Supplemental oxygen does not modulate responses to acetylcholine or ascorbic acid in the forearm of patients with congestive heart failure

2000 ◽  
Vol 99 (1) ◽  
pp. 57-63 ◽  
Author(s):  
Karen J. MURCHIE ◽  
Garry L. JENNINGS ◽  
Bronwyn A. KINGWELL
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Blood Flow ◽  
Ascorbic Acid ◽  
Supplemental Oxygen ◽  
Left Ventricular ◽  
Percentage Increase ◽  
Acid Infusion ◽  
Oxygen Inhalation ◽  
Adrenergic Antagonist

Despite providing symptomatic relief in patients with congestive heart failure (CHF), supplemental oxygen (O2) has been demonstrated to increase total peripheral resistance. The present study investigated the possibility that O2 inhalation reduces nitric oxide (NO) bioavailability, using endothelium-dependent (acetylcholine) and -independent (phentolamine) vasodilators, and the antioxidant ascorbic acid. Ten patients (nine male and one female) with primary left ventricular failure participated in the study. Forearm venous occlusion plethysmography was used to study blood flow responses to acetylcholine and the α-adrenergic antagonist phentolamine during inhalation of either room air or 100% O2, with and without the simultaneous infusion of ascorbic acid. Neither O2 inhalation (3.9±0.4 compared with 3.8±0.3 ml⋅min-1⋅100 ml-1) nor ascorbic acid infusion (5.2±0.4 compared with 5.5±0.4 ml⋅min-1⋅100 ml-1) affected resting forearm blood flow. The percentage increase from basal blood flow after acetylcholine infusion was not altered by either O2 inhalation or ascorbic acid infusion (room air, 140±55%; O2, 118±46%; ascorbic acid, 147±39%; ascorbic acid+O2, 109±31%). O2 inhalation did, however, reduce the dilation induced by phentolamine (room air, 131±24%; O2, 80±14%; P < 0.05). These data indicate that oxygen inhalation does not increase forearm vascular resistance. Secondly, preservation of reactivity to acetylcholine during O2 inhalation suggests that degradation of NO by O2-derived free radicals is not enhanced. Attenuation of phentolamine-induced vasodilation during O2 inhalation, however, implies increased adrenergic activity, which may possibly exacerbate the detrimental effects of elevated sympathetic activity in CHF.

Volume expansion potentiates cardiac sympathetic afferent reflex in dogs

2001 ◽  
Vol 280 (2) ◽  
pp. H576-H581 ◽  
Author(s):  
Wei Wang ◽  
Harold D. Schultz ◽  
Rong Ma
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Coronary Blood Flow ◽  
Volume Expansion ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Blood Volume Expansion ◽  
Cardiac Sympathetic Afferent Reflex

Our previous study (27) showed that the cardiac sympathetic afferent reflex (CSAR) was enhanced in dogs with congestive heart failure. The aim of this study was to test whether blood volume expansion, which is one characteristic of congestive heart failure, potentiates the CSAR in normal dogs. Ten dogs were studied with sino-aortic denervation and bilateral cervical vagotomy. Arterial pressure, left ventricular pressure, left ventricular epicardial diameter, heart rate, and renal sympathetic nerve activity were measured. Coronary blood flow was also measured and, depending on the experimental procedure, controlled. Blood volume expansion was carried out by infusion of isosmotic dextran into a femoral vein at 40 ml/kg at a rate of 50 ml/min. CSAR was elicited by application of bradykinin (5 and 50 μg) and capsaicin (10 and 100 μg) to the epicardial surface of the left ventricle. Volume expansion increased arterial pressure, left ventricular pressure, left ventricular diameter, and coronary blood flow. Volume expansion without controlled coronary blood flow only enhanced the RSNA response to the high dose (50 μg) of epicardial bradykinin (17. 3 ± 1.9 vs. 10.6 ± 4.8%, P < 0.05). However, volume expansion significantly enhanced the RSNA responses to all doses of bradykinin and capsaicin when coronary blood flow was held at the prevolume expansion level. The RSNA responses to bradykinin (16. 9 ± 4.1 vs. 5.0 ± 1.3% for 5 μg, P < 0.05, and 28.9 ± 3.7 vs. 10.6 ± 4.8% for 50 μg, P < 0.05) and capsaicin (29.8 ± 6.0 vs. 9.3 ± 3.1% for 10 μg, P < 0.05, and 34.2 ± 2.7 vs. 15.1 ± 2.7% for 100 μg, P < 0.05) were significantly augmented. These results indicate that acute volume expansion potentiated the CSAR. These data suggest that enhancement of the CSAR in congestive heart failure may be mediated by the concomitant cardiac dilation, which accompanies this disease state.

Sympathetic reflex control of subcutaneous blood flow in patients with congestive heart failure

1986 ◽  
Vol 70 (5) ◽  
pp. 513-522 ◽  
Author(s):  
Eli Kassis ◽  
Ole Amtorp ◽  
Knud Skagen
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Blood Flow ◽  
Left Ventricular ◽  
Transmural Pressure ◽  
Receptor Blockade ◽  
Sympathetic Stimulation ◽  
Nerve Blockade ◽  
Control Subjects ◽  
Β Receptor

1. Central and local regulation of forearm subcutaneous vascular resistance (FSVR) during postural changes were studied in congestive heart failure (CHF). Blood flow was measured by the local 133Xe-washout technique. Nine patients with severe CHF (baseline angiographic ejection fraction, 23 ± 2%, mean ± sem; cardiac index, 2.2 ± 0.2 litres min−1 m−2; increased left ventricular pressures and dimensions) were compared with seven control subjects who had normal cardiac performance. 2. Baseline FSVR and plasma concentrations of noradrenaline and adrenaline were substantially higher in patients with CHF than control subjects. However, the patients, like control subjects, increased FSVR by 46 ± 3% in response to increase in local venous transmural pressure and disclosed a normal response to decrease in forearm perfusion pressure. Both responses to changes in vascular transmural pressure were preserved after either proximal nervous blockade or local β-receptor blockade. 3. Central sympathetic stimulation was induced with use of 45° upright tilt. Control subjects developed vasoconstriction (FSVR increased by 59 ± 5%), which was completely abolished after proximal nerve blockade. Patients with CHF developed vasodilatation (FSVR decreased by 24 ± 8%), which was not only abolished but reversed after proximal nerve blockade (FSVR increased by 22 ± 7%), probably owing to the increased humoral vasoconstrictor activity. The paradoxical vasodilator response to central sympathetic stimulation in these patients was reversed after local β-receptor blockade (FSVR increased by 19 ± 9%). 4. The local vasoconstrictor reflex responsiveness and intrinsic vascular reactivity were not affected by the augmented baseline sympathetic vasoconstrictor activity in patients with CHF. Central sympathetic stimulation seems to elicit a β-adrenergic reflex effect intended to improve perfusion of the subcutaneous tissue in these patients.

Inhibition of NO production increases myocardial blood flow and oxygen consumption in congestive heart failure

2002 ◽  
Vol 282 (6) ◽  
pp. H2278-H2283 ◽  
Author(s):  
Jay H. Traverse ◽  
Yingjie Chen ◽  
Mingxiao Hou ◽  
Robert J. Bache
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Blood Flow ◽  
Oxygen Consumption ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
No Production ◽  
Before And After ◽  
Rapid Ventricular Pacing

Coronary blood flow (CBF) and myocardial oxygen consumption (MV˙o 2) are reduced in dogs with pacing-induced congestive heart failure (CHF), which suggests that energy metabolism is downregulated. Because nitric oxide (NO) can inhibit mitochondrial respiration, we examined the effects of NO inhibition on CBF and MV˙o 2 in dogs with CHF. CBF and MV˙o 2 were measured at rest and during treadmill exercise in 10 dogs with CHF produced by rapid ventricular pacing before and after inhibition of NO production with N G-nitro-l-arginine (l-NNA, 10 mg/kg iv). The development of CHF was accompanied by decreases in aortic and left ventricular (LV) systolic pressure and an increase in LV end-diastolic pressure (25 ± 2 mmHg). l-NNA increased MV˙o 2 at rest (from 3.07 ± 0.61 to 4.15 ± 0.80 ml/min) and during exercise; this was accompanied by an increase in CBF at rest (from 31 ± 2 to 40 ± 4 ml/min) and during exercise (both P < 0.05). Althoughl-NNA significantly increased LV systolic pressure, similar increases in pressure produced by phenylephrine did not increase MV˙o 2. The findings suggest that NO exerts tonic inhibition on respiration in the failing heart.

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