Acute cardiovascular response to isocapnic hypoxia. I. A mathematical model

2000 ◽  
Vol 279 (1) ◽  
pp. H149-H165 ◽  
Author(s):  
Mauro Ursino ◽  
Elisa Magosso

A mathematical model of the acute cardiovascular response to isocapnic hypoxia is presented. It includes a pulsating heart, the systemic and pulmonary circulation, a separate description of the vascular bed in organs with the higher metabolic need, and the local effect of O2 on these organs. Moreover, the model also includes the action of several reflex regulatory mechanisms: the peripheral chemoreceptors, the lung stretch receptors, the arterial baroreceptors, and the hypoxic response of the central nervous system. All parameters in the model are given in accordance with the physiological literature. The simulated overall response to a deep hypoxia (28 mmHg) agrees with the experimental data quite well, showing a biphasic pattern. The early phase (8–10 s), caused by activation of peripheral chemoreceptors, exhibits a moderate increase in mean systemic arterial pressure, a decrease in heart rate, a quite constant cardiac output, and a redistribution of blood flow to the organs with higher metabolic need at the expense of other organs. The later phase (20 s) is characterized by the activation of lung stretch receptors and by the central nervous system hypoxic response. During this phase, cardiac output and heart rate increase together, and blood flow is restored to normal levels also in organs with lower metabolic need. The model may be used to gain a deeper understanding of the role of each mechanism in the overall cardiovascular response to hypoxia.

1972 ◽  
Vol 56 (1) ◽  
pp. 67-77
Author(s):  
M. G. EMILIO ◽  
G. SHELTON

1. A series of breathing movements which are effective in ventilating the lungs are accompanied by a marked increase in pulmonary blood flow and a decrease in pulmocutaneous arterial pressure. This reaction must involve considerable vasodilation of the pulmonary vascular bed. 2. Similar vasodilation is produced by artificial inflation of the lungs via an implanted cannula. Nitrogen is not so effective as air in producing the vasodilation, whereas oxygen is more effective. It is suggested that both stretch receptors in the lungs and chemical receptors in lungs or blood are involved in the reaction. 3. The level of anaesthesia is important in determining the degree of vasodilation response to the different stimuli. It is concluded that the central nervous system is the site where interaction occurs between signals from stretch receptors and chemical receptors and from the breathing movements themselves. Experiments with atropine suggest that the efferent pathway is in the vagus nerve. 4. Recordings from free-swimming, unanaesthetized toads show that the vasodilation response occurs as part of normal diving-emergence behaviour.


1985 ◽  
Vol 93 (6) ◽  
pp. 786-793 ◽  
Author(s):  
Steven O. Short ◽  
Paul C. Goodwin ◽  
Jory N. Kaplan ◽  
Josef M. Miller

Cochlear blood flow (CBF) was studied with a commercially available laser Doppler system in 20 guinea pigs. The cochlea was exposed to permit placement of the laser Doppler probe over the intact lateral wall of the basal turn. Ketamine and xylazine were used for anesthesia, and blood pressure was monitored from the femoral artery. In some cases, skin blood flow was monitored with a second laser Doppler system, and cardiac output was monitored with an ultrasonic Doppler system placed over the right brachiocephalic artery. We found that the laser Doppler signal is composed primarily of blood flow supplied by the internal auditory artery. Local pressure on the contents of the internal auditory canal after occipital craniotomy was found to reduce CBF to 15% of its original value in a reversible fashion. There was no change in CBF after bilateral occlusion of the common carotid arteries. There appears to be a mechanism governing CBF that stabilizes its value In the face of changes in blood pressure and cardiac output. This is similar to the vascular behavior of the central nervous system. Through the use of positive airway pressure and blood removal at different rates, cardiac output could be depressed to varying degrees. The magnitude of decrease in CBF was clearly related to the rate at which cardiac output and blood pressure dropped. This was confirmed when intravenous phenylephrine was given in sequential and Increasing doses. CBF increased as blood viscosity decreased, as expected according to the vascular behavior of the central nervous system. Our findings indicate that the laser Doppler system provides a reliable, valid, and cochlear noninvasive measure of blood flow dynamics.


2002 ◽  
Vol 96 (2) ◽  
pp. 438-441 ◽  
Author(s):  
Thomas Peter Weber ◽  
Andreas Meissner ◽  
Jörg Stypmann ◽  
Maike Grosse Hartlage ◽  
Hugo Van Aken ◽  
...  

Background In patients undergoing colonoscopy, naloxone has vasodilative properties. However, it remains unclear whether this effect is mediated by central or peripheral mechanisms. The aim of this study was to investigate whether these effects are mediated by an effect of naloxone on the central nervous system. Methods Twenty dogs were chronically instrumented for measurement of hemodynamic parameters. Splanchnic blood flow was determined using colored microspheres. Transthoracic echocardiographic examinations were performed to measure cardiac output. In each animal, two experiments were performed in a random order: experiment 1 was determination of splanchnic blood flow before and 5 min after intravenous administration of naloxone (63 microg/kg), and experiment 2 was determination of splanchnic blood flow before and 5 min after administration of naloxone methiodide (63 microg/kg), which does not cross the blood-brain barrier. Results Naloxone, but not naloxone methiodide, significantly increased blood flow to the stomach (from 0.41 +/- 0.022 to 0.9 +/- 0.016# ml x g (-1) x min(-1) with naloxone), jejunum (from 0.31 +/- 0.024 to 0.83 +/- 0.083# ml x g(-1) x min(-1) with naloxone), colon (from 0.41 +/- 0.057 to 0.68 +/- 0.008# ml x g(-1) x min(-1) with naloxone), spleen (from 1.45 +/- 0.21 to 2.13 +/- 0.25# ml x g(-1) x min(-1) with naloxone), pancreas (from 0.97 +/- 0.021 to 1.25 +/- 0.005# ml x g(-1) x min(-1) with naloxone), and kidneys (from 3.24 +/- 0.108 to 5.31 +/- 0.26# ml x g(-1) x min(-1) with naloxone), without altering cardiac output or arterial blood pressure in conscious dogs. There were no differences in the hemodynamics or cardiac output between the two experiments. Data are presented as mean +/- SD. Conclusions The increased splanchnic perfusion after naloxone is not caused by direct peripheral vascular effects or increased cardiac output. Indirect vasodilative effects on splanchnic vessels mediated by actions of naloxone on the central nervous system account for the increased gastrointestinal perfusion after naloxone in dogs.


2021 ◽  
Author(s):  
Asif Hasan Sharif

The fractal component in the complex fluctuations of the human heart rate represents a dynamic feature that is widely observed in diverse fields of natural and artificial systems. It is also of clinical significance as the diminishing of the fractal dynamics appears to correlate with heart disease processes and adverse cardiac events in old age. While the autonomic nervous system directly controls the pacemaker cells of the heart, it does not provide an immediate characterization of the complex heart rate variability (HRV). The central nervous system (CNS) is known to be an important modulator for various cardiac functions. However, its role in the fractal HRV is largely unclear. In this research, human experiments were conducted to study the influence of the central nervous system on fractal dynamics of healthy human HRV. The head up tilt (HUT) maneuver is used to provide a perturbation to the autonomic nervous system. The subsequent fractal effect in the simultaneously recorded electroencephalography and beat-to-beat heart rate data was examined. Using the recently developed multifractal factorization technique, the common multifractality in the data fluctuation was analyzed. An empirical relationship was uncovered which shows the increase (decrease) in HRV multifractality is associated with the increase (decrease) in multifractal correlation between scale-free HRV and the cortical expression of the brain dynamics in 8 out of 11 healthy subjects. This observation is further supported using surrogate analysis. The present findings imply that there is an integrated central-autonomic component underlying the cortical expression of the HRV fractal dynamics. It is proposed that the central element should be incorporated in the fractal HRV analysis to gain a more comprehensive and better characterization of the scale-free HRV dynamics. This study provides the first contribution to the HRV multifractal dynamics analysis in HUT. The multivariate fractal analysis using factorization technique is also new and can be applied in the more general context in complex dynamics research.


2020 ◽  
Vol 8 (6) ◽  
pp. 1146-1149

This note explains about “Parkinson Disease which may be a long-term disorder of the central nervous system”. The research paper focuses on analysis of symptoms of “Parkinson Disease” to predict the disease in early stage. Concept of FCMs was used to interpret the diagnostic symptoms of “Parkinson Disease”. The target is to draw connection between the symptoms and provide likely explanation.


1981 ◽  
Vol 241 (4) ◽  
pp. H479-H485 ◽  
Author(s):  
J. W. Holaday ◽  
M. O'Hara ◽  
A. I. Faden

The possible involvement of pituitary endorphins in the pathophysiology of shock was evaluated by measuring cardiorespiratory variables after naloxone injection in conscious hypophysectomized and sham-hypophysectomized rats subjected to controlled hemorrhage. Additionally, the role of the central nervous system (CNS) in mediating the cardiodepressant effects of endorphins in shock was studied. After the induction of hypovolemic shock (20 min at below 40 mmHg), hypophysectomized and sham-hypophysectomized rats received intraventricular (ivt) injections of naloxone HCl (10 micrograms) or an equivalent volume of saline (20 microliters over 20 s). In sham-hypophysectomized rats, both injections significantly elevated mean arterial pressure and pulse pressure; however, the increase produced by naloxone was significantly greater than that produced by saline. By contrast, hypophysectomized rats showed no response to naloxone or saline. Intravenous (iv) administration of naloxone HCl (3 mg/kg) or saline to these same hypophysectomized rats 15 min after ivt administration had no additional cardiovascular effects; as before, only animals with intact pituitaries responded to naloxone. Heart rate and respiration rate were unaffected by ivt or iv naloxone. From these data we suggest that pituitary endorphins contribute to the pathophysiology of hypovolemic shock, at least in part through actions within the CNS.


1999 ◽  
Vol 5 (S2) ◽  
pp. 1340-1341
Author(s):  
E. Bushong ◽  
M. E. Martone ◽  
C. Foster ◽  
M. H. Ellisman

Each astrocyte forms an extensive network of fine processes within the surrounding neural tissue, interacting extensively with neighboring neurons and blood vessels. Fine glial processes surround synapses and probably modulate synaptic transmission. Glial endfeet on capillaries are responsible for transport of ions and metabolites and possibly control blood flow. Alterations in these fine structures may be of significance in brain function and disease. Glial fibrillary acidic protein (GFAP) is an intermediate filament found in astrocytes of the central nervous system. GFAP is commonly found in the perikarya and processes of protoplasmic and fibrous type astrocytes. Immunohistochemical labeling of GFAP is extensively used as a means of determining the location and shape of astrocytes. However, its labeling pattern varies with brain region (e.g. cortex vs. hippocampus), with cell state (natural vs. reactive astrocytes), and with the specific α- GFAP antibody used. Furthermore, Golgi-stained or dye-filled astrocytes show numerous small appendages or vellate structures that conform to the surrounding tissue and do not stain for GFAP.


1997 ◽  
Vol 272 (5) ◽  
pp. H2361-H2368 ◽  
Author(s):  
R. L. Davisson ◽  
M. D. Travis ◽  
J. N. Bates ◽  
A. K. Johnson ◽  
S. J. Lewis

This study examined whether the stereoselective actions of S-nitrosocysteine (SNC) in the central nervous system involves the activation of stereoselective SNC recognition sites. We examined the effects produced by intracerebroventricular injection of the L- and D-isomers of SNC (L- and D-SNC) on mean arterial blood pressure, heart rate, and vascular resistances in conscious rats. We also examined the hemodynamic effects produced by intracerebroventricular injections of 1) L-cystine, the major non-nitric oxide (NO) decomposition product of L-SNC, 2) the parent thiols L- and D-cysteine, and 3) the bulky S-nitrosothiol L-S-nitroso-gamma-glutamylcysteinylglycine [L-S-nitrosoglutathione, (L-SNOG)]. Finally, we examined the decomposition of L- and D-SNC and L-SNOG to NO on their addition to brain homogenates. The intracerebroventricular injection of L-SNC (250-1,000 nmol) produced falls in mean arterial pressure, increases in heart rate, and a dose-dependent pattern of changes in hindquarter, renal, and mesenteric vascular resistances. The intracerebroventricular injections of D-SNC, L-cystine, and L-SNOG produced only minor effects. The intracerebroventricular injection of L-cysteine produced pressor responses and tachycardia, whereas D-cysteine was inactive. L- and D-SNC decomposed equally to NO on addition to brain homogenates. L-SNOG decomposed to similar amounts of NO as L- and D-SNC. These results suggest that SNC may activate stereoselective SNC recognition sites on brain neurons and that S-nitrosothiols of substantially different structure do not stimulate these sites. These recognition sites may be stereoselective membrane-bound receptors for which L-SNC is the unique ligand.


1995 ◽  
Vol 7 (3) ◽  
pp. 549 ◽  
Author(s):  
AJ Llanos ◽  
RA Riquelme ◽  
FA Moraga ◽  
G Cabello ◽  
JT Parer

The fetal llama exposed to an intense degree of hypoxaemia did not increase cerebral blood flow, but showed a marked peripheral vasoconstriction. The same cardiovascular response is observed in fetal sheep submitted to a extremely severe hypoxaemia, when the initial compensatory vasodilatory mechanisms in brain and heart fail. To investigate whether the fetal llama responses to acute hypoxaemia are adaptive, or whether they are the result of a breakdown of mechanisms of blood flow redistribution that favours the central nervous system, we studied seven fetal llamas (0.6-0.7 of gestation) chronically-catheterized during 1 h of graded and progressive hypoxaemia. Fetal ascending aorta blood gases and fetal cardiac output and its distribution (radiolabelled-microspheres) were measured after 60 min of normoxaemia (B) and at the end of 20 min (H20), 40 min (H40) and 60 min (H60) of hypoxaemia. Data were analysed by ANOVA and Newman-Keuls tests. Each treatment resulted in a lower (P < 0.05) percentage of haemoglobin saturation than hypoxaemia; H40 was lower than H20, and H60 was lower than H20 and H40. No statistical difference was observed among treatments for cardiac output or cerebral blood flow. These results demonstrate that fetal cardiac output and brain blood flow are maintained at all degrees of hypoxaemia, indicating that these cardiovascular responses are an adaptive response in the llama fetus, rather than an index of cardiorespiratory decompensation.


PEDIATRICS ◽  
1949 ◽  
Vol 3 (2) ◽  
pp. 253-253

Gives the facts and correlation needed to understand the simple workings of the central nervous system. Serves as a preface to start the student with three dimensional orientation towards neurology and psychiatry, leading up to a description of the principal disease entities. The chapters on cerebral blood flow, the types of neurons in the autonomic system and the motor areas of the cerebral cortex have been largely rewritten. The author is Bullard Professor of Neuropathology, Harvard Medical School and Psychiatrist in Chief, Massachusetts General Hospital.


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