47 +/- 4 mmHg X l-1 X min-1, and heart rate did not change. Only after elimination of the buffering by heart rate by use of cholinergic receptor blockade (atropine 0.1 mg/kg) or ventricular pacing could buffering of the vasoconstrictor responses to alpha-adrenergic receptor agonists be demonstrated. Thus in conscious dogs the primary mechanism for buffering increases in arterial pressure induced by alpha-adrenergic receptor agonists is compensatory changes in heart rate and cardiac output with little buffering of total peripheral resistance.

Chemical activation of thin-fiber phrenic afferents. 2. Cardiovascular responses

1991 ◽  
Vol 70 (1) ◽  
pp. 77-86 ◽  
Author(s):  
S. N. Hussain ◽  
A. Chatillon ◽  
A. Comtois ◽  
C. Roussos ◽  
S. Magder
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Chemical Activation ◽  
Cardiovascular Responses ◽  
Arterial Flow ◽  
Aortic Blood Flow ◽  
Thin Fiber ◽  
The Right

To assess the effects of groups III and IV (thin-fiber) phrenic afferents on arterial pressure, heart rate, and distribution of cardiac output, we injected capsaicin into phrenic arteries of in situ isolated and innervated left diaphragms of dogs anesthetized with chloralose, vagotomized, and mechanically ventilated. Blood flow in the ascending aorta, common carotid, renal, superior mesenteric, and femoral arteries was measured by electromagnetic and Doppler flow probes. Injection of 1 mg capsaicin into the left phrenic artery produced congruent to 15% increase in mean arterial pressure and congruent to 7% increase in heart rate with no change in aortic flow. Phrenic arterial flow decreased by 64%, renal arterial flow by 16%, and superior mesenteric arterial flow by 10%, whereas carotid flow increased by 13% and flow to the right gastrocnemius muscle did not change. Mean arterial pressure, heart rate, and blood flow distribution (with the exception of the decline in phrenic blood flow) returned to baseline within 60 s of the injection. Injection of 1.5 mg capsaicin into the right isolated and innervated gastrocnemius produced congruent to 35% increase in mean arterial pressure, 17% rise in heart rate, and no change in aortic blood flow. Phrenic and carotid arterial flow rose by 240 and 41%, respectively, whereas renal and superior mesenteric flow declined by 50 and 20%, respectively. In conclusion, thin-fiber phrenic afferents have an excitatory effect on arterial pressure and heart rate. They redistribute blood flow away from the renal and intestinal vascular beds and toward the carotid vascular bed. On the other hand, the cardiovascular reflex from thin-fiber phrenic afferents seems less potent than that from limb muscle afferents.

GABAergic effects on the depressor responses elicited by stimulation of central nucleus of the amygdala

1999 ◽  
Vol 276 (1) ◽  
pp. H242-H247 ◽  
Author(s):  
John Ciriello ◽  
Stefanie Roder
Keyword(s):  
Arterial Pressure ◽  
Receptor Antagonist ◽  
Wistar Rats ◽  
Cardiovascular Responses ◽  
Systemic Arterial Pressure ◽  
The Other ◽  
Central Nucleus ◽  
Male Wistar Rats ◽  
The Mean ◽  
Stimulation Of

GABAergic inputs have been demonstrated in the central nucleus of the amygdala (ACe). However, the contribution of these inhibitory inputs to the cardiovascular responses elicited from the ACe is not known. Experiments were done in chloralose-anesthetized, paralyzed, and artificially ventilated male Wistar rats to investigate the effects of microinjections of GABA, the selective GABAA-receptor antagonist bicuculline, or the GABAB-receptor antagonist phaclofen, in the ACe on the mean arterial pressure (MAP) and heart rate (HR) responses elicited byl-glutamate (Glu) stimulation of the ACe. Microinjections of Glu in the ACe elicited decreases in MAP (−13.7 ± 1.6 mmHg) and HR (−5.3 ± 1.9 beats/min). The MAP and HR responses elicited by Glu stimulation of the ACe were significantly reduced (89%) by the prior microinjection of GABA in the same ACe site. In addition, at some sites in the ACe at which microinjection of Glu did not elicit depressor responses, Glu injections in the presence of phaclofen elicited decreases in MAP (−9.5 ± 1.0 mmHg) and variable changes in HR. On the other hand, the magnitude of the depressor responses elicited during stimulation of the ACe site in the presence of bicuculline was significantly attenuated (60%), whereas phaclofen had no effect on the magnitude of the depressor responses elicited by Glu stimulation of the ACe. These data suggest that GABAergic mechanisms in the ACe alter the excitability of ACe neurons involved in mediating changes in systemic arterial pressure and HR.

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