The influence of acute starvation on the cardiovascular responses to lower body subatmospheric pressure or to standing in man

The cardiovascular responses to lower body subatmospheric pressure or to standing were measured in the same nine normal male subjects after a 12 h and after a 48 h fast. After the 48 h fast there was a significant reduction in diastolic blood pressure and forearm vascular resistance (relative to the values after a 12 h fast) when subjects were supine. During exposure to lower body subatmospheric pressure, subjects who had fasted for 48 h showed an inability to maintain systolic blood pressure, accompanied by an impairment of forearm vasoconstriction and an exaggerated tachycardia (relative to their responses after a 12 h fast). Similar disorders of cardiovascular homoeostasis were seen on standing. The results are consistent with an inhibition of sympathetic nervous activity after a 48 h fast, but other possibilities are discussed.     

Effects of resistance training on cardiovascular responses to lower body negative pressure in the elderly

The purpose of the present study was to determine whether resistance training alters the cardiovascular responses to submaximal lower body negative pressure (LBNP) in the elderly. Twenty‐one subjects were randomized into a control (C: n=10; 70 ± 3 years, mean ± SD) or a resistance training (TR: n=11; 67 ± 7 years) group. Subjects in the TR underwent 12 weeks of training consisting of three sets of 8–12 contractions at ?60–80% of their initial maximal one repetition, three times per week, on 10 different machines. Before (Pre) and after (Post) training, all subjects underwent exposures of LBNP of ?10, ?20 and ?40 Torr and muscle biopsy sampling at the vastus lateralis. TR increased (P≤0·05) knee extension (Pre=379 ± 140 N, Post=534 ± 182 N) and chest press (Pre=349 ± 137 N, Post=480 ± 192 N) strength. Neither body weight nor percentage body fat were altered (P >0·05) by training. Resistance training increased (P≤0·05) cross‐sectional area in both Type I (4203 ± 1196 to 5248 ± 1728 μm²) and Type II (3375 ± 1027 to 4286 ± 1892 μm²) muscle fibres. Forearm blood flow, forearm vascular conductance, mean arterial pressure, and heart‐rate responses to LBNP were not altered by the training. These data suggest that the cardiovascular responses of elderly to LBNP are unaffected by 12 weeks of whole‐body resistance training despite increases in muscle strength and size.     

The effects of the antagonists of the renin-angiotensin system on cardiovascular response to lower-body subatmospheric pressure in the anaesthetized cat

1. Lower-body subatmospheric (negative) pressure led to a prompt reduction in central venous pressure and arterial blood pressure. Arterial blood pressure was then restored within 30 s and there was a tachycardia. These reflex responses have been used to investigate the role angiotensin plays in blood pressure control. 2. The initial plasma renin activity (2.9 ng of angiotensin I h-1 ml-1) did not change during the brief lowering of pressure. Before pressure was lowered neither the angiotensin-converting enzyme inhibitor nor a competitive antagonist, [Sar1, Ala8]-angiotensin II, lowered arterial pressure. 3. Nevertheless, after inhibition of the renin-angiotensin system by these agents, the reduction in blood pressure induced by lower-body negative pressure became greater and the blood pressure recovery was impaired. 4. The findings suggest that angiotensin, at a blood concentration which has no direct effect on blood pressure, interacts with the sympathetic nervous system to maintain arterial blood pressure.     

The effect of adrenaline upon cardiovascular and metabolic functions in man

On three separate occasions, at least 1 week apart, seven young healthy male subjects received intravenous infusions of either adrenaline, 50 ng min-1 kg-1 (high A), adrenaline, 10 ng min-1 kg-1 (low A) or sodium chloride solution (saline: 154 mmol of NaCl/l) plus ascorbic acid, 1 mg/ml (control), over 30 min. Venous adrenaline concentrations of 2.19 +/- 0.15 nmol/l, 0.73 +/- 0.08 nmol/l and 0.15 +/- 0.03 nmol/l were achieved during the high A, low A and control infusions respectively. Heart rate rose significantly by 19 +/- 3 beats/min (high A) and by 6 +/- 1 beats/min (low A). Heart rate remained significantly elevated 30 min after cessation of the high A infusion, despite venous plasma adrenaline concentration having fallen to control levels. The diastolic blood pressure fell during the high A and low A infusions, but the systolic blood pressure rose only during the high A infusion. Vasodilatation occurred in the calf vascular bed during both high A and low A infusions. The changes in hand blood flow and hand vascular resistance were not statistically significant, although there was a tendency to vasoconstriction during the infusion of adrenaline. Metabolic rate rose significantly by 23.5 +/- 1.8% (high A) and by 11.8 +/- 1.6% (low A). Metabolic rate remained elevated between 15 and 30 min after termination of the high A infusion. There was an initial transient increase in respiratory exchange ratio (RER) during the adrenaline infusions. During the later stages of the adrenaline infusions and after their cessation, RER fell, probably reflecting increased fat oxidation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Circulating adrenaline and blood pressure: the metabolic effects and kinetics of infused adrenaline in man

Abstract. Six normotensive volunteers were infused with L-adrenaline at 001, 003, 005, 0075 and 010 μg/kg^-1 min^-1, each increment lasted 10 min. Plasma adrenaline rose from 0–27 to 4–61 nmol/1, and there were dose-related increases in plasma renin activity, blood glucose, plasma cyclic AMP and plasma free fatty acids, but not in plasma noradrenaline and cyclic GMP. Levels of circulating adrenaline previously noted in essential hypertensives had minimal cardiovascular effects. The secretion rate of adrenaline and its rate of clearance from the circulation were calculated from plasma samples taken during an hour-long infusion (0–083 ± 0006 μg kg^-1 min^-1) of L-adrenaline in the same individuals. The secretion rate ranged from 1 40 to 601 nmol/min with a mean (±SEM, 6) of 2–82 ±0–76 nmol/min. Mean clearance (±SEM, 6) was 9–41 ± 1 -37 1/min and ranged from 4–86 to 14.611/min. The decline of plasma adrenaline following the infusion was biexponential.
Plasma adrenaline is unlikely to be of primary importance in the elevation of blood pressure, either directly, via renin release or by noradrenaline release via presynaptic beta receptors. However, variation in clearance between subjects limits the use of plasma levels as an interindividual index of adrenal release of adrenaline. The relationship between sympathoadrenal activity and plasma adrenaline may be further perturbed by equilibration between the circulation and sites of tissue uptake. The lower levels of plasma adrenaline than of noradrenaline appear to result from both a slower rate of secretion and a higher rate of clearance from the circulation.     

Continuous intravenous infusion of naloxone does not change behavioral,cardiovascular, or inflammatory responses to subcutaneous formalin in the rat

The opioid antagonist, naloxone, produces equivocal effects on the magnitude of nociceptive responses in several animal models of persistent pain, including the formalin test. Hindpaw injection of dilute formalin produces not only inflammation but also phasic (Phase 1) and persistent (Phase 2) behavioral and cardiovascular nociceptive responses in the rat. To test the hypothesis that endogenous opioid systems contribute to the magnitude of responses to intraplantar formalin injection, we evaluated the effects of continuous naloxone administration (0.01–100 mg/kg per h, i.v.) on formalin-evoked hindpaw inflammation, on behavioral indices of pain, flinching and licking pain behavior, and on changes in mean arterial pressure and heart rate. We report that naloxone, at doses less than 100 mg/kg per h, did not change any formalin-evoked response. Although the 100 mg/kg per h dose significantly decreased these responses, it also produced muscle rigidity and profound bradycardia. We conclude that endogenous opioids do not significantly modulate the nociceptive processing induced by subcutaneous formalin.     

Effect of cold pressure test and 2-deoxy-D-glucose infusion on plasma renin activity in man

Abstract. It has been reported that catecholamines stimulate plasma renin activity (PRA) in vivo and in vitro. Yet the respective roles of endogenous epinephrine and norepinephrine are still debated. Therefore two tests were performed in human subjects: the cold pressure and the 2-deoxy-d -glucose tests. During these tests and on a control day, blood samples were taken at short intervals for PRA; in some subjects the excretion of epinephrine (E) and norepinephrine (NE) was also measured. In 9 healthy males the cold pressure test induced an immediate NE response with increase of systolic and diastolic blood pressure without change in the blood glucose concentration. There was no significant change in the mean value of PRA although in four subjects some rise of PRA occurred. The 2-deoxy-d -glucose induced, in response to an intracellular glucopaenia, an E discharge with a rise in the blood glucose concentration. In all 8 healthy males a striking rise of PRA was observed. Neither hyperglycaemia nor the concomitant decline of serum potassium could explain this rise of PRA, since the same changes during oral glucose test were not accompanied by a similar elevation. Patients with Addison's disease of tuberculous origin responded in a normal fashion to the cold pressure test, but failed to present a hyperglycaemia and a rise of PRA in response to 2-deoxy-d -glucose. This indicates that an intact adrenal medulla was required for the last stimulus but not for the former. From these studies in man it would appear that endogenous epinephrine stimulates renin more strongly than norepinephrine.     

Cardiovascular and metabolic responses to low dose adrenaline infusion: an invasive study in humans

Cardiovascular and metabolic responses to intravenous infusions of adrenaline (ADR), which raised arterial plasma ADR in a stepwise fashion from 0.3 to 1.3, 2.3 and 6.0 nmol/l, were studied in 11 healthy volunteers. ADR evoked marked and concentration-dependent increases in stroke volume and cardiac output (thermodilution), as well as decreases in the vascular resistances of the systemic circulation, calf and adipose tissue. These changes were significant from 1.3 nmol/l ADR. Less marked effects were found on blood pressure and heart rate. Significant arterial ADR concentration-effect relationships were found for cyclic AMP, glycerol, glucose, lactate and noradrenaline, but not for insulin. Cyclic AMP and glycerol were significantly elevated at 1.3, glucose at 2.3, but lactate not below 6.0 nmol/l ADR. Increases in adipose tissue blood flow and arterial glycerol levels were correlated (P less than 0.001), suggesting a metabolic component in the blood flow response of adipose tissue. Invasive haemodynamic measurements revealed that ADR at arterial concentrations within the lower physiological range had considerable effects on cardiac output and vascular resistances, despite moderate changes in the conventional non-invasive haemodynamic variables blood pressure and heart rate. ADR elicited clear-cut responses at arterial plasma concentrations attained during various kinds of mild to moderate stress.     

Comparison of intravenous and topical lidocaine in attenuating the cardiovascular responses to endotracheal intubation

We administered lidocaine intravenously or topically to the larynx to compare the cardiovascular response to intubation between the two techniques and to determine if these responses were related to blood levels of lidocaine. Sixteen patients were randomly selected into group A (100 mg intravenous lidocaine) or group B (160 mg topical lidocaine). Neither method was completely effective in abolishing hypertension and tachycardia on intubation. The increase in pulse rate (PR) was more significant than the rise in mean arterial pressure (MAP) and was of longer duration. Significant increases in MAP were evident for less than two minutes in group A and less than three minutes in group B. Significant increases in PR were observed for approximately four minutes in group A and six minutes in group B. The average lidocaine blood level in group A was approximately 20 times that in group B at the time of intubation. The more prolonged and more significant increase in PR observed in group B indicates that intravenous administration of lidocaine may be superior to topical administration.     

利多卡因缓解静脉输液中疼痛的效果观察

目的：探讨2％盐酸利多卡因注射液在静脉输液穿刺中缓解疼痛的效果,以减轻患者疼痛,提高其舒适度。方法：选择2012年1～6月在本院住院输液的患者60例,随机分为对照组和观察组各30例,观察组按实验设计方法选择好静脉,应用2％盐酸利多卡因注射液4ml浸湿纱布,湿敷拟穿刺输液点3rnin后穿刺静脉输液;对照组采用的生理盐水4ml浸湿纱布湿敷穿刺点3rain行输液作对照,观察两组患者疼痛情况。结果：两组患者疼痛程度比较有统计学意义（P〈0．05）。结论：应用2％盐酸利多卡因注射液湿敷穿刺点3min后,有缓解疼痛的作用。     

Vitamin C modifies the cardiovascular and microvascular responses to cigarette smoke inhalation in man

Both neutrophil margination and increases in the non-invasively assessed parameter, isovolumetric venous congestion cuff pressure (Pv(i)), are symptomatic of some inflammatory diseases. Neutrophil margination occurs primarily, though not exclusively, at the post-capillary endothelial surface. The local haemodynamic changes resulting from margination may be responsible for the observed increases in Pv(i). Smoke inhalation has been shown in animal studies to cause an increase in post-capillary neutrophil margination by mechanisms that can be blocked by oral vitamin C administration. We looked for indices of a relationship between margination and Pv(i) in man, using cigarette smoke inhalation as a pathophysiological challenge. We also examined the effect of prophylactic vitamin C on the response. Smoke inhalation was associated with highly significant increases in both Pv(i) and heart rate. After vitamin C pre-treatment, no increase in Pv(i) was observed in response to the smoke inhalation; however, whilst heart rate still increased significantly, the duration of this response was attenuated. The results suggest that vitamin C affords protection against some of the cardiovascular and microvascular changes associated with cigarette smoke inhalation in man. They also support the notion that non-invasive assessment of changes in Pv(i) may provide a measurable index of systemic changes in inflammatory conditions.     

鱼骨图在小儿静脉留置输液中的运用效果观察

目的提高小儿静脉留置输液质量。方法将2013-01—03住院患儿735例随机分成对照组和观察组,对照组369例均采用常规护理,观察组366例运用鱼骨图进行干预护理。结果观察组一次性穿刺成功率,病人家属满意度显著高于对照组（P〈0.01）,置管后并发症堵管（P〈0.01）、渗漏（P〈0.01）、静脉炎（P〈0.05）显著低于对照组,留置时间长于对照组（P〈0.01）,差异有统计学意义。结论运用鱼骨图实施静脉留置输液,提高了穿刺成功率,减少了并发症,延长了留置时间,提高了家属满意度。     

Effect of plantar micromechanical stimulation on cardiovascular responses to immobility

OBJECTIVE: We investigated the cardiovascular responses of adult women to the influence of extended quiet sitting and the extent to which these responses may be reversed by micromechanical stimulation of the plantar surface. DESIGN: The cardiovascular responses of 20 healthy adult women (mean age, 55.9 +/- 4.45 yrs) were observed during quiet sitting with and without exposure to a plantar-based micromechanical stimulation. Beat-to-beat heart rate via electrocardiogram was acquired along with preexposure and postexposure blood pressures, from which heart rate variability and mean arterial pressure were determined. Seven stimulus frequencies (0, 15, 22, 44, 60, 90, and 120 Hz, all at 0.2 x g, peak to peak) were tested on each subject. RESULTS: Over one-half of the women tested (11/20) exhibited a significant resting tachycardia (mean, 8.3 +/- 0.5 beats/min) with a corresponding decline in their systolic blood pressure (9.45 +/- 1.8 mm Hg) after 20 mins of quiet sitting. Plantar stimulation at 44 Hz (25 mum, peak to peak) was able to completely reverse the effect of immobility in this group, resulting in a heart rate decline of 2.5 beats/min (P < 0.0001) and a decrease of only 1 mm Hg in systolic pressure (P = 0.006). CONCLUSION: We interpret these results to suggest that the immobility of quiet sitting has a profound effect on the cardiovascular systems in a large fraction of otherwise healthy women, perhaps due to inadequate muscle tone leading to venous insufficiency. Simple external stimulation of the plantar surface seems to be capable of preventing these cardiovascular stress-based responses.     

Cardiac and whole-body [3H]noradrenaline kinetics during adrenaline infusion in man.

1. To investigate the possible role of adrenaline as a modulator of noradrenaline release from the sympathetic nervous system, the responses of cardiac and whole-body noradrenaline kinetics to intravenous infusions of adrenaline (30 ng min-1 kg-1) and matching saline placebo were determined at rest and during supine bicycle exercise in 16 patients undergoing cardiac catheterization, in whom beta-adrenoceptor antagonists had been discontinued for 72 h. 2. At rest and compared with placebo, infusion of adrenaline was associated with a small increase in arterial plasma noradrenaline from 211 +/- 29 pg/ml to 245 +/- 29 pg/ml (P less than 0.05). Increases in whole-body noradrenaline spillover to arterial plasma were larger (from 282 +/- 40 ng min-1 m-2 to 358 +/- 41 ng min-1 m-2, P less than 0.01) and there was a trend towards an increase in whole-body noradrenaline clearance. Cardiac noradrenaline clearance was modestly increased during adrenaline infusion, but cardiac noradrenaline spillover was not altered despite increases in heart rate and coronary sinus plasma flow. Adrenaline infusion was associated with symptomatic myocardial ischaemia in four of 14 patients with coronary heart disease. 3. Supine bicycle exercise was associated with significant increases in peripheral noradrenaline concentrations and in cardiac and whole-body noradrenaline spillover. The increases on exercise were not significantly different for these variables during saline and adrenaline infusions. 4. Infusion of adrenaline to produce 'physiological' increases in plasma adrenaline concentration was associated with an increase in total noradrenaline release, as assessed by whole-body noradrenaline spillover to plasma.(ABSTRACT TRUNCATED AT 250 WORDS)