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Biomedical subjects

J Juchmes

Publications and source records attributed to J Juchmes.

At least 19 recordsLinked to original sources
PubMed1989

Contribution of peripheral blood pooling to central hemodynamic disturbances during endotoxin insult in intact dogs.

The aim of the present study was to determine possible effects of Escherichia coli endotoxin on peripheral vascular compliance and relate them to concomitant central hemodynamic disturbances. Endotoxin was infused at 0.25 micrograms/kg.min during 2 h in six anesthetized dogs, while six additional animals served as controls. Vascular compliance of the systemic circulation was calculated in intact animals from the changes in CVP after known changes in systemic blood volume. In control dogs, vascular compliance averaged 2.3 ml/mm Hg.kg body weight. During slow endotoxin infusion, cardiovascular effects were measurable only after a certain period of time had elapsed from the start of endotoxin insult and consisted of hypotension associated with systemic vasodilation. Systemic BP decreased gradually from 124 to 68 mm Hg while vascular compliance was finally increased by 100%, when compared to control values. This latter rise was responsible for a reduction in the cardiac preloads. Pulmonary wedge pressure and CVP were decreased from 7.1 to 3.4 and from 4.5 to 2.6 mm Hg, respectively. However, parallel to the decrease in left ventricular preload, endotoxin induced a progressive decrease in left ventricular afterload. Because of the balance in ventricular loading, cardiac output remained almost unchanged. After volume loading (dextran 30 ml/kg), cardiac output was remarkably increased from 3.28 to 6.24 L/min.m2 while peripheral vasodilation was not affected by this maneuver. It is concluded that low dose endotoxin infusion induces in dogs a hemodynamic pattern similar to human sepsis. The left ventricular loading changes are related to an enhanced systemic vascular compliance from 2.3 to 4.5 ml/mm Hg.kg. High flow shock state is encountered provided peripheral blood pooling is compensated by adequate volume replacement.

Animals↗
PubMed1988

[Relation between endurance time and maximal oxygen consumption during supramaximal running].

The relationship between speed and the maximal length of time supramaximal runs can be sustained (temps-limite, tlim) has been studied in seven male subjects (physical education students). Within the range of intensity studied, tlim strictly depends on maximal oxygen consumption (VO2max). The relationship between tlim and the relative energy cost of the exercises per unit of time (E), calculated by subtracting the maximal power of aerobic metabolism (Emaxox) from E, removes the interindividual differences of tlim. The function tlim = f(E-Emaxox) is described by an empirical equation of the form: tlim = a.exp[-b(E-Emaxox)] (r = 0.979; P less than 0.001), where the parameters a and b are respectively equal to 330.8 and 0.14 and where tlim, E and Emaxox are respectively expressed in seconds and in watts per kg of body weight.

Adult↗
PubMed1987

Effects of intravascular volume expansion on lung fluid balance in a canine model of septic shock.

We tested the early effects of endotoxin on both the permeability of capillary membranes and microvascular pressure. One group of dogs (n = 8) were fluid loaded (30 ml/kg dextran-40) after having been subjected to a 2-h Escherichia coli endotoxin infusion (0.25 micrograms/kg X min). A second control group of animals (n = 6) was submitted to a similar (25 ml/kg) volume loading over an equivalent 30-min period. We estimated extravascular lung water (EVLW), calculated the effective pulmonary capillary pressure, and determined the alveolar-capillary filtration coefficient (Kf) after volume loading. Only the septic animals consistently showed elevated EVLW values consistent with pulmonary edema. The results showed, however, that the Kf calculated for the dogs that received endotoxin was no different from that of control group (Kf = 0.005 ml/kg X min X mm Hg). Instead, endotoxin constricted the pulmonary veins which led to a considerable rise in microvascular hydrostatic pressure above the level at which the lungs could not resist edema formation. We conclude that acute pulmonary edema that follows endotoxin insult and subsequent therapeutic volume replacement is due to an increased filtration force instead of an alteration in the microvascular permeability.

Animals↗
PubMed1987

A comparison of Escherichia coli endotoxin single bolus injection with low-dose endotoxin infusion on pulmonary and systemic vascular changes.

The purpose of this study was to compare effects of single bolus endotoxin injection with sustained low-dose endotoxin infusion on systemic and pulmonary hemodynamics in anesthetized dogs. When administered as a bolus (.01 mg/kg), endotoxin induced systemic vascular changes whose evolution could be divided into two consecutive phases. In the early phase, marked hepatic venoconstriction caused a rise in portal pressure followed by abrupt decreases in both cardiac output and blood pressure. Mean pulmonary artery pressure remained unchanged. Because of lowered blood flow, both peripheral and pulmonary resistances increased. The rise in the latter was due to a prominent vasoconstriction of pulmonary arteries. Following a partial spontaneous recovery from shock, the late phase was characterized by a low-output state combined with high systemic vascular resistances. In contrast, when endotoxin was given at a slow infusion rate (250 ng/kg/min) over a 2-hour period of time, cardiovascular effects were basically different from the preceding ones, and they were measurable only after a certain period of time had elapsed from the start of endotoxin insult. First, blood pressure decreased gradually, while cardiac output remained almost unchanged. Therefore, peripheral resistance was decreased. Second, in the pulmonary circulation, the site of vasoconstriction was shifted from arteries to veins. We conclude that there is a fundamental difference in the response of the dog's systemic and pulmonary circulation as a function of endotoxin administration as either a bolus or slow infusion. This difference might be due to sudden elevated portal pressure responsible for an abrupt cardiovascular collapse in dogs subjected to bolus injection.

Animals↗
PubMed1987

Pulmonary hydrostatic microvascular pressure changes and lung fluid balance during histamine infusion in intact dogs.

The effects of histamine on systemic and pulmonary hemodynamics of dogs were studied in six intact animals. Histamine infusion resulted in an almost immediate, precipitous fall in blood pressure (BP), pulmonary capillary wedge pressure (PCWP), and right atrial pressure (RA) as well as an increase in heart rate. Partial recovery occurred about 5 minutes after infusion was stopped. Cardiac output did not change significantly. Consequently, the calculated peripheral resistance decreased afterwards. Hepatic portal pressure rose significantly after 2 minutes of histamine infusion with partial recovery in about 5 minutes. Suprahepatic venous pressure did not change significantly. Although pulmonary arterial pressure did not necessarily rise, total pulmonary vascular resistance increased in every dog. If the absolute level in pulmonary arterial resistance remained greater (Ra 105 mm Hg/liter-1 min X kg-1) than the level of venous resistance (Rv 70 mm Hg/liter-1 min X kg-1), the relative increase in venous resistance (100%) was higher than the increase in Ra (35%). On the other hand, effective capillary pulmonary pressure remained unchanged. Central blood volume and extravascular lung water increased upon histamine infusion and returned rapidly to baseline when histamine infusion was stopped. No significant changes occurred in either effective pulmonary compliance and arterial blood gas values. Our data lead us to conclude that histamine's major action occurs in the venous pulmonary segments; pulmonary and splanchnic blood pooling is responsible for a fall in cardiac preload; and an increase in extravascular lung water and central blood volume with unchanged effective pulmonary pressure might be explained by an increase in microvascular surface area.

Animals↗
PubMed1986

Lack of defective cardiac oxidative metabolism in intact dogs subjected to a prolonged low-dose infusion of Escherichia coli endotoxin.

The aim of the present study was to determine possible direct adverse effects of a 2-hour Escherichia coli endotoxin infusion (50 ng kg-1 min-1) on myocardial oxidative carbohydrate metabolism. The experiments were performed in intact dogs to assay glucose and lactate cardiac uptake and relate them to oxygen consumption (MVO2), CO2 production, and myocardial hemodynamics. Coronary sinus blood flow (CSBF) was measured by thermodilution, and the arteriovenous differences in glucose, lactate, pyruvate, O2, and CO2 were determined by blood samples obtained simultaneously from the carotid artery and sinus coronary. The adequacy of CSBF in meeting cardiac oxygen needs was evaluated by calculating the percentage of anaerobic metabolic rate (% AMR). During endotoxin infusion, CSBF was significantly lowered by 33% while mean aortic blood pressure was decreased by 43%. Cardiac index exhibited a minimal reduction of 14%. Mean arterial blood glucose decreased 30% and arterial lactate increased 100%. Despite the progressively developing hypoglycemia, cardiac glucose uptake increased 140%. Although MVO2 was reduced to 70% of control value, lactate uptake increased 50%. Throughout the experimental period, the % AMR remained negative. Under endotoxin infusion, up to 78% of the cardiac CO2 production was derived from carbohydrate utilization, as compared to 40% prior to endotoxin infusion. Our findings suggest the absence of any toxic action by an endotoxin-sustained infusion on cardiac oxidative metabolism.

Animals↗
PubMed1985

[Hemodynamic and respiratory effects of the perfusion of low-dose endotoxin in intact heparinized dogs].

In the anesthetized dog, a low dose perfusion of endotoxin (50 ng X kg-1 X min-1) produces hemodynamic and metabolic perturbations generally similar to those clinically found in man during the hemodynamic phase of septic shock. These modifications are observed after about 30 minutes following the beginning of the perfusion. They constitute: 1) an arterial vasodilatation responsible for a hypotension without a significant modification of the cardiac output; 2) a drop in the left ventricular filling pressure; 3) a progressive metabolic acidosis; 4) a moderate arterial hypoxia that is independent of an alveolar hypoventilation. To these perturbations is added the contemporary development of a leucopenia associated with a thrombopenia. This mode of endotoxin administration seems to us to constitute a satisfactory experimental model for studying the circulatory injuries due to hyperdynamic septic shock.

Animals↗
PubMed1983

The arterial baroreflex and the cardiopulmonary reflex in borderline hypertension.

An elevation of the cardiopulmonary baroreflex control of the forearm vascular resistances due to an impairment of the arterial baroreflex has been postulated in borderline hypertension. The purpose of the study is to verify this hypothesis. The arterial baroreflex sensitivity, measured by the phenylephrine method is similar in borderline hypertensive and normotensive subjects of the same age. The forearm and the splanchnic vascular resistances are studied in borderline hypertension and normotension during leg negative body pressure at -40 and -70 mmHg. Baseline forearm resistances are higher in borderline hypertension. The increase of forearm resistance is similar in borderline hypertension and normotension when variations are expressed in percentage of the basal values. The elevation of plasma norepinephrine is similar in the two groups. The tachycardia and the elevation of splanchnic resistances are similar in borderline hypertensive and normotensive subjects. We conclude that: The arterial baroreflex is acting normally in borderline hypertension. The cardiopulmonary baroreflex control of the forearm vascular resistances is normal in borderline hypertension. The elevation of the basal forearm vascular resistances is not due to a sympathetic hyperactivity.

Adult↗
PubMed1982

[Tachycardia induced by a hot bath].

When immersed in plain water at 40 degrees C, normal young adults experience an important increase in the heart rate. beta adrenergic receptor blockade by propranolol (40 and 80 mg) reduces this tachycardia by 25%. The increase in the heart rate depends on orthosympathetic stimulation, on parasympathetic inhibition and on a Q10 effect related to the blood temperature acting on the sino-auricular node.

Adult↗
PubMed1982

[Effects of a hypocaloric protein diet on changes in arterial pressure produced by adrenaline infusion].

In 9 obese patients, epinephrine infusion (10 microgram/min) did not significantly modify the mean arterial blood pressure (MBP) in basal conditions. This infusion reduced MBP (-7 mm Hg, p less than 0.05) after 13 days of protein-supplemented fasting. This difference in the cardio-vascular reactivity to circulatory epinephrine could contribute to the decrease in the arterial blood pressure observed during protein-supplemented fasting.

Blood Pressure↗
PubMed1982

[Changes in plasma volume in submaximal exertion of short duration].

Changes in plasma fluid volume and hyperlactacidemia were measured in nine healthy young men who had been running 10 min on a motor-driven treadmill (work rate from 40 to 90% V0, max). Our results show that there is a linear relationship between reduction of plasma fluid volume and intensity from 50% of max. For a given intensity the reduction of plasma fluid volume is a function of hyperlactacidemia.

Humans↗
PubMed1980

[Endurance after propranolol in the human execution of a general dynamic exercise].

The effects of a single oral dose of 40 mg propranolol on endurance time and on the maximum oxygen consumption were studied in eight healthy young men. They were running on a motor-driven treadmill (work rate from 80 to 150% VO2 max. The VO2 max and endurance time were decreased to an average of 10 and 30% of controls respectively. The relationship between the endurance time and the relative work load (VO2/VO2 max) remained unchanged after beta-adrenoceptor blockade. The reduction of the endurance time following beta-adrenoceptor blockade is a consequence of the reduction of the VO2 max.

Adult↗
PubMed1979

[Effect of horizontal immersion into water at 38 degrees C on the urinary elimination of catecholamines].

The urinary excretion of noradrenaline, adrenaline and creatinine has been studied in normal young individuals during a water bath at 38 degrees C for 40 minutes. The noradrenalinuria and the ratio noradrenalinuria/creatininuria are decreased, indicating an inhibition of the vasomotor activity of the orthosympathetic system. This inhibition is related to the consequence of the external hydrostatic pressure of the water filling the intrathoracic venous reservoirs and increasing the systemic blood pressure at the sino-baroreceptor level, hyperthermia playing a very limited role.

Adult↗