scholarly journals Attenuated muscle metaboreflex-induced increases in cardiac function in hypertension

2013 ◽  
Vol 305 (10) ◽  
pp. H1548-H1554 ◽  
Author(s):  
Javier A. Sala-Mercado ◽  
Marty D. Spranger ◽  
Rania Abu-Hamdah ◽  
Jasdeep Kaur ◽  
Matthew Coutsos ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Cardiac Function ◽  
Peripheral Resistance ◽  
Artery Occlusion ◽  
Left Ventricular ◽  
Exercise Intolerance ◽  
Muscle Metaboreflex ◽  
Cardiac Responses

Sympathoactivation may be excessive during exercise in subjects with hypertension, leading to increased susceptibility to adverse cardiovascular events, including arrhythmias, infarction, stroke, and sudden cardiac death. The muscle metaboreflex is a powerful cardiovascular reflex capable of eliciting marked increases in sympathetic activity during exercise. We used conscious, chronically instrumented dogs trained to run on a motor-driven treadmill to investigate the effects of hypertension on the mechanisms of the muscle metaboreflex. Experiments were performed before and 30.9 ± 4.2 days after induction of hypertension, which was induced via partial, unilateral renal artery occlusion. After induction of hypertension, resting mean arterial pressure was significantly elevated from 98.2 ± 2.6 to 141.9 ± 7.4 mmHg. The hypertension was caused by elevated total peripheral resistance. Although cardiac output was not significantly different at rest or during exercise after induction of hypertension, the rise in cardiac output with muscle metaboreflex activation was significantly reduced in hypertension. Metaboreflex-induced increases in left ventricular function were also depressed. These attenuated cardiac responses caused a smaller metaboreflex-induced rise in mean arterial pressure. We conclude that the ability of the muscle metaboreflex to elicit increases in cardiac function is impaired in hypertension, which may contribute to exercise intolerance.

Chronic Ablation of TRPV1 Sensitive Skeletal Muscle Afferents Attenuates the Muscle Metaboreflex

2021 ◽  
Author(s):  
Joseph Mannozzi ◽  
Mohamed-Hussein Al-Hassan ◽  
Beruk Lessanework ◽  
Alberto Alvarez ◽  
Danielle Senador ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Skeletal Muscle ◽  
Blood Flow ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Intrathecal Administration ◽  
Exercise Intolerance ◽  
Stroke Work ◽  
Muscle Metaboreflex

Exercise intolerance is a hallmark symptom of cardiovascular disease and likely occurs via enhanced activation of muscle metaboreflex- induced vasoconstriction of the heart and active skeletal muscle which, thereby limits cardiac output and peripheral blood flow. Muscle metaboreflex vasoconstrictor responses occur via activation of metabolite-sensitive afferent fibers located in ischemic active skeletal muscle, some of which express Transient Receptor Potential Vanilloid 1 (TRPV1) cation channels. Local cardiac and intrathecal administration of an ultra-potent noncompetitive, dominant negative agonist resiniferatoxin (RTX) can ablate these TRPV1 sensitive afferents. This technique has been used to attenuate cardiac sympathetic afferents and nociceptive pain. We investigated whether intrathecal administration (L4-L6) of RTX (2 μg/kg) could chronically attenuate subsequent muscle metaboreflex responses elicited by reductions in hindlimb blood flow during mild exercise (3.2 km/h) in chronically instrumented conscious canines. RTX significantly attenuated metaboreflex induced increases in mean arterial pressure (27 ± 5.0 mmHg vs. 6 ± 8.2 mmHg), cardiac output (1.40 ± 0.2 L/min vs. 0.28 ± 0.1 L/min) and stroke work (2.27 ± 0.2 L*mmHg vs. 1.01 ± 0.2 L*mmHg). Effects were maintained until 78 ± 14 days post RTX at which point the efficacy of RTX injection was tested by intra-arterial administration of capsaicin (20 μg/kg). A significant reduction in the mean arterial pressure response (+45.7 ± 6.5 mmHg pre RTX vs +19.7 ± 3.1mmHg post RTX) was observed. We conclude that intrathecal administration of RTX can chronically attenuate the muscle metaboreflex and could potentially alleviate enhanced sympatho-activation observed in cardiovascular disease states.

Norepinephrine-induced beta 1-adrenergic peripheral vasodilation in conscious dogs

1985 ◽  
Vol 249 (1) ◽  
pp. H49-H56 ◽  
Author(s):  
S. F. Vatner ◽  
D. R. Knight ◽  
T. H. Hintze
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Peripheral Resistance ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Adrenergic Blockade ◽  
Peripheral Vasodilation

Norepinephrine (NE) elicits alpha-adrenergic vasoconstriction and beta 1-adrenergic increases in heart rate and myocardial contractility. To determine whether NE can also elicit peripheral beta 1-adrenergic vasodilation, conscious dogs were studied after recovery from instrumentation for the measurement of cardiac output, arterial pressure, and left ventricular (LV) pressure and calculations of LV dP/dt and total peripheral resistance (TPR). NE, after pretreatment with hexamethonium and phentolamine, reduced mean arterial pressure 40 +/- 5% from 117 +/- 9 mmHg and TPR 60 +/- 5% from 0.058 +/- 0.007 mmHg X ml-1 X min and increased cardiac output 55 +/- 11% from 2,159 +/- 188 ml/min. beta 1-Adrenergic blockade with atenolol reversed the vasodilation induced by NE completely, while at this time isoproterenol was still able to reduce peripheral resistance further, by 67 +/- 7%, indicating that beta 2-adrenergic receptors were not blocked. Administration of phentolamine to intact dogs caused a fall in mean arterial pressure (23 +/- 5%) and TPR (34 +/- 5.4%) and an endogenous increase in plasma NE (2,987 +/- 905 pg/ml) and epinephrine (584 +/- 92 pg/ml). These increases in cardiac output and decreases in TPR were also reversed by atenolol (0.5 mg/kg). Moreover, this dose of atenolol blocked the increases in iliac blood flow induced by local injection of NE in the limb. Thus, in the presence of alpha-adrenergic receptor blockade, either administration of NE or release of endogenous NE elicits potent peripheral vasodilation, which appears to involve a beta 1-adrenergic receptor mechanism.

Hemodynamic responses to acute carboxyhemoglobinemia in the rat

1983 ◽  
Vol 244 (3) ◽  
pp. H320-H327 ◽  
Author(s):  
W. E. Kanten ◽  
D. G. Penney ◽  
K. Francisco ◽  
J. E. Thill
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Cardiac Index ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Peripheral Resistance ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Stroke Work

The effects of carbon monoxide on the hemodynamics of the adult rat were investigated. A number of parameters were measured using an open-chest, chloralose-urethan anesthetized preparation. Our experiments showed this anesthetic agent to have several advantages over pentobarbital sodium. One group inhaled 150 ppm CO for 0.5-2 h, carboxyhemoglobin (HbCO) reaching 16%. Heart rate, cardiac output, cardiac index, dF/dtmax (aortic), and stroke volume rose significantly; mean arterial pressure, total peripheral resistance, and left ventricular systolic pressure fell, whereas stroke work, left ventricular dP/dtmax, and stroke power changed little. These effects were evident at a HbCO saturation as low as 7.5% (0.5 h). A second group inhaled 500 ppm CO for 5-48 h, HbCO reaching 35-38%. The same parameters changed in the same direction as in the first group, with mean arterial pressure and peripheral resistance remaining depressed, while heart rate, cardiac output, cardiac index, and stroke volume remained elevated. Heart rate and arterial systolic pressure were also monitored in conscious rats; rats in one group inhaled 500 ppm CO for 24 h, and rats in a second group were injected with a bubble of pure CO ip. In both cases heart rate was sharply elevated and blood pressure depressed as HbCO saturation increased. Both parameters recovered on CO washout. There was no significant difference between the response to inhaled vs. injected CO.

Cardiac function in fetal sheep during two weeks of hypoxemia

1994 ◽  
Vol 266 (6) ◽  
pp. R1778-R1785 ◽  
Author(s):  
M. Kamitomo ◽  
L. D. Longo ◽  
R. D. Gilbert
Keyword(s):  
Arterial Pressure ◽  
Cardiac Function ◽  
Ventricular Function ◽  
Left Ventricular ◽  
Pressure Sensitivity ◽  
Sensitivity Curve ◽  
Fetal Sheep ◽  
Cardiac Responses ◽  
Ovine Fetal

Although several studies have examined fetal cardiac responses to acute hypoxemia, relatively little is known of the response to prolonged hypoxemia. To determine the effects of long-term hypoxemia on ovine fetal cardiac function, we measured right (QRV) and left ventricular outputs (QLV) and determined the effects of increasing preload (ventricular function curve) and afterload (arterial pressure sensitivity curve) on the left ventricle. Six days after fetal surgical instrumentation with catheters and electromagnetic flow probes (approximately 123 days gestation), we administered N2 into the maternal trachea for 14 days to reduce maternal PO2 to approximately 55 Torr (hypoxemic group, Hyp, n = 6). Normoxic animals were used as controls (Cont, n = 6). With the onset of hypoxemia, fetal arterial PO2 was reduced from approximately 27 to approximately 18 Torr. Fetal heart rate in Hyp fetuses decreased approximately 22% on day 14 compared with Cont (P < 0.05). Mean arterial pressure in the Hyp group was higher than that of Cont but not significantly so. Right and left atrial pressures were not affected by hypoxemia. QRV in Hyp fetuses was maintained on day 1 but decreased significantly by day 3 (approximately 19%) and further decreased on days 7 (approximately 28%) and 14 (approximately 34%). QLV was not depressed until day 7 (approximately 20%), with a further decrease on day 14 (approximately 38%). In association with the decreased QLV the plateau of the ventricular function curve in Hyp fetuses was depressed significantly on days 7 and 14. In contrast, the slope of the arterial pressure sensitivity curve in the Hyp group did not differ from Cont.(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanism of decreased cardiac output during ANP infusion in conscious anephric dogs

1992 ◽  
Vol 262 (1) ◽  
pp. R120-R125
Author(s):  
H. L. Mizelle ◽  
C. A. Gaillard ◽  
R. D. Manning ◽  
J. E. Hall
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Blood Cells ◽  
Venous Return ◽  
Control Period ◽  
Peripheral Resistance ◽  
Circulating Blood Volume

Atrial natriuretic peptide (ANP) may decrease cardiac output (CO) by lowering circulating blood volume (BV) or by altering the vasculature in a manner that would decrease venous return. The purpose of this study was to determine the role of decreased BV in mediating the decrease in CO during acute infusion of ANP. BV was measured by dilution of 51Cr-labeled red blood cells in seven trained conscious splenectomized dogs studied after unilateral (UNX) and total (TNX) nephrectomy. BV, hematocrit (Hct), CO, mean arterial pressure (MAP), and total peripheral resistance (TPR) were determined during a 90-min control period and 270 min of infusion of ANP (20 ng.kg-1.min-1 iv). In UNX dogs, ANP decreased BV from 60.9 +/- 1.4 to 58.6 +/- 1.4 ml/kg and increased Hct from 39.3 +/- 1.8% to 41.1 +/- 1.8% (P less than 0.05). MAP was not changed and CO fell to a low that was 86 +/- 2% of control (P less than 0.05) 240 min after starting ANP. TPR increased significantly during ANP infusion. All variables returned to control after ANP was stopped. In the same dogs studied 24 h after TNX, MAP averaged 111 +/- 5 mmHg during control and did not change during ANP infusion. CO fell to a low of 82 +/- 3% of control (P less than 0.05) after 120 min of infusion and remained reduced until after the ANP was stopped.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Elevated vascular resistance and afterload reduce the cardiac output response to dobutamine in early growth-restricted rats in adulthood

2011 ◽  
Vol 106 (9) ◽  
pp. 1374-1382 ◽  
Author(s):  
Vladislava Zohdi ◽  
M. Jane Black ◽  
James T. Pearson
Keyword(s):  
Cardiac Output ◽  
Cardiac Function ◽  
Peripheral Resistance ◽  
Early Growth ◽  
Left Ventricular ◽  
Growth Restriction ◽  
Protein Diet ◽  
Ventricular Pressure ◽  
Control Group ◽  
Increased Risk

Epidemiological studies have linked intra-uterine growth restriction (IUGR) with an increased risk of CVD later in life. The aim of the present study was to examine the effect of maternal protein restriction on cardiac function in adulthood during dobutamine (DOB) stimulation. IUGR was induced in Wistar Kyoto dams through administration of a low-protein diet (LPD; 8·7 % casein) during pregnancy and lactation; the control group received a normal-protein diet (NPD; 20 % casein). At 14 weeks of age, cardiac function was assessed in male and female NPD (eight females and eight males) and LPD offspring (ten females and ten males) by pressure volumetry using an anaesthetised closed-chest approach. We determined mean arterial pressure (MAP), heart rate and left ventricular pressure–volume indices under baseline conditions and DOB stimulation (2 and 4 μg/kg per min). During β-adrenergic activation in LPD offspring, increases in cardiac output (CO, P < 0·018) and stroke volume (SV, P < 0·005) were attenuated in comparison with NPD offspring, while increases in ejection fraction and the maximal rate of ventricular pressure development were not affected. LPD females maintained a smaller end-diastolic volume (P < 0·017). MAP did not differ between the groups and did not change significantly during DOB infusion. Arterial elastance and total peripheral resistance decreased in all rats but remained significantly elevated in LPD offspring (P < 0·015 and < 0·01). Early growth restriction did not affect ventricular contractility but led to an increased afterload and impaired the ability to increase SV and CO during β-adrenergic stimulation.

Hemodynamic effects of neurohypophyseal peptides with antidiuretic activity in dogs

1985 ◽  
Vol 249 (5) ◽  
pp. H1001-H1008 ◽  
Author(s):  
J. Schwartz ◽  
J. F. Liard ◽  
C. Ott ◽  
A. W. Cowley
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Plasma Renin Activity ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Plasma Renin ◽  
Hemodynamic Effects ◽  
Antidiuretic Activity

Arginine vasopressin (AVP) is known to produce increases in total peripheral resistance (TPR) and mean arterial pressure (MAP) and decreases in heart rate (HR), cardiac output (CO), and plasma renin activity (PRA). Some recent observations with AVP and synthetic analogues have suggested that under certain conditions, AVP can induce cardiovascular and reninsecretory responses in the opposite directions. To characterize the receptors mediating these responses, the effects of AVP, oxytocin, and synthetic neurohypophyseal analogues with specific antidiuretic, vasoconstrictor, or oxytocic activities were studied in conscious dogs. AVP and 2-phenylalanine-8-ornithine-oxytocin (Phe2Orn8OT, a selective vasoconstrictor agonist) produced similar responses when infused at 10 ng X kg-1 X min-1. That is, TPR and MAP increased, and CO, HR, and PRA decreased. Pretreatment with a selective vasoconstrictor antagonist, [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid) 2-(O-methyl)tyrosine]AVP, abbreviated d(CH2)5Tyr(Me)-AVP (10 micrograms/kg), blocked the actions of Phe2Orn8OT. However, in the presence of d(CH2)5Tyr(Me)AVP, AVP actually decreased TPR and increased CO, HR, and PRA. An analogue with selective antidiuretic activity, 4-valine-8-D-AVP (VDAVP, 10 ng X kg-1 X min-1), produced the same effects as the combination of vasopressin plus d(CH2)5Tyr(Me)AVP. Neither the effects of VDAVP nor of AVP plus antagonist were blocked by propranolol (1 mg/kg). These data indicate that vasopressin, by its antidiuretic activity, produces cardiovascular effects that are opposite to many of those produced by its vasoconstrictor action and that these effects are not dependent on mediation by beta-adrenoceptors.

Effects of arteriovenous fistula on systemic and pulmonary circulations

1964 ◽  
Vol 207 (6) ◽  
pp. 1319-1324 ◽  
Author(s):  
Jiro Nakano ◽  
Christian De Schryver
Keyword(s):  
Cardiac Output ◽  
Blood Transfusion ◽  
Arterial Pressure ◽  
Left Atrial ◽  
Pulmonary Arterial Pressure ◽  
Peripheral Resistance ◽  
Systemic Arterial Pressure ◽  
Left Ventricular ◽  
Stroke Work ◽  
Pulmonary Arterial

The effects of arteriovenous fistulas of different magnitudes on cardiovascular dynamics were studied in anesthetized dogs. It was found that A-V fistula decreases mean systemic arterial pressure, effective systemic blood flow, total and pulmonary peripheral resistances, whereas it increases heart rate, total cardiac output, stroke volume, left atrial pressure, pulmonary arterial pressure, and systemic peripheral resistance. The magnitude of the above hemodynamic changes was essentially proportional to the size of the fistula. At equivalent increments in total cardiac output produced by A-V fistula and blood transfusion, the former condition causes a greater increase in pulmonary arterial pressure than the latter, although both conditions decrease the pulmonary peripheral resistance by the same degree. It was also found that, at equivalent left atrial pressures, left ventricular stroke work with A-V fistula was greater than that with blood transfusion.

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.

Cardiovascular Effects of Moxibustion at Jen Chung (Go-26) during Halothane Anesthesia in Dogs

1975 ◽  
Vol 03 (03) ◽  
pp. 245-261 ◽  
Author(s):  
Do Chil Lee ◽  
Myung O. Lee ◽  
Donald H. Clifford
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Halothane Anesthesia

The cardiovascular effects of moxibustion at Jen Chung (Go-26) in 10 dogs under halothane anesthesia were compared to 5 dogs under halothane anesthesia without moxibustion and 5 dogs under halothane anesthesia in which moxibustion was effected at a neutral or non-acupuncture site. Cardiac output, stroke volume, heart rate, mean arterial pressure, central venous pressure, total peripheral resistance, pH, PaCO2, PaO2 and base deficit were measured over a two-hour period. A significant increase in cardiac output and stroke volume and a significant decrease in the total peripheral resistance were observed in the group which was stimulated by moxibustion at Jen Chun (Go-26). Heart rate, mean arterial pressure and pulse pressure were significantly increase during the early part of the two-hour period in the same group. The cardiovascular effects of moxibustion at Jen Chung (Go-26) which were observed at the end of the two hours were also present in two dogs in which measurements were continued for two additional hours.

Sign in / Sign up

Export Citation Format

Share Document