The Relationship between Oxygen Delivery and Consumption in the Conscious Rat before and after Expansion of Body Fluid Volumes

1984 ◽  
Vol 66 (1) ◽  
pp. 91-98 ◽  
Author(s):  
J. M. Ledingham ◽  
S. Gofford ◽  
S. J. W. Evans

1. Oxygen consumption and delivery (defined as the product of cardiac output, haemoglobin concentration and arterial oxygen saturation) and haemodynamic variables were examined in the conscious resting rat throughout the day and after the expansion of body fluid volumes. Cardiac output was measured in arbitrary units by electromagnetic flowmetry and oxygen consumption by respirometry. 2. The variability of blood pressure in the basal state was significantly less than that of cardiac output. 3. Oxygen consumption was significantly correlated with cardiac output and oxygen delivery. 4. In studies undertaken throughout the day, both oxygen consumption and delivery fell in the afternoon and there was evidence that the relationship between these two variables was curvi- rather than recti-linear. 5. During oral sodium chloride administration for 7 days, blood pressure rose and some evidence was found for an alteration in the relationship between oxygen consumption and delivery, with an excess of delivery relative to consumption, particularly on the first day of salt loading. 6. Intravenous injection of sodium chloride solution (0.171 mol/l) did not alter the relationship between oxygen consumption and delivery. 7. Expansion of blood volume, while the packed cell volume was maintained nearly constant, raised oxygen delivery transiently and evidence was obtained that the relationship between oxygen consumption and delivery was altered, with oxygen delivery rising relatively more than oxygen consumption. 8. The findings are discussed in relation to the autoregulatory hypothesis of circulatory control and for the role of autoregulation in hypertensive states. The importance of relating oxygen delivery to metabolic requirements in studies of the role of autoregulation is emphasized.

Author(s):  
Jaana Humaloja ◽  
Markus B. Skrifvars ◽  
Rahul Raj ◽  
Erika Wilkman ◽  
Pirkka T. Pekkarinen ◽  
...  

Abstract Background In neurocritically ill patients, one early mechanism behind secondary brain injury is low systemic blood pressure resulting in inadequate cerebral perfusion and consequent hypoxia. Intuitively, higher partial pressures of arterial oxygen (PaO2) could be protective in case of inadequate cerebral circulation related to hemodynamic instability. Study purpose We examined whether the association between PaO2 and mortality is different in patients with low compared to normal and high mean arterial pressure (MAP) in patients after various types of brain injury. Methods We screened the Finnish Intensive Care Consortium database for mechanically ventilated adult (≥ 18) brain injury patients treated in several tertiary intensive care units (ICUs) between 2003 and 2013. Admission diagnoses included traumatic brain injury, cardiac arrest, subarachnoid and intracranial hemorrhage, and acute ischemic stroke. The primary exposures of interest were PaO2 (recorded in connection with the lowest measured PaO2/fraction of inspired oxygen ratio) and the lowest MAP, recorded during the first 24 h in the ICU. PaO2 was grouped as follows: hypoxemia (< 8.2 kPa, the lowest 10th percentile), normoxemia (8.2–18.3 kPa), and hyperoxemia (> 18.3 kPa, the highest 10th percentile), and MAP was divided into equally sized tertiles (< 60, 60–68, and > 68 mmHg). The primary outcome was 1-year mortality. We tested the association between hyperoxemia, MAP, and mortality with a multivariable logistic regression model, including the PaO2, MAP, and interaction of PaO2*MAP, adjusting for age, admission diagnosis, premorbid physical performance, vasoactive use, intracranial pressure monitoring use, and disease severity. The relationship between predicted 1-year mortality and PaO2 was visualized with locally weighted scatterplot smoothing curves (Loess) for different MAP levels. Results From a total of 8290 patients, 3912 (47%) were dead at 1 year. PaO2 was not an independent predictor of mortality: the odds ratio (OR) for hyperoxemia was 1.16 (95% CI 0.85–1.59) and for hypoxemia 1.24 (95% CI 0.96–1.61) compared to normoxemia. Higher MAP predicted lower mortality: OR for MAP 60–68 mmHg was 0.73 (95% CI 0.64–0.84) and for MAP > 68 mmHg 0.80 (95% CI 0.69–0.92) compared to MAP < 60 mmHg. The interaction term PaO2*MAP was nonsignificant. In Loess visualization, the relationship between PaO2 and predicted mortality appeared similar in all MAP tertiles. Conclusions During the first 24 h of ICU treatment in mechanically ventilated brain injured patients, the association between PaO2 and mortality was not different in patients with low compared to normal MAP.


1994 ◽  
Vol 267 (1) ◽  
pp. R84-R88 ◽  
Author(s):  
M. Huang ◽  
M. L. Leblanc ◽  
R. L. Hester

The study tested the hypothesis that the increase in blood pressure and decrease in cardiac output after nitric oxide (NO) synthase inhibition with N omega-nitro-L-arginine methyl ester (L-NAME) was partially mediated by a neurogenic mechanism. Rats were anesthetized with Inactin (thiobutabarbital), and a control blood pressure was measured for 30 min. Cardiac output and tissue flows were measured with radioactive microspheres. All measurements of pressure and flows were made before and after NO synthase inhibition (20 mg/kg L-NAME) in a group of control animals and in a second group of animals in which the autonomic nervous system was blocked by 20 mg/kg hexamethonium. In this group of animals, an intravenous infusion of norepinephrine (20-140 ng/min) was used to maintain normal blood pressure. L-NAME treatment resulted in a significant increase in mean arterial pressure in both groups. L-NAME treatment decreased cardiac output approximately 50% in both the intact and autonomic blocked animals (P < 0.05). Autonomic blockade alone had no effect on tissue flows. L-NAME treatment caused a significant decrease in renal, hepatic artery, stomach, intestinal, and testicular blood flow in both groups. These results demonstrate that the increase in blood pressure and decreases in cardiac output and tissue flows after L-NAME treatment are not dependent on a neurogenic mechanism.


Neurology ◽  
2021 ◽  
pp. 10.1212/WNL.0000000000012065
Author(s):  
Yuan Ma ◽  
Deborah Blacker ◽  
Anand Viswanathan ◽  
Susanne J. van Veluw ◽  
Daniel Bos ◽  
...  

ObjectiveLarge systolic blood pressure (SBP) variability has been proposed as a novel risk factor for dementia above and beyond SBP levels, but the underlying neuropathology is largely unknown. We investigated the relationship among visit-to-visit SBP variability, cognitive deterioration and underlying neuropathological changes.MethodsWe used longitudinal data (between 2005 and 2019) from the National Alzheimer’s Coordinating Center. 13,284 dementia-free participants aged≥50 years were followed over a median of 5.0 (interquartile range: 3.1-7.6) years. Neuropathology data were available in 1,400 autopsied participants. Visit-to-visit SBP variability was quantified from repeated annual SBP measurements. Cognitive deterioration was defined as conversion from normal cognition to mild cognitive impairment (MCI) or dementia, or from MCI to dementia.ResultsLarger visit-to-visit SBP variability was associated with cognitive deterioration (adjusted odds ratio comparing extreme quintiles: 2.64; 95%CI:2.29-3.04, P <0.001). It was also associated with a higher burden of vascular pathology (including microinfarcts, white matter lesion, atherosclerosis of the circle of Willis and arteriolosclerosis) and with neurofibrillary tangle pathology assessed by Braak staging (All P < 0.05). The association with cognitive deterioration and vascular pathology appeared stronger among those with normal cognition versus MCI at baseline. These findings were observed after adjusting for age, sex, mean SBP and other confounding variables. Similar results were observed for diastolic BP variability.ConclusionLarger visit-to-visit SBP variability was associated with cognitive deterioration. It was also associated with cerebrovascular pathology and neurofibrillary tangles. These results suggest the intertwined role of vascular and Alzheimer's disease pathology in the etiology of dementia.


2010 ◽  
Vol 22 (3) ◽  
pp. 369-378 ◽  
Author(s):  
Joey C. Eisenman ◽  
Mark A. Sarzynski ◽  
Jerod Tucker ◽  
Kate A. Heelan

The purpose of this study was to examine if offspring physical activity may affect the relationship between maternal overweight and offspring fatness and blood pressure (BP). Subjects included 144 maternal-child pairs (n = 74 boys and 70 girls, mean age = 7.3 yrs). Maternal prepregnancy BMI was determined by self-report. Offspring characteristics included resting systolic and diastolic BP, body fatness by dual energy x-ray absorbtiometry, and moderate-to-vigorous physical activity (MVPA) using the Actigraph accelerometer. Children whose mothers were overweight or obese prepregnancy (Prepreg OW) were significantly larger and fatter than children from mothers with a normal prepregnancy BMI (Prepreg NORM). Prepreg OW children also had higher mean arterial pressure than Prepreg NORM children. BP values were not different across maternal Prepreg BMI/MVPA groups. Percent fat was significantly different across Prepreg BMI/MVPA groups. Prepreg OW children that did not meet the daily recommended value of MVPA were the fattest. Prepreg OW children that attained 360 min of MVPA/day had a mean percent body fat that was similar to Prepreg NORM children of either MVPA group.


1991 ◽  
Vol 260 (2) ◽  
pp. H632-H637 ◽  
Author(s):  
D. S. O'Leary

When large changes in baseline blood flow occur in regional vascular beds (i.e., in skeletal muscle between rest and dynamic exercise or in skin between normothermia and hyperthermia) opposite conclusions are often drawn regarding the magnitude of a given vasomotor response (such as baroreflex vasoconstriction during hypotension) using regional resistance versus conductance. This report analyzes the relationship between changes in regional resistance or conductance and the contribution of the responses in the maintenance of blood pressure. The main supposition is that the appropriate index of baroreflex responses should reflect the importance of the response in the maintenance of blood pressure. Through differential analysis of the relationship between changes in resistance and conductance on arterial pressure, it can be seen that in terms of resistance, the effect of a given change in resistance on arterial pressure is greatly dependent on the baseline level of resistance. For conductance, while a modest baseline effect exists when cardiac output changes markedly, at a constant cardiac output, the same change in regional conductance always causes the same change in arterial pressure regardless of the initial value of conductance. Conclusions drawn are that while neither resistance nor conductance is a perfect index of vasomotor responses, changes in conductance far better reflect the importance of the response in pressure regulation than do changes in regional resistance.


2020 ◽  
Vol 1 (1) ◽  
pp. 72-9
Author(s):  
Alfan Mahdi Nugroho ◽  
Yusmein Uyun ◽  
Annemarie Chrysantia Melati

Analgesia epidural telah diperkenalkan secara rutin sebagai salah satu modalitas analgesia pada proses persalinan sejak lama. Hubungan antara analgesia epidural persalinan dengan demam intrapartum pada maternal sudah disebutkan pada beberapa literatur. Demam didefinisikan sebagai peningkatan suhu tubuh lebih dari 38 oC yang didapat dari dua kali pemeriksaan. Beberapa teori yang disebutkan antara lain perubahan termoregulasi, infeksi pada ibu-janin dan inflamasi non-infeksi yang dimediasi oleh sitokin proinflamasi. Namun demikian berbagai mekanisme analgesia epidural dapat menyebabkan demam masih terus diteliti. Identifikasi demam pada ibu saat persalinan merupakan hal yang penting untuk dilakukan karena memiliki konsekuensi klinis pada ibu dan neonatus. Pada ibu ditemukan suhu yang meningkat dikaitkan dengan peningkatan denyut jantung ibu, curah jantung, konsumsi oksigen, dan produksi katekolamin. Sedangkan pada janin demam intrapartum dapat menyebabkan sepsis, perubahan skor APGAR, peningkatan kebutuhan bantuan napas dan kejadian kejang. Efek demam pada ibu dan janin masih terus dipelajari, sehingga suatu saat didapatkan cara pencegahan yang paling baik yang pada akhirnya menghindarkan keraguan untuk melakukan analgesia persalinan.   Fever during labour epidural analgesia Abstract Epidural analgesia has been routinely introduced as one of the analgesia modalities during labour. Literature has mentioned the relationship between epidural analgesia and intrapartum fever among mothers. Fever is defined as increased temperature above 38 oC in more than two measurements. Several theories have been proposed, inculing thermoregulation changes, mother-fetal infection, and non-infectious inflammation mediated by proinflammatory cytokines. However, these mechanisms have been continued to evolve. Fever identification in pregnant women is essential to recognize clinical consequences to both mothers and neonates. Increased temperature in mothers is associated with increased heart rate, cardiac output, oxygen consumption, and catecholamines production. Meanwhile, in neonates intrapartum fever is related to sepsis, APGAR score changes, the need of respiratory support and incidence of neonatal seizure. Therefore, these consequences are extensively studied in order to determine the appropriate prevention.


1963 ◽  
Vol 41 (1) ◽  
pp. 1949-1953 ◽  
Author(s):  
Margaret Beznák ◽  
P. Hacker

Subcutaneous injection of 40 mg/kg isoproterenol is followed within 2 minutes by a fall in blood pressure and peripheral resistance, by tachycardia, and by an increase in cardiac output. It seems likely that these hemodynamic changes are a consequence of a direct action of isoproterenol on the myocardium. Isoproterenol also causes a significant increase in the oxygen consumption of the rats. The increased oxygen demand of the tissues may play a role in maintaining the hemodynamic changes for periods of more than an hour after isoproterenol. Signs of histological damage in the myocardium begin to appear without affecting the function of the cardiovascular system, as measured by the tests used.


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