Effects of Experimentally Produced Heart Failure on the Peripheral Vascular Response to Severe Exercise in Conscious Dogs

The interactions between yohimbine (selective α2-antagonist) with noradrenaline (mixed agonist) and phenylephrine (selective α1-agonist) were studied in the canine dorsal pedal artery in an attempt to characterize the peripheral vascular response to adrenergic agents before and after the development of congestive heart failure in the dog. The contractile responses of the dorsal pedal artery to potassium chloride were also examined. Both noradrenaline and phenylephrine contracted the dorsal pedal artery in a concentration-dependent manner before and at peak heart failure, the responses to the agonists being enhanced at heart failure. The responses of the artery to potassium were not modified by congestive heart failure. Yohimbine caused concentration-dependent antagonism of noradrenaline, without altering the magnitude of the maximum response, providing pA2 values ranging from 8.26 to 7.06 against low and high concentrations of noradrenaline, respectively, before heart failure development. Following heart failure, the pA2 values for yohimbine against noradrenaline remained unchanged, but slopes from the Arunlakshana–Schild plots were significantly different from unity, implying a noncompetitive antagonism. The pA2 values of yohimbine against phenylephrine were at least 10 orders of magnitude lower than those against noradrenaline. After congestive heart failure, yohimbine was even less effective against high concentrations of phenylephrine. These findings suggest that enhanced vasoconstriction during heart failure results, in part, from increased α1-adrenoceptor mechanisms in peripheral arterial smooth muscle.Key words: vascular α-adrenoceptors, congestive heart failure, dorsal pedal artery, yohimbine, noradrenaline.

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Humoral Immunity in Heart Failure

Cardiovascular & Haematological Disorders - Drug Targets ◽

10.2174/1871529x18666180518101527 ◽

2019 ◽

Vol 19 (1) ◽

pp. 14-18 ◽

Cited By ~ 2

Author(s):

Amrita Sarkar ◽

Khadija Rafiq

Keyword(s):

Heart Failure ◽

Humoral Immunity ◽

Treatment Strategies ◽

Pathophysiological Mechanism ◽

Peripheral Vascular ◽

Cardiac Inflammation ◽

Humoral Immune ◽

Humoral Immune System ◽

New Treatment ◽

Immunity Function

Cardiovascular Disease (CVD) is a class of diseases that involve disorders of heart and blood vessels, including hypertension, coronary heart disease, cerebrovascular disease, peripheral vascular disease, which finally lead to Heart Failure (HF). There are several treatments available all over the world, but still, CVD and heart failure became the number one problem causing death every year worldwide. Both experimental and clinical studies have shown a role for inflammation in the pathogenesis of heart failure. This seems related to an imbalance between pro-inflammatory and anti-inflammatory cytokines. Cardiac inflammation is a major pathophysiological mechanism operating in the failing heart, regardless of HF aetiology. Disturbances of the cellular and humoral immune system are frequently observed in heart failure. This review describes how B-cells play a specific role in the heart failure states. There is an urgent need to identify novel therapeutic targets and develop advanced therapeutic strategies to combat the syndrome of HF. Understanding and describing the elements of the humoral immunity function are essential and may suggest potential new treatment strategies.

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

International Journal of Psychophysiology ◽

10.1016/j.ijpsycho.2008.05.215 ◽

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

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Chronic therapy with an ETA/B receptor antagonist in conscious dogs during progression of congestive heart failure Intracellular Ca2+ regulation and nitric oxide mediated coronary relaxation

Cardiovascular Research ◽

10.1016/s0008-6363(00)00183-8 ◽

2000 ◽

Vol 48 (2) ◽

pp. 332-345 ◽

Cited By ~ 7

Author(s):

Y Shen

Keyword(s):

Nitric Oxide ◽

Heart Failure ◽

Congestive Heart Failure ◽

Receptor Antagonist ◽

Conscious Dogs ◽

Chronic Therapy ◽

Coronary Relaxation

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Abstract 17638: Systemic Cardiovascular Effects of Intravenous Urocortin 2 and Urocortin 3 in Patients with Heart Failure and Healthy Volunteers

Circulation ◽

10.1161/circ.130.suppl_2.17638 ◽

2014 ◽

Vol 130 (suppl_2) ◽

Author(s):

Colin G Stirrat ◽

Sowmya Venkatasubramanian ◽

Tania Pawade ◽

Andrew Mitchell ◽

Anoop Shah ◽

...

Keyword(s):

Heart Failure ◽

Blood Pressure ◽

Cardiac Index ◽

Healthy Volunteers ◽

Diastolic Blood Pressure ◽

Cardiovascular Effects ◽

Peripheral Vascular ◽

Patients With Heart Failure ◽

Group A ◽

Urocortin 3

Introduction: Urocortin 2 (UCN 2) and urocortin 3 (UCN 3) are endogenous peptide hormones with an emerging role in the pathophysiology and treatment of heart failure. For the first time, we examined the systemic cardiovascular effects of both UCN 2 and UCN 3 in healthy volunteers and patients with heart failure. Methods: Seven healthy volunteers (Group A) and nine patients with stable chronic heart failure (Group B, New York Heart Association class II and III, left ventricular ejection fraction <35%) on optimal medical therapy underwent non-invasive oscillometric sphygmomanometry and impedance cardiography during incremental intravenous infusions of sodium nitroprusside (0.15/0.5/1.5 μg/kg/min), UCN 2 (0.16/0.48/1.6 μg/min), UCN 3 (5/15/50 μg/min) and saline placebo in a randomised double blind two-way cross over study. Results: Other than diastolic blood pressure (78 vs 72 mmHg for Group A and B respectively, p<0.05), haemodynamic variables were similar at baseline of each infusion and were unchanged by saline placebo infusion (p>0.05 for all). SNP, UCN2 and UCN 3 infusions increased heart rate and cardiac index, and reduced systolic and diastolic blood pressure and peripheral vascular resistance index (PVRI) in both healthy volunteers and patients with heart failure (p<0.05 for all; see Figure 1). There were no significant differences in the changes in cardiac index or PVRI between healthy volunteers and patients with heart failure during either UCN 2 or UCN 3 infusions (p>0.05). Conclusion: Intravenous UCN 2 and especially UCN 3 increase cardiac output and reduce peripheral vascular resistance. This favourable haemodynamic profile suggests that UCN 2 and UCN 3 hold exciting therapeutic potential for the treatment of acute heart failure.

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Peripheral vascular responses to hyperthermia in the rat

Journal of Applied Physiology ◽

10.1152/jappl.1988.64.6.2582 ◽

1988 ◽

Vol 64 (6) ◽

pp. 2582-2588 ◽

Cited By ~ 115

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.

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