scholarly journals Cerebral Blood Flow Autoregulation in Acute Intracranial Hypertension

1994 ◽  
Vol 14 (3) ◽  
pp. 519-525 ◽  
Author(s):  
John Hauerberg ◽  
Marianne Juhler

The present series of experiments was carried out to investigate CBF autoregulation during fixed levels of acute increased intracranial pressure (ICP). Three groups of six rats each, one with normal ICP (8 mm Hg), one with moderately increased ICP (30 mm Hg), and one with severely increased ICP (50 mm Hg), were investigated. ICP was maintained by continuous infusion of lactated Ringer solution into the cisterna magna. Cerebral perfusion pressure (CPP), calculated as mean arterial blood pressure – ICP, was increased by intravenously infused norepinephrine and decreased by controlled bleeding. In all groups the corresponding autoregulation curve included a plateau where CBF was independent of changes in CPP, demonstrating intact autoregulation. However, a significant shift of the lower limit of autoregulation (LL) toward lower CPP levels during severe intracranial hypertension was observed (p < 0.006). In the controls the LL was found at CPP = 73 ±6 mm Hg, in moderately increased ICP the LL was 59 ± 4 mm Hg, and in severely increased ICP the LL was 51 ±4 mm Hg. These results indicate that an acute elevation of ICP activates a reserve capacity of cerebral resistance vessels that dilate further below the normal physiological LL to maintain CBF at low levels of CPP.

2004 ◽  
Vol 287 (3) ◽  
pp. H1404-H1409 ◽  
Author(s):  
Dan P. Stephens ◽  
Adham R. Saad ◽  
Lee Ann T. Bennett ◽  
Wojciech A. Kosiba ◽  
John M. Johnson

Previous studies have provided evidence of a non-noradrenergic contributor to reflex cutaneous vasoconstriction in humans but did not identify the transmitter responsible. To test whether neuropeptide Y (NPY) has a role, in two series of experiments we slowly reduced whole body skin temperature (TSK) from 34.5 to 31.7°C. In protocol 1, Ringer solution and the NPY receptor antagonist BIBP-3226 alone were delivered intradermally via microdialysis. In protocol 2, yohimbine plus propranolol (Yoh + Pro), Yoh + Pro in combination with BIBP-3226, and Ringer solution were delivered to antagonize locally the vasomotor effects of NPY and norepinephrine. Blood flow was measured by laser Doppler flowmetry (LDF). Mean arterial blood pressure (MAP) was monitored at the finger (Finapres). In protocol 1, cutaneous vascular conductance (CVC) fell by 45%, to 55.1 ± 5.6% of baseline at control sites ( P < 0.05). At BIBP-3226-treated sites, CVC fell by 34.1% to 65.9 ± 5.0% ( P < 0.05; P < 0.05 between sites). In protocol 2, during body cooling, CVC at control sites fell by 32.6%, to 67.4 ± 4.3% of baseline; at sites treated with Yoh + Pro, CVC fell by 18.7%, to 81.3 ± 4.4% of baseline ( P < 0.05 vs. baseline; P < 0.05 vs. control) and did not fall significantly at sites treated with BIBP-3226 + Yoh + Pro ( P > 0.05; P < 0.05 vs. other sites). After cooling, exogenous norepinephrine induced vasoconstriction at control sites ( P < 0.05) but not at sites treated with Yoh + Pro + BIBP-3226 ( P > 0.05). These results indicate that NPY participates in sympathetically mediated cutaneous vasoconstriction in humans during whole body cooling.


1988 ◽  
Vol 65 (2) ◽  
pp. 964-970 ◽  
Author(s):  
T. I. Musch ◽  
A. Bruno ◽  
G. E. Bradford ◽  
A. Vayonis ◽  
R. L. Moore

Two different open-circuit techniques of measuring metabolic rate were examined in rats at rest and during exercise. With one technique ambient air was drawn through a tightly fitting mask that was secured to the rat's head, whereas with the other technique the rat was placed into and ambient air was drawn through a Plexiglas box. Two series of experiments were performed. In series I, two groups were studied that consisted of rats that had received myocardial infarctions produced by coronary arterial ligations and rats that had received sham operations. In this series of experiments O2 uptake (VO2) and CO2 production (VCO2) were measured at rest, during four levels of submaximal exercise, and during maximal treadmill exercise in the same group of rats by use of both techniques in random order. VO2, VCO2, and the calculated respiratory exchange ratio (R) were similar at rest, during the highest level of submaximal exercise (20% grade, 37 m/min), and during maximal exercise; however, VO2 and VCO2 were significantly lower with the metabolic box technique compared with the mask technique during the three lowest work loads (5% grade, 19 m/min; 10% grade, 24 m/min; and 15% grade, 31 m/min). These differences appeared to be associated with a change in gait produced when the mask was worn. In series II, the arterial blood gas and acid-base responses to both submaximal and maximal exercise were measured using both techniques in a group of instrumented rats that had a catheter placed into the right carotid artery.(ABSTRACT TRUNCATED AT 250 WORDS)


2021 ◽  
Author(s):  
Parisa Naraei ◽  
Alireza Sadeghian

Intracranial pressure (ICP), the pressure within the cranium reflects three elements: cerebrospinal fluid, brain tissue and blood pressure. High ICP (above 20 mmHg) is called intracranial hypertension (ICH) which is due to the tumour, swelling or the internal bleeding of brain and may cause secondary damage to the brain. ICP is a crucial parameter in diagnosis of brain injuries. Two models which utilize machine learning techniques to anticipate ICH and assist in clinical decision making were developed in the present thesis. ICP can be monitored through the invasive techniques (i.e., inserting an intraventricular catheter through the skull). Despite the high accuracy, the episodes of ICH can also be manually identified only after placement of catheter which is accompanied by lots of technical difficulties. Furthermore, the ICP signal might not be available continuously or may include unwanted noise that could introduce more complication to the diagnosis and treatment procedure. Considering the difficulties of the invasive techniques, a non-invasive model, capable to predict the ICH helps to save time, estimate the missing ICPs, predict the ICP in advance and accelerate medical intervention. The present thesis introduces two machine learning models to resolve the current limitations: 1- Non-invasive prediction of ICP labels 10 minutes in advance where the status of ICP (normal / ICH) is predicted based on the two components extracted from the physiological signals such as mean arterial blood pressure and respiration rate. 2- Wavelet – clustering where a machine learning solution for ICP estimation using a hybrid wavelet clustering is proposed. The episodes of ICP and derived from ICP (such as cerebral perfusion pressure) are excluded from the second model.


1974 ◽  
Vol 60 (3) ◽  
pp. 901-908
Author(s):  
M. G. EMíLIO

1. The respiratory exchanges through the lungs and skin of frogs and the time courses of blood gas concentrations were studied during emergence and diving periods. 2. Most of the total oxygen uptake is carried out through the lungs. The partial pressure of oxygen in arterial blood falls to very low levels a few minutes after diving, showing that the cutaneous respiratory surface cannot compensate for the lack of lung respiration. 3. Most of the metabolic carbon dioxide is disposed of through the skin. Although the skin output is maintained through diving periods, there is an important rise in the partial pressure of carbon dioxide in blood following submergence. However, the total concentration of CO2 in the blood decreases, as does the blood pH value. 4. This phenomenon is probably the result of a metabolic acidosis due to the switching on of anaerobic processes during diving periods.


1988 ◽  
Vol 254 (3) ◽  
pp. H525-H531
Author(s):  
G. J. Crystal

To evaluate the effect of hemodilution per se on coronary hemodynamics, experiments were performed in 36 anesthetized, open-chest dogs whose left anterior descending coronary artery (LAD) was perfused selectively with either normal arterial blood or arterial blood diluted with lactated Ringer solution. LAD blood flow (CBF) was measured with an electromagnetic flowmeter and its transmural distribution assessed with 15-microns radioactive microspheres. LAD perfusion pressure was set at the normal level (approximately 100 mmHg) or at 50% of that level to simulate coronary insufficiency. Dilator reserve capacity was calculated from ratio of reactive hyperemic peak flow following release of 90-s occlusion to control (preocclusion) flow. Systemic hemodynamic parameters were maintained near control values during coronary hemodilution. With perfusion pressure normal, graded hemodilution caused progressive, transmurally uniform increases in CBF that showed a nonlinear relationship to inflow hematocrit. Increased peak reactive hyperemic flow and decreased dilator reserve ratio indicated that both reduced viscosity and vasodilation contributed to increased CBF during hemodilution. Hypotension alone reduced CBF, with greater effect in the subendocardium. Additional hemodilution returned CBF to normotensive value, but relative subendocardial hypoperfusion persisted. The present study provides fundamental information on effects of hemodilution on coronary hemodynamics without the systemic responses that complicated previous studies utilizing whole body exchange transfusions.


1980 ◽  
Vol 8 (4) ◽  
pp. 474-478 ◽  
Author(s):  
A. W. Duncan ◽  
M. T. Gleeson

A case of traumatic cerebral oedema is reported in which the infusion of small volumes of stable plasma protein solution (SPPS) resulted in acute and massive increases in intracranial pressure. The batch of SPPS responsible was found to have high levels of prekallikrein activator which is thought to be the cause of the systemic hypotension previously described with plasma proteins solutions. A second batch of SPPS with low levels of prekallikrein activator generated much smaller increases in intracranial pressure. The mechanism of this phenomenon is discussed and a recommendation made for the cautious use of SPPS when intracranial hypertension is present or suspected.


1982 ◽  
Vol 52 (2) ◽  
pp. 287-294 ◽  
Author(s):  
H. V. Forster ◽  
J. P. Klein ◽  
L. H. Hamilton ◽  
J. P. Kampine

This study was designed to determine whether 1) arterial PCO2 (PaCO2) increases when inspired PCO2 (PICO2) is increased from less than 0.4 Torr (eupnea) to 7 or 14 Torr, and 2) ventilatory sensitivity to CO2 (delta VE/ delta PaCO2) is greater at low levels of PICO2 (7–21 Torr) than it is at higher levels (28–42 Torr). Human subjects were studied while seated in an environmental chamber that permitted alteration of PICO2 by changing the chamber PCO2. In study 1, arterial blood was sampled over the final 5 min of a eupneic period and again 10–15 min later when PICO2 was 7 or 14 Torr. With this protocol, PACO2 was increased above eupnea by 0.7 (P less than 0.02) and 0.9 Torr (P less than 0.01) when PICO2 was 7 and 14 Torr, respectively. In study 2, arterial blood was sampled every 5 min during two 1-h periods of eupnea that were separated by 3 h during which PICO2 was increased by 7 Torr each 0.5 h. With this protocol there was no consistent difference in PACO2 between eupneic periods and periods when PICO2 was 7–14 Torr. There was a progressively increased hypercapnia as PICO2 was increased from 7 to 42 Torr. The delta VE/ delta PaCO2 was less than half for data obtained at low relative to high PICO2. The two studies demonstrated that measurement error and physiologic variation necessitate using a “powerful” experimental design (study 1) to detect small increases in PaCO2. On the basis of these results, we have concluded that there is no apparent reason to postulate a sensory mechanism other than the carotid and intracranial chemoreceptors to account for the hyperpnea during CO2 inhalation. Specifically, isocapnic hyperpnea probably does not occur.


2020 ◽  
Vol 74 (10) ◽  
pp. 1263-1273
Author(s):  
Lorilee S.L. Arakaki ◽  
Wayne A. Ciesielski ◽  
D. Michael McMullan ◽  
Kenneth A. Schenkman

In critically ill patients, direct knowledge of intracellular pO2 would allow for identification of cellular hypoxia, which when prolonged leads to organ failure. We have developed a visible–near-infrared optical system that noninvasively measures myoglobin saturation, which is directly related to intracellular pO2, from the surface of the skin. We used an animal model of graded hypoxia from low levels of inspired oxygen ( n = 5) and verified that low intracellular pO2 is correlated with high steady-state serum lactate values. In addition, the pO2 gradient between arterial blood and inside muscle cells was 83 mm Hg at 21% O2, but fell to 24 mm Hg at 8% O2. Continuous myoglobin saturation measurement in skeletal muscle displayed the same trends as cerebral oxygenation with no lag in changes over time, demonstrating its relevance as a measure of systemic oxygenation.


1992 ◽  
Vol 263 (4) ◽  
pp. R945-R953 ◽  
Author(s):  
V. L. Tucker ◽  
K. E. Simanonok ◽  
E. M. Renkin

Blood-tissue transport of 131I-labeled bovine serum albumin (BSA) during intravenous infusion of synthetic atrial natriuretic peptide (ANP) was examined in anesthetized male Wistar rats. Plasma volumes were maintained at pre-ANP levels by infusion of 2% BSA in lactated Ringer solution (LR) to minimize compensatory responses to ANP-induced hypovolemia. 131I-BSA clearance was measured over 30 min, and 125I-BSA was injected terminally to correct for intravascular volume. Thirty-minute infusion of 20 ng.kg-1.min-1 ANP resulted in a tissue-selective increase in 131I-BSA clearance in jejunum and colon compared with controls given LR only. Smaller but significant increases in tracer clearance also were observed in fat, kidney, left ventricle, and skeletal muscle exposed to 400 ng.kg-1.min-1 ANP. The observed elevation in tracer albumin extravasation was not associated with any measurable increase in tissue extravascular water content. Furthermore, it was shown that coupling of 131I-BSA transport to filtration induced by hindlimb venous congestion was similar in control and ANP-treated rats. In a second series of experiments, plasma ANP levels were determined after 30-min ANP infusions from 0 to 180 ng.kg-1.min-1. Significant linear associations between physiological ANP levels (62-578 pg/ml) and 131I-BSA clearance were demonstrable for small intestine, colon, fat, kidney, and skeletal muscle but not for skin, heart, diaphragm, and lung. We conclude that raising plasma ANP by infusion of the synthetic peptide results in a filtration-independent, tissue-selective increase in albumin transport. Tissue uptake of albumin is a potential mechanism for extrarenal fluid shift during circulatory volume overload.


1988 ◽  
Vol 255 (1) ◽  
pp. R73-R81 ◽  
Author(s):  
T. J. Malkinson ◽  
K. E. Cooper ◽  
W. L. Veale

Adult male Wistar rats were anesthetized with urethan (1.5 g/kg). They were unable to maintain body temperature (Tb) in a warm (32 degrees C) or cool (9 degrees C) environment or at a laboratory room temperature of 22 degrees C. Tb was allowed to fall to 35.8, 34.5, or 33.3 degrees C, and prostaglandin E1 (PGE1, 400 ng) was delivered into a lateral cerebral ventricle. An immediate feverlike rise in Tb resulted, accompanied by vigorous shivering. Animals were vasoconstricted throughout. When Tb was raised to and maintained at 38.3 or 39.5 degrees C, animals also responded with a fever; however, the magnitude of the fever diminished as the starting Tb increased. In a series of experiments in which Tb was maintained (36.8-37.4 degrees C) by means of a heating pad, PGE1 delivered into a lateral cerebral ventricle or into the anterior hypothalamus caused a dose-dependent change in Tb, which was similar in time of onset, magnitude, and duration to that observed in conscious animals. This fever was accompanied by shivering and increased O2 uptake, heart rate, arterial blood pressure, respiratory rate, and intracranial pressure during the rising phase of the fever, and vasodilation of the paws occurred during defeveresence. Animals were also able to develop a dose-dependent rise in Tb in response to purified human interleukin 1.


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