Decreased Cardiac Output in Infants of Mothers Who Abused Cocaine

PEDIATRICS ◽  
1990 ◽  
Vol 85 (1) ◽  
pp. 30-32 ◽  
Author(s):  
Margot van de Bor ◽  
Frans J. Walther ◽  
Mahmood Ebrahimi

Cocaine increases the level of circulating catecholamines by blocking the catecholamine reuptake receptors. The effect of intrauterine cocaine exposure on cardiac output was studied in 15 full-term newborn infants whose mothers used cocaine during pregnancy. A total of 22 healthy nonexposed full-term infants served as a control group. On the first day of life, cardiac output (183 ± 12 vs 235 ± 13 mL/kg per minute, mean ± SD; P < .05) and stroke volume (1.3 ± 0.1 vs 1.9 ± 0.1 mL/kg, mean ± SD; P < .005) were lower and arterial blood pressure (60 ± 2 vs 41 ± 2 mmHg, mean ± SD; P < .001) higher in the infants exposed to cocaine. On day 2, cardiac output, stroke volume, and mean arterial blood pressure were similar, probably because of the gradual excretion of cocaine and its metabolites by the infant. It was speculated that an increase in plasma norepinephrine levels is responsible for the cardiovascular effects of intrauterine cocaine exposure.

1992 ◽  
Vol 263 (5) ◽  
pp. R1147-R1155 ◽  
Author(s):  
J. A. Taylor ◽  
G. A. Hand ◽  
D. G. Johnson ◽  
D. R. Seals

Our purpose was to test the hypothesis that human aging alters sympathoadrenal-circulatory control of arterial blood pressure during orthostasis. Plasma catecholamine and hemodynamic adjustments to two different forms of orthostatic stress, lower body suction (-10 to -50 mmHg) and standing, were determined in 14 young (26 +/- 1 yr) and 13 older (64 +/- 1) healthy, normally active men. During quiet supine rest, cardiac output tended to be lower and systemic vascular resistance higher in the older men, but no other differences were observed. On average, arterial blood pressure was well maintained during both forms of orthostasis in the two groups; the older men actually demonstrated better maintenance of pressure (P < 0.05) and a lesser incidence of orthostatic hypotension than the young men during lower body suction. Despite a blunted reflex tachycardia during orthostatic stress (P < 0.05), cardiac output tended to decrease less in the older men because of a smaller decline in stroke volume (P < 0.05, suction only), whereas the reflex increases in systemic vascular resistance were not different in the two groups. The whole forearm vasoconstrictor response tended to be attenuated in the older men during lower body suction, but was identical in the two groups with standing. Forearm skin vascular resistance was unaltered during lower body suction in both groups. Orthostasis-evoked increases in antecubital venous plasma norepinephrine concentrations were similar in the young and older men, whereas little or no increases in plasma epinephrine concentrations were observed in either group.(ABSTRACT TRUNCATED AT 250 WORDS)


2012 ◽  
Vol 112 (11) ◽  
pp. 1832-1838 ◽  
Author(s):  
Tatsuya Arai ◽  
Kichang Lee ◽  
Robert P. Marini ◽  
Richard J. Cohen

The purpose of this study was to introduce and validate a new algorithm to estimate instantaneous aortic blood flow (ABF) by mathematical analysis of arterial blood pressure (ABP) waveforms. The algorithm is based on an autoregressive with exogenous input (ARX) model. We applied this algorithm to diastolic ABP waveforms to estimate the autoregressive model coefficients by requiring the estimated diastolic flow to be zero. The algorithm incorporating the coefficients was then applied to the entire ABP signal to estimate ABF. The algorithm was applied to six Yorkshire swine data sets over a wide range of physiological conditions for validation. Quantitative measures of waveform shape (standard deviation, skewness, and kurtosis), as well as stroke volume and cardiac output from the estimated ABF, were computed. Values of these measures were compared with those obtained from ABF waveforms recorded using a Transonic aortic flow probe placed around the aortic root. The estimation errors were compared with those obtained using a windkessel model. The ARX model algorithm achieved significantly lower errors in the waveform measures, stroke volume, and cardiac output than those obtained using the windkessel model ( P < 0.05).


2000 ◽  
Vol 279 (2) ◽  
pp. R531-R538 ◽  
Author(s):  
Tobias Wang ◽  
Michael Axelsson ◽  
Jorgen Jensen ◽  
J. Michael Conlon

The cardiovascular actions of python bradykinin (BK) and substance P (SP) have been investigated in the anesthetized ball python, Python regius. Bolus intra-arterial injections of python BK (0.03–3 nmol/kg) produced concentration-dependent increases in arterial blood pressure, heart rate (HR), and cardiac output concomitant with small decreases in systemic resistance and stroke volume. Intra-arterial injection of 3 nmol/kg python BK produced a tenfold increase in circulating concentration of norepinephrine, but epinephrine levels did not change. BK-induced tachycardia was attenuated (>90%) by the β-adrenergic receptor antagonist sotalol, and the hypertensive response was attenuated (>70%) by the α-adrenergic receptor antagonist prazosin, indicating that effects of python BK are mediated at least in part by activation of the extensive network of adrenergic neurons present in vascular tissues. Bolus intra-arterial injections of python SP in the range 0.01–30 pmol/kg produced concentration-dependent decreases in arterial blood pressure and systemic peripheral resistance concomitant with increases in cardiac output and stroke volume but with only minor effects on HR. The data suggest that kinins play a physiologically important role in cardiovascular regulation in the python.


1964 ◽  
Vol 19 (5) ◽  
pp. 833-838 ◽  
Author(s):  
Bengt Saltin ◽  
Jesper Stenberg

Four subjects worked on a treadmill or a bicycle ergometer for 180 min at oxygen uptakes of 75% of the individual's max Vo2; after 90 min rest, the exercise was resumed and a maximal work load was tried. Repeated circulatory studies were made. The body weight decreased 3.1 kg (3.2–5.2%), but the reduction in blood volume was less than 5%. During submaximal exercise the major change in the hemodynamic response was a decrease in stroke volume (from 126 to 107 ml). Oxygen uptake and cardiac output increased slightly. There was a decrease of about 10% in systolic, diastolic, and mean arterial blood pressure during the 180 min of exercise. When the work was performed in a supine position there was the same reduction in the stroke volume as in the sitting work position. At the maximal work oxygen uptake, cardiac output, heart rate, and blood pressure attained almost normal values but there was a marked decrease in both work time and blood lactates. dehydration; blood volume; arterial blood pressure; circulatory reaction Submitted on January 31, 1964


1986 ◽  
Vol 251 (1) ◽  
pp. R82-R90 ◽  
Author(s):  
J. W. Hubbard ◽  
R. H. Cox ◽  
B. J. Sanders ◽  
J. E. Lawler

Normotensive Wistar-Kyoto (WKY) rats and borderline hypertensive rats (BHR) were exposed to aversive classical conditioning procedures and chronically instrumented with arterial catheters and electromagnetic flow probes around the ascending aorta. After postoperative recovery, hemodynamic measurements and blood samples were obtained from conscious animals at rest and during aversive conditioning. The cardiovascular response to the behavioral stress consisted of a significant increase in mean arterial blood pressure, total peripheral resistance index, cardiac index, heart rate, and aortic dP/dt for both strains. However, the elevated vascular resistance seen in the BHR resulted in a significantly greater increase in mean arterial blood pressure (21 mmHg) compared with the WKY rats (14 mmHg). In addition, the BHR showed a significantly (P less than 0.05) greater plasma norepinephrine concentration (760 +/- 99 pg/ml) in response to the stress than did the WKY rats (559 +/- 53 pg/ml). These data suggest that an increase in cardiac output, elevated vascular resistance, and increased sympathetic drive may contribute to the development of stress-induced hypertension in this animal model.


2018 ◽  
Vol 1 (108) ◽  
pp. 2-8
Author(s):  
Kęstutis Bunevičius ◽  
Albinas Grunovas ◽  
Jonas Poderys

Background. Occlusion pressure intensity influences the blood flow intensity. Immediately after the cuff pressure is released, reactive hyperaemia occurs. Increased blood flow and nutritive delivery are critical for an anabolic stimulus, such as insulin. The aim of study was to find which occlusion pressure was optimal to increase the highest level of post occlusion reactive hyperaemia. Methods. Participants were randomly assigned into one of the four conditions (n = 12 per group): control group without blood flow restriction, experimental groups with 120; 200 or 300 mmHg occlusion pressure. We used venous occlusion plethysmography and arterial blood pressure measurements. Results. After the onset of 120 and 200 mm Hg pressure occlusion, the blood flow intensity significantly decreased. Occlusion induced hyperaemia increased arterial blood flow intensity 134 ± 11.2% (p < .05) in the group with 120 mmHg, in the group with 200 mmHg it increased 267 ± 10.5% (p < .05), in the group with 300 mmHg it increased 233 ± 10.9% (p < .05). Applied 300 mmHg occlusion from the 12 minute diastolic and systolic arterial blood pressure decreased statistically significantly. Conclusions. Occlusion manoeuvre impacted the vascular vasodilatation, but the peak blood flow registered after occlusion did not relate to applied occlusion pressure. The pressure of 200 mmHg is optimal to impact the high level of vasodilatation. Longer than 12 min 300 mmHg could not be recommended due to the steep decrease of systolic and diastolic blood pressures.


1991 ◽  
Vol 261 (1) ◽  
pp. H172-H180 ◽  
Author(s):  
L. M. Sassen ◽  
K. Bezstarosti ◽  
W. J. Van der Giessen ◽  
J. M. Lamers ◽  
P. D. Verdouw

Effects of pretreatment with L-propionylcarnitine (50 mg/kg, n = 9) or saline (n = 10) were studied in open-chest anesthetized pigs, in which ischemia was induced by decreasing left anterior descending coronary artery blood flow to 20% of baseline. After 60 min of ischemia, myocardium was reperfused for 2 h. In both groups, flow reduction abolished contractile function of the affected myocardium and caused similar decreases in ATP (by 55%) and energy charge [(ATP + 0.5ADP)/(ATP + ADP + AMP); decrease from 0.91 to 0.60], mean arterial blood pressure (by 10-24%), the maximum rate of rise in left ventricular pressure (by 26-32%), and cardiac output (by 20-30%). During reperfusion, “no-reflow” was attenuated by L-propionylcarnitine, because myocardial blood flow returned to 61 and 82% of baseline in the saline- and L-propionylcarnitine-treated animals, respectively. Cardiac output of the saline-treated animals further decreased (to 52% of baseline), and systemic vascular resistance increased from 46 +/- 3 to 61 +/- 9 mmHg.min.l-1, thereby maintaining arterial blood pressure. In L-propionylcarnitine-treated pigs, cardiac output remained at 75% of baseline, and systemic vascular resistance decreased from 42 +/- 3 to 38 +/- 4 mmHg.min.l-1. In both groups, energy charge but not the ATP level of the ischemic-reperfused myocardium tended to recover, whereas the creatine phosphate level showed significantly more recovery in saline-treated animals. We conclude that L-propionylcarnitine partially preserved vascular patency in ischemic-reperfused porcine myocardium but had no immediate effect on “myocardial stunning.” Potential markers for long-term recovery were not affected by L-propionylcarnitine.


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