Catecholamines and Haemodynamics in Fixed Essential Hypertension

1979 ◽  
Vol 57 (s5) ◽  
pp. 193s-196s ◽  
Author(s):  
E. Agabiti-Rosei ◽  
C. Alicandri ◽  
R. Fariello ◽  
G. Muiesan

1. Arterial plasma catecholamines and haemodynamic status were simultaneously studied in 27 patients with fixed essential hypertension (WHO I—II). 2. Total arterial plasma catecholamines were found to be directly related to mean arterial pressure and to calculated total peripheral resistance, and they were inversely related to stroke index. 3. The degree of total peripheral resistance reduction after α-receptor blockade (phentolamine 10 mg intravenously) and the degree of mean arterial pressure reduction after combined α- and β-receptor blockade (labetalol 100 mg intravenously) were directly related to pretreatment plasma catecholamine concentrations. 4. These findings support the view that the sympathetic nervous system, as evaluated by plasma catecholamine concentration, may have an important role in maintaining hypertension in a subgroup of patients, contributing mainly to the degree of peripheral vasoconstriction.

1978 ◽  
Vol 55 (s4) ◽  
pp. 69s-71s ◽  
Author(s):  
Y. Miura ◽  
K. Kobayashi ◽  
H. Sakuma ◽  
H. Tomioka ◽  
M. Adachi ◽  
...  

1. Plasma noradrenaline concentrations and haemodynamic status were simultaneously studied in young patients with uncomplicated essential hypertension and in age-matched normal controls. 2. Resting plasma noradrenaline in the controls tended to increase slightly, but progressively, with age. The hypertensive subjects had significantly higher plasma noradrenaline concentrations than those in the controls, but these values did not show any age-related variation. The response of plasma noradrenaline to the standing position tended to increase with age in the controls, whereas plasma noradrenaline in the hypertensive subjects showed a wide range of responses without any fixed relationship with age. 3. The cardiac index was significantly greater in the labile hypertensive subjects than in the controls, whereas total peripheral resistance was significantly greater in the sustained hypertensive subjects than in the labile patients and in the controls. Mean arterial pressure in these patients was closely related with the values of total peripheral resistance rather than with the cardiac index. 4. Of the patients with raised plasma noradrenaline 80% showed significantly increased values of either total peripheral resistance or cardiac index. Plasma noradrenaline was correlated significantly to total peripheral resistance, and marginally to mean arterial pressure. 5. These findings support the view that sympathetic nervous overactivity is an important factor underlying the haemodynamic findings in these patients.


1987 ◽  
Vol 253 (4) ◽  
pp. H728-H736
Author(s):  
A. M. Fujii ◽  
S. F. Vatner

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.


1979 ◽  
Vol 57 (s5) ◽  
pp. 359s-362s ◽  
Author(s):  
P. Van Brummelen ◽  
A. Man In 't Veld ◽  
M. A. D. H. Schalekamp

1. Blood pressure, systemic haemodynamics, plasma volume, renin and aldosterone were measured during placebo treatment and after 1, 4 and 12 weeks of hydrochlorothiazide in 13 patients with uncomplicated essential hypertension. Nine of these patients were also studied after 24 and 36 weeks of treatment. 2. Mean arterial pressure was lowered significantly during hydrochlorothiazide treatment. In seven patients the fall in mean arterial pressure was greater than 10% (responders); four of these were studied for 36 weeks. The remainder were considered non-responders. 3. Hydrochlorothiazide lowered cardiac output. The maximal decrease was observed after 12 weeks of treatment (P < 0·01). In responders this was followed by a return to pretreatment values and a significant decrease in total peripheral resistance, whereas in non-responders cardiac output remained reduced and total peripheral resistance was permanently elevated. 4. Changes in plasma volume, renin and aldosterone were not significantly different in responders and non-responders although non-responders tended to show a greater degree of plasma volume depletion and a more pronounced increase in plasma aldosterone. 5. Thus it is unlikely that the initial decrease in cardiac output is an important determinant of the long-term haemodynamic effect of thiazide diuretics.


1999 ◽  
Vol 86 (1) ◽  
pp. 285-293 ◽  
Author(s):  
Stephen S. Blevins ◽  
Martha J. Connolly ◽  
Drew E. Carlson

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.


1977 ◽  
Vol 52 (6) ◽  
pp. 591-597 ◽  
Author(s):  
R. Fagard ◽  
A. Amery ◽  
T. Reybrouck ◽  
P. Lijnen ◽  
L. Billiet ◽  
...  

1. Plasma renin concentration, intra-arterial pressure, cardiac output and total peripheral resistance have been studied in 50 patients with essential hypertension and normal renal function. 2. Total peripheral resistance and plasma renin were negatively correlated (r = −0·45), indicating that ‘high-renin’ essential hypertension is not necessarily associated with arteriolar vasoconstriction. 3. The inverse relation between mean arterial pressure and plasma renin (r = −0·46) suggests a role for the renal baroreceptor mechanism in the suppression of renin in ‘low-renin’ hypertension. 4. Cardiac output was positively related to plasma renin concentration (r = +0·42). 5. Multiple regression analysis indicates that the described relationships were independent of age.


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 ◽  
...  

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.


1975 ◽  
Vol 03 (03) ◽  
pp. 245-261 ◽  
Author(s):  
Do Chil Lee ◽  
Myung O. Lee ◽  
Donald H. Clifford

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.


Pteridines ◽  
2003 ◽  
Vol 14 (3) ◽  
pp. 94-101 ◽  
Author(s):  
Remigiusz Zieba ◽  
Elzbieta Czarnecka ◽  
Małgorzata Wągrowska-Danilewicz ◽  
Malgorzata Dzielska-Olczak ◽  
Julita Graczyk

Abstract The aim of this study was to establish the effect of naturally occurring antioxidant - carnosine - on the doxorubicin induced cardiotoxicity in a rabbit model. For this purpose we evaluated the influence of doxorubicin administration alone and in a combined therapy with carnosine on the haemodynamic parameters and on the degree of cardiac muscle cells alterations in rabbits. The rabbits were divided into four groups. One group of rabbits was injccted with doxorubicin in a dose of 2 mg kg-1 weekly for 7 weeks to induce congestive heart failure. Another group of rabbits received the same doses of doxorubicin simultaneously with carnosine in a dose of 100 mg kg1 p.o. daily for 9 weeks. Administration of carnosine was started 1 week prior to the first dose of doxorubicin and was ended one week after the administration of the last dose of doxorubicin. The control groups of animals received 0.9% NaCl and carnosine alone. The following haemodynamic parameters were estimated: heart rate, mean arterial pressure, cardiac index, stroke index and total peripheral resistance. Registration of the haemodynamic parameters in rabbits was performed by Doppler method. Carnosine normalised the values of mean arterial pressure in rabbits receiving doxorubicin, and increased the values of cardiac index and stroke index. The influence of carnosine on total peripheral resistance was not statistically significant, but there was a decreasing tendency. The degree of cardiac muscle cell alterations was examined by light microscopy using Mean Total Score technique. The histopathological studies revealed smaller damage of cardiac muscle in rabbits which received doxorubicin and carnosine, in comparison to animals receiving doxorubicin alone. Carnosine seems to be car dioprotective during doxorubicin administration


1987 ◽  
Vol 253 (6) ◽  
pp. H1335-H1341 ◽  
Author(s):  
T. L. Smith ◽  
T. G. Coleman ◽  
K. A. Stanek ◽  
W. R. Murphy

A new technique is described that allows minute-to-minute recordings of cardiac output and arterial pressure in unanesthetized rats for periods of 24 h and longer. Rats were instrumented with electromagnetic flow probes and arterial catheters. An electrical and hydraulic swivel was interposed between the rat and recording apparatus to allow free range of movement. Data were collected and analyzed once each minute by computer. Average 24-h values (mean +/- SD) for the following hemodynamic variables were determined in eight rats [expressed where appropriate as a function of body weight (BW)]: cardiac output (98.1 +/- 14.7 ml/min), cardiac index (29.2 +/- 4.4 ml.min-1.100 g BW-1), mean arterial pressure (92.5 +/- 7.8 mmHg), heart rate (347 +/- 45 beats/min), peak aortic flow (403 +/- 32 ml/min), stroke volume (282 +/- 26 microliters), stroke volume index (84.4 +/- 8.1 microliters/100 g BW), and total peripheral resistance index (3.26 +/- 0.46 mmHg.ml-1.min.100 g BW). These results provide a data base of hemodynamic values for unanesthetized adult, Sprague-Dawley male rats, which has not been previously available. In addition, cardiac index, mean arterial pressure, and total peripheral resistance index demonstrated diurnal variation. Diurnal variation contributed substantially to the overall variance observed within these variables. Hourly variance was also substantial and indicates the use of continuous recordings for short-term experiments.


1995 ◽  
Vol 82 (4) ◽  
pp. 877-883. ◽  
Author(s):  
Rom A. Stevens ◽  
David Beardsley ◽  
J. Lee White ◽  
Tzu-Cheg Kao ◽  
Rod Gantt ◽  
...  

Background Spinal and epidural injection of local anesthetics are used to produce sympathetic block to diagnose and treat certain chronic pain syndromes. It is not clear whether either form of regional anesthesia produces a complete sympathetic block. Spinal anesthesia using tetracaine has been reported to produce a decrease in plasma catecholamine concentrations. This has not been demonstrated for epidural anesthesia in humans with level of anesthesia below C8. One possible explanation is that spinal anesthesia results in a more complete sympathetic block than epidural anesthesia. To examine this question, a cross-over study was performed in young, healthy volunteers. Methods Ten subjects underwent both spinal and epidural anesthesia with lidocaine (plain) on the same day with complete recovery between blocks. By random assignment, spinal anesthesia and epidural anesthesia were induced via lumbar injection. Before and 30 min after local anesthetic injection, a cold pressor test (CPT) was performed. Blood was obtained to determine epinephrine and norepinephrine plasma concentrations at four stages: (1) 20 min after placing peripheral catheters, (2) at the end of a 2-min CPT (before conduction block), (3) 30 min after injection of epidural or spinal lidocaine, and (4) at the end of a second CPT (during anesthesia). Mean arterial pressure, heart rate, noninvasive cardiac index, and analgesia to pin-prick were monitored. Results Neither spinal nor epidural anesthesia changed baseline resting values of catecholamines or any hemodynamic variable, except heart rate, which was slightly decreased during spinal anesthesia. Median level of analgesia was T4 during spinal and T3 during epidural anesthesia. CPT before conduction block reliably increased heart rate, mean arterial pressure, cardiac index, epinephrine, and norepinephrine. Conduction block attenuated the increase in response to CPT only in mean arterial pressure (spinal and epidural) and cardiac index (spinal only). Neither technique blocked the increase in heart rate, norepinephrine, or epinephrine to CPT. Conclusions Spinal anesthesia did not result in a more complete attenuation of the sympathetic response to a CPT than did epidural anesthesia. In response to the CPT, spinal anesthesia blocked the increase in cardiac index, and epidural anesthesia resulted in a decrease in total peripheral resistance compared to the pre-anesthesia state. The differences between the techniques are not significant and are of uncertain clinical implications.


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