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At least 1,207 records · Page 67Linked to original sources
PubMed1982

The influence of behavioural state on the cardiovascular system of newborn lambs.

The influence of behavioural state, as defined by clinical observation and EEG recording, on cardiac output, heart rate, stroke volume and blood pressure was investigated in eight newborn lambs during the first 2 weeks of life. Cardiac output was measured using the technique of thermodilution. Highest mean value (mean +/- SEM) of cardiac output was found in the very alert awake state in week 1, 271 +/- 16 ml/min per kg. Other values were significantly lower; quiet sleep, 173 +/- 4 ml/min per kg; rapid-eye-movement sleep, 191 +/- 7 ml/min per kg; quiet awake, 174 +/- 3 ml/min per kg; alert awake, 180 +/- 5 ml/min per kg. Similar values were found in week 2. These values of cardiac output were lower than those previously reported for newborn lambs except in the very alert awake state. Heart rate was significantly lower during sleep than in the awake states in week 1. The heart rate was found to be significantly higher in all states except the very alert awake state in week 2 compared with week 1. Stroke volume was significantly higher in rapid-eye-movement sleep, 1.08 +/- 0.06 ml/kg, and in the very alert awake state, 1.16 +/- 0.09 ml/kg, compared with the other states in week 1, but only in the very alert awake state in week 2. Blood pressure was highest in the very alert awake state in both weeks. These findings demonstrate that behavioural state has a very significant influence on the cardiovascular system during newborn life in lambs, particularly on cardiac output values, which in the very alert awake and rapid-eye-movement sleep states significantly exceed values in the other states.

Animals↗
PubMedDate not supplied

Fluorescence histochemical observations on the adrenergic innervation of the cardiovascular system in the aged rat.

The Falck-Hillarp fluorescence technique was applied to tissue samples of the heart and certain vessels of both 4 and 24 month Wistar rats. It appeared that with increasing age, the density and fluorescence intensity of the cardiac sympathetic innervation was maintained at a level comparable to the young adult (4 month) in the atria, left ventricle and in the region of the sino-atrial node. Similarly the adrenergic innervation of the coronary vasculature, particularly in the atrium was maintained into old age. In contrast the adrenergic innervation of the common and internal carotid arteries and abdominal aorta was very sparse in the 24 month rat compared to the young adult in which these vessels were surrounded by dense fluorescent plexuses. Peripheral arteriolar innervation in the pancreas was apparently similar in both age-groups. The present study suggests that the density of adrenergic innervation varies within the constituents of the cardiovascular system in aged rats.

Adrenergic Fibers↗
PubMed1999

[Effect of the long distance truck driving in Hokkaido on cardiovascular system].

We took the blood pressure and ECG of 8 male truck drivers who drive long distances in Hokkaido and observed the conditions under which they work. Most of their driving routes included steep passes, and the weather and the road conditions became worse in winter. Their tasks were not only the driving and waiting but also such manual labor as loading, etc. The mean driving distance of one route was 705 km and it ranged from 159 km to 1,210 km. The mean number of working hours was 27.8 h, and it ranged from 9.2 h to 46.9 h. Blood pressure was higher when driving or loading than when resting or on a day off. The mean systolic blood pressure was over 140 mmHg in 6 cases, and arrhythmia occurred frequently in 4 cases during driving or loading. In 2 cases, in which the driver met with accident, the blood pressure was remarkably high and arrhythmia occurred frequently. Most drivers worked for a very long time in poor conditions and environment. The results of our study suggested that such a heavy work load will affect the cardiovascular system.

Accidents, Traffic↗
PubMed2006

Cross-talk between the kidney and the cardiovascular system.

In recent years, increasing evidence has been provided that even minor renal dysfunction is a powerful cardiovascular risk factor that induces typical cardiovascular alterations and thus predisposes to coronary heart disease as well as to noncoronary cardiovascular problems. This first had been noted in patients with diabetes but now has been confirmed amply in patients without diabetes as well. Numerous heterogeneous abnormalities have been described in patients with early renal dysfunction (e.g., microalbuminuria, reduced estimated GFR). One final common pathway seems to be endothelial cell dysfunction. The link between albuminuria and generalized endothelial cell dysfunction (as indicated by diminished flow-mediated vasodilation, markers of endothelial cell dysfunction, sloughed off endothelial cells, and high transcapillary albumin escape rate) is unclear. In patients with early renal dysfunction, a long list of classical and nonclassical cardiovascular risk factors have been identified: Elevated asymmetric dimethyl-l-arginine concentrations, markers of microinflammation, oxidative stress, features of metabolic syndrome, abnormal adipokine concentrations, dyslipidemia, inappropriate activation of the renin-angiotensin system, and sympathetic overactivity. The mechanisms that link dysfunction of the kidney and the cardiovascular system are being sought. The most interesting unifying concept, however, is deranged fetal programming linking nephron underdosing to the increased cardiovascular risk.

Cardiovascular System↗
PubMed1979

Recovery rate of the cardiovascular system in rabbits following short-term halothane anesthesia.

Mean arterial pressure, cardiac output and heart rate were determined in eight male New Zealand white rabbits while conscious and after being anesthetized with halothane plus nitrous oxide for 15 minutes. Delivery of the anesthetic agent was stopped and the measurement repeated at 15, 30, 60 and 210 minutes. In a separate experiment blood samples were obtained for plasma renin activity in six rabbits before anesthesia, after 15 minutes of halothane plus nitrous oxide administration, and again 210 minutes after cessation of the anesthesia. Later, this experiment was repeated with the same rabbits except that they were allowed to breathe room air instead of the anesthesia. The halothane anesthesia resulted in decreased mean arterial pressure and cardiac output, but these returned to the preanesthetic levels by 15 minutes after stopping the anesthesia. Heart rate increased during halothane administration, and although it tended to return toward control levels after cessation of the halothane, heart rate was still elevated 210 minutes later. Halothane plus nitrous oxide produced an increase in plasma renin activity, which then subsided to normal by 210 minutes following anesthesia; breathing room air did not result in increases in plasma renin activity. These studies revealed that although short-term anesthesia with halothane plus nitrous oxide resulted in cardiovascular changes in rabbits, after cessation of the anesthetic agent the cardiovascular system quickly returned to normal.

Animals↗
PubMed2003

Dynamics of nitric oxide release in the cardiovascular system.

The endothelium plays a critical role in maintaining vascular tone by releasing nitric oxide (NO). Endothelium derived NO diffuses to smooth muscles, triggering their relaxation. The dynamic of NO production is a determining factor in signal transduction. The present studies were designed to elucidate dynamics of NO release from normal and dysfunctional endothelium. The nanosensors (diameter 100-300 nm) exhibiting a response time better than 100 micros and detection limit of 1.0 x 10(-9) mol L(-1) were used for in vitro monitoring of NO release from single endothelial cells from the iliac artery of normotensive (WKY) rats, hypertensive (SHR) rats, and normal and cholesterolemic rabbits. Also, the dynamics and distribution of NO in left ventricular wall of rabbit heart were measured. The rate of NO release was much higher (1200 +/- 50 nmol L(-1) s(-1)) for WKY than for SHR (460 +/- 10 nmol L(-1) s(-1)). Also, the peak NO concentration was about three times higher for WKY than SHR. Similar decrease in the dynamics of NO release was observed for cholesterolemic rabbits. The dynamics of NO release changed dramatically along the wall of rabbit aorta, being highest (0.86 +/- 0.12 micromol L(-1)) for the ascending aorta, and lowest for the iliac aorta (0.48 +/- 0.15 micromol L(-1)). The distribution of NO in the left ventricular wall of rabbit heart was not uniform and varied from 1.23 +/- 0.20 micromol L(-1) (center) to 0.90 +/- 0.15 micromol L(-1) (apex). Both, the maximal concentration and the dynamics of NO release can be useful diagnostic tools in estimating the level of endothelial dysfunction and cardiovascular system efficiency.

Animals↗
PubMed1996

Presence of vasomotor and respiratory rhythms in the discharge of single medullary neurons involved in the regulation of cardiovascular system.

We analyzed the discharges of 77 single neurons located in the rostral ventrolateral medulla (RVLM, n = 25), caudal ventrolateral medulla (CVLM, n = 18), lateral tegmental field (LTF, n = 19) and caudal raphe nuclei (n = 15). These recordings were made from 36 vagotomized and sinoaortic denervated cats that were either decerebrate (n = 27) or anesthetized with urethane (n = 9) and from 3 decerebrate cats with intact sinoartic and vagal nerves. These neurons were classified as sympathetic-related (n = 61) if spike triggered averaging showed that their naturally occurring discharges were correlated to either the cardiac related (2-6 Hz) or a faster (10 Hz) oscillation in inferior cardiac sympathetic nerve discharge. Neurons were classified as sympathetic-unrelated (n = 16) if they lacked these characteristics. We used autoregressive spectral techniques to detect additional slower oscillations hidden in the variability of neuronal discharge and possibly correlated to the oscillations of systolic arterial pressure (SAP). This analysis revealed the existence of a low frequency (LF) oscillation (0.12 +/- 0.02 Hz) in the discharges of 36 sympathetic-related and 9 sympathetic-unrelated neurons. In relation to 35 neurons in 21 animals there was also an LF component in SAP variability. In 29 instances the LF neuronal discharges and SAP variabilities were significantly correlated. In addition, there was a high frequency (HF) oscillation (0.34 +/- 0.06 Hz) in the discharges of 59 medullary neurons. In 56 cases the HF in neuronal discharge variability cohered to that in SAP variability. These data are the first to demonstrate the existence of an LF component in the discharges of individual medullary neurons, at least some of which were likely to be involved in the regulation of the cardiovascular system. Since these oscillations were evident in cats with section of sinoaortic and vagal nerves, they likely reflect central rhythmogenic properties.

Animals↗
PubMed2002

Verification of protector effect of the norepinephrine and felypressin upon the cardiovascular system under action of the lidocaine hydrochloride and prilocaine hydrochloride in anesthetized rats.

Vasoconstrictor substances, as norepinephrine and epinephrine, were mixtured to local anesthetics to decrease their toxic effects and to prolong the depth of the anesthesia. However, these catecholamines produce systolic and diastolic hypertension. The effects of felypressin, a synthetic vasoconstrictor, upon arterial blood pressure and heart are lesser than those of norepinephrine or epinephrine, but due to its effects like oxytocin these catecholamines are yet the most used vasoconstrictors in association with lidocaine or another anesthetic salt. These vasoconstrictors are contraindicated for some physician, mainly for cardiac patients. But, are the catecholamines or is the salt the most dangerous components of the local anesthetic? The effects of the salt and catecholamines are opposite, but which of these exercises their effects first when inside blood vessel? Singi et al. [Pharmacol. Res. 44 (2001)] demonstrated that the first effect is always of the salt and that norepinephrine promotes protector effects upon guinea-pig isolated heart against lidocaine action. But, is this true for in vivo animals? The present study was performed with the aiming to answer this question and to verify if felypressin can induce the same effect of the norepinephrine. Fourteen Rattus norvegicus albinus, weighing 350g on average, were used. After being anesthetized with sodic thiopental, they were tracheostomizeds and one jugular and one carotid were cannuled for application of substances and to record the blood arterial pressure, respectively. The ECG was gotten through electrodes located in the front and back paws of the animals. The animals were separated in two groups, each one with seven rats. The lidocaine hydrochloride 2% in the doses of 600 microg and 3% in the doses of 900 microg acted on the cardiovascular system reducing the arterial pressure and modifying the electrocardiogram, while the prilocaine hydrochloride, in the same doses, also reduced the arterial pressure, but did not modify the electrocardiogram. When norepinephrine was associated to lidocaine 3% hydrochloride, it was possible to observe that this salt always exercised its effect first and a protective effect against the fall of pressure produced for the lidocaine. The same protective effect did not occur when felypressin was associated with prilocaine hydrochloride 3%.

Anesthesia↗
PubMed2006

22q11 deletion syndrome: a review of some developmental biology aspects of the cardiovascular system.

The morphology and molecular genetics of the 22q11 deletion syndrome cardiovascular anomalies are reviewed. Special emphasis is given to TBX1, recently identified and considered to be the potential key gene for this clinical syndrome. The TBX1 downstream molecular pathways modulating the normal development of the pharyngeal apparatus are also discussed, and emphasis is given to the possible, equally fundamental role of downstream molecular pathway disruption in causing the clinical 22q11 deletion phenotype features.

Animals↗
PubMed1986

[Reactivity of the cardiovascular system and of the pressor neurohumoral systems in hypertension patients].

Correlations between sympathoadrenal, renin-angiotensin and cardiovascular (BP and heart rate) response to psychoemotional and physical stress and antebrachial skin vascular response to noradrenaline were examined in patients with essential hypertension. Four groups of patients were identified on the basis of the magnitude of variation in the examined parameters. The progress of the disease over the past two years was assessed in all patients. The prognosis was particularly unfavorable in the "hyperreactive" group which showed a set of distinctive features: increased vascular response to noradrenaline, a greater BP rise in response to stress, greater sympathoadrenal activation, increased neuroticism, as well as significantly older age of the patients and greater severity and duration of the disease. No intergroup differences in plasma renin activity could be demonstrated. Possible use of vascular response to noradrenaline, and BP and plasma catecholamine variation in response to psychoemotional stress as criteria for the assessment of the severity and outcome of essential hypertension is discussed.

Adrenal Glands↗
PubMed1981

[Parameters of bradykinin interaction with cardiovascular system receptors].

The equation describing kinetics of interaction between bradykinin and cardiovascular receptors resembles the equations describing depressive adrenergic and some cholinergic reactions in dogs, rabbits and white rats. In this study of bradykinin receptor state, in order to describe quantitatively hypotensive action of different bradykinin doses on interaction of this peptide with receptors, bradykinin had to be injected intraaortally. The data obtained revealed that the greatest efficiency of kininergic reaction occurred in dogs whereas the least--in white rats.

Animals↗
PubMed2003

A biochemical rationale for the discrete behavior of nitroxyl and nitric oxide in the cardiovascular system.

The redox siblings nitroxyl (HNO) and nitric oxide (NO) have often been assumed to undergo casual redox reactions in biological systems. However, several recent studies have demonstrated distinct pharmacological effects for donors of these two species. Here, infusion of the HNO donor Angeli's salt into normal dogs resulted in elevated plasma levels of calcitonin gene-related peptide, whereas neither the NO donor diethylamine/NONOate nor the nitrovasodilator nitroglycerin had an appreciable effect on basal levels. Conversely, plasma cGMP was increased by infusion of diethylamine/NONOate or nitroglycerin but was unaffected by Angeli's salt. These results suggest the existence of two mutually exclusive response pathways that involve stimulated release of discrete signaling agents from HNO and NO. In light of both the observed dichotomy of HNO and NO and the recent determination that, in contrast to the O2/O2- couple, HNO is a weak reductant, the relative reactivity of HNO with common biomolecules was determined. This analysis suggests that under biological conditions, the lifetime of HNO with respect to oxidation to NO, dimerization, or reaction with O2 is much longer than previously assumed. Rather, HNO is predicted to principally undergo addition reactions with thiols and ferric proteins. Calcitonin gene-related peptide release is suggested to occur via altered calcium channel function through binding of HNO to a ferric or thiol site. The orthogonality of HNO and NO may be due to differential reactivity toward metals and thiols and in the cardiovascular system, may ultimately be driven by respective alteration of cAMP and cGMP levels.

Animals↗