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Biomedical subjects

A Perel

Publications and source records attributed to A Perel.

At least 73 records · Page 4Linked to original sources
PubMed1990

Timing of corticosteroid treatment. Effect of lung lymph dynamics in air injury in awake sheep.

In paired experiments, we studied the effects of high-dose methylprednisolone on the acute pulmonary injury caused by 4 h of venous air embolization in 19 chronically instrumented, unanesthetized sheep with lung lymph fistulas. We compared the effect of methylprednisolone (30 mg/kg intravenous bolus) given before embolization, early (1 H) in the course of embolization, late (3 h) in the course of embolization, or after embolization (at the beginning of the recovery period). We measured pulmonary hemodynamics and lymph dynamics. In six sheep we also fixed lung tissue for semiquantitative histology, and in some we measured leukocyte concentrations in blood and in pulmonary lymph. Methylprednisolone did not significantly affect pulmonary hemodynamics but it largely prevented lung injury when it was given before embolization. It also lessened the degree of lung injury when it was given during embolization, although this effect became less marked as treatment was delayed. Methylprednisolone had no effect on lung injury when given after embolization was completed (4 h). We found fewer leukocytes attached to air emboli and fewer endothelial cell gaps in the lungs of sheep given methylprednisolone as prophylaxis. Leukocyte counts were lower in lung lymph and higher in the circulating blood of methylprednisolone-treated sheep. We conclude that methylprednisolone has a preventive effect on air embolism lung injury, such that its effect is greater when given earlier during the development of injury.

Acute Disease↗
PubMed1989

The effect of tidal volume and intravascular volume state on systolic pressure variation in ventilated dogs.

Both tidal volume and effective blood volume may affect the variation in the arterial pressure waveform during mechanical ventilation. The systolic pressure variation (SPV), which is the difference between the maximal and minimal systolic pressure values following one positive pressure breath was analyzed in 10 anesthetized and ventilated dogs, during ventilation with tidal volumes of 15 and 25 ml/kg. The dogs were studied during normovolemia, hypovolemia (after bleeding of 30% of estimated blood volume) and hypervolemia (after retransfusion of shed blood with additional 50 ml/kg of plasma expander). The SPV reflected hemodynamic changes and was maximal during hypovolemia and minimal during hypervolemia. Unlike all other hemodynamic parameters it was also affected by the tidal volume and significantly increased at higher tidal volumes during each volume state. We conclude that the SPV and its components are useful parameters in evaluating the intravascular volume state. They also reflect the magnitude of the tidal volume employed.

Animals↗
PubMed1989

QRS-activated ventilation during general anesthesia for extracorporeal shock wave lithotripsy.

High frequency ventilation has been claimed to improve the efficiency of extracorporeal shock wave lithotripsy (ESWL) by minimizing the movement of urinary stones during the procedure. A ventilatory mode, QRS-activated ventilation, was developed in which the stones remain motionless during the delivery of shock waves. As the shock wave is triggered to occur approximately 20 milliseconds after the R wave of the QRS complex, the mechanical breath was synchronized to occur approximately 150 ms later. QRS-activated ventilation is used in 16 patients undergoing ESWL under general anesthesia. Tidal volume was set at 3 ml/kg (234 +/- 36 ml; mean +/- SD) at a rate that equaled the heart rate (71 +/- 9 beats/min). The time between the R wave and the initiation of mechanical breath (T1) was 124 +/- 25 ms, time of mechanical breath itself (T2) was 431 +/- 67 ms, and time between end of T2 and next R wave (T3) was 264 +/- 84 ms. End-tidal CO2 measured by the large breath technique was 28.1 +/- 4.8 mmHg. During the clinical use of QRS-activated ventilation and during earlier studies using an EKG simulator and a test lung, the shock wave occurred invariably at end-expiration even at high heart rates.

Adult↗
PubMed1989

The arterial pressure waveform during acute ventricular failure and synchronized external chest compression.

Methods for mechanical cardiac support by intermittent increases in the intrathoracic pressure have recently been described. In the present study the responses of the arterial pressure waveform to mechanical ventilation with and without synchronized external chest compression (SEC) in the presence of acute ventricular failure (AVF) were evaluated by measuring the systolic pressure variation (SPV). SPV, the difference between the maximal and minimal values of systolic blood during a single positive pressure breath, consists of delta up and delta down components when systolic blood pressure during a short apnea is used as reference value. During intermittent positive pressure ventilation (IPPV) alone, AVF caused SPV to decrease significantly from 8.8 +/- 4.0 to 5.7 +/- 1.9 mm Hg, and further to 3.1 +/- 1.1 mm Hg after volume loading (P less than 0.02). The decrease in SPV was due to a significant decrease in the delta down component, whereas the delta up became the major component of the reduced SPV. The application of SEC caused significant increases in the delta down, delta up, and overall SPV during AVF without volume loading. However, during AVF with volume loading, SEC increased only the delta up component of the SPV, signifying a transient increase in the left ventricular stroke output. It is concluded that the disappearance of the delta down component of the SPV is characteristic of congestive heart failure. Analysis of the arterial waveform offers a readily available monitoring tool for the differentiation of the possible effects on increased intrathoracic pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1988

Systolic pressure variation is greater during hemorrhage than during sodium nitroprusside-induced hypotension in ventilated dogs.

The systolic pressure variation (SPV), which is the difference between the maximal and minimal values of the systolic blood pressure (SBP) after one positive-pressure breath, was studied in ventilated dogs subjected to hypotension. Mean arterial pressure was decreased to 50 mm Hg for 30 minutes either by hemorrhage (HEM, n = 7) or by continuous infusion of sodium nitroprusside (SNP, n = 7). During HEM-induced hypotension the cardiac output was significantly lower and systemic vascular resistance higher compared with that in the SNP group. The systemic, central venous, pulmonary capillary wedge pressures, and heart rates, were similar in the two groups. Analysis of the respiratory changes in the arterial pressure waveform enabled differentiation between the two groups. The SPV during hypotension was 15.7 +/- 6.7 mm Hg in the HEM group, compared with 9.1 +/- 2.0 mm Hg in the SNP group (P less than 0.02). The delta down, which is the measure of decrease of SBP after a mechanical breath, was 20.3 +/- 8.4 and 10.1 +/- 3.8 mm Hg in the HEM and SNP groups, respectively, during hypotension (P less than 0.02). It is concluded that increases in the SPV and the delta down are characteristic of a hypotensive state due to a predominant decrease in preload. They are thus more important during absolute hypovolemia than during deliberate hypotension.

Animals↗
PubMed1987

Systolic blood pressure variation is a sensitive indicator of hypovolemia in ventilated dogs subjected to graded hemorrhage.

Systolic pressure variation (SPV) is defined as the difference between the maximum and minimum values of systolic blood pressure following a single positive pressure breath. An increase in the SPV is known to occur clinically during hypovolemia. This study aims to quantify SPV during graded hemorrhage in ventilated dogs, and to compare its reliability relative to other hemodynamic indicators of hypovolemia. Ten anesthetized dogs were mechanically ventilated with a fixed tidal volume. A continuously inflated vest was applied around the chest to maintain the ratio of lung to chest wall compliance similar to that of humans (0.83 +/- 0.12). SPV was further divided into delta up and delta down components relative to apneic (5 s) systolic blood pressure. Dogs were bled 5, 10, 20, and 30% of their estimated blood volume. The measured parameters best correlated to the amount of bleeding were SPV (rs = 0.993), delta down (rs = 0.981), and cardiac output (rs = 0.976). The SPV and its delta down component correlated to the degree of hemorrhage as well as the CO and the pulmonary capillary wedge pressure, and significantly better than the central venous pressure and the mean systemic blood pressure. Thus, SPV and its delta down component are accurate indicators of hypovolemia in ventilated dogs subjected to hemorrhage.

Animals↗
PubMed1987

Dependence of oxygen consumption on cardiac output in sepsis.

We studied the relationship between oxygen consumption (Vo2) and cardiac output in 17 hemodynamically stable, septic and eight nonseptic ICU patients. Each received 300 ml of fresh-frozen plasma or 25% albumin with up to 500 ml of crystalloids, in addition to regular maintenance fluids; this treatment increased pulmonary wedge pressure (WP) by 3 to 4 mm Hg. Measurements were performed before and after approximately 5 h of volume loading. Because cardiac index (CI) decreased as WP increased in four septic and three nonseptic patients, we grouped the data according to the state of flow instead of the recording time sequence. From low to high flows, mean CI increased in septic patients and nonseptic patients. Oxygen delivery (Do2) increased in septic and nonseptic patients. Vo2 remained unchanged in nonseptic patients, while it increased in septic patients. Accordingly, arteriovenous oxygen difference narrowed in nonseptic patients from 4.46 +/- 1.62 to 3.59 +/- 1.21 ml/dl (p less than .05) but did not change in septic patients. In the septic group, the difference in CI between high and low flows was significantly (p less than .05) greater in survivors than in nonsurvivors. We conclude that the septic state is accompanied by a peripheral oxygen deficit, which can be partially reversed by maintaining an above-normal CI and Do2.

Abscess↗
PubMed1987

Hemorrhagic shock prevents lung microvascular permeability and hypoxemia associated with complement activation in the awake sheep.

The effect of hemorrhagic hypotension on pulmonary dysfunction induced by complement activation was studied in 43 awake sheep, divided into six groups: Group I (n = 6), pulmonary vascular pressure was increased by inflation of a left atrial balloon; group II (n = 9), the complement system was activated by infusion of zymosan activated plasma (ZAP); group III (n = 5), hemorrhagic shock of 50 torr was induced for 3 hr; group IV (n = 10), hemorrhagic shock was induced as in group III, and after 2 hr of shock, ZAP was infused; group V (n = 8), 5 mg/kg of indomethacin was administered before ZAP infusion; group VI (n = 5), pretreatment with indomethacin as in group V, hemorrhagic shock and ZAP as in group IV. ZAP infusion in group II led to a fall in WBC to 2,600/ml (P less than 0.001), and a rise in mean pulmonary artery pressure to 41.1 torr (P less than 0.001) and in pulmonary shunting (QS/QT) to 29.4% (P less than 0.001). Arterial oxygen tension (PaO2) fell to 62.0 torr (P less than 0.001), pulmonary lymph flow (QL) rose to 14.0 ml/hr (P less than 0.01), and lymph protein clearance (L/P.QL) to 8.9 ml/hr (P less than 0.01). Plasma thromboxane B2 (TxB2) increased to 2.43 ng/ml (P less than 0.025) and pulmonary lymph TxB2 to 3.02 ng/ml (P less than 0.005). Hemorrhagic shock was followed by a rise in PaO2 to 97.5 torr (P less than 0.01), a fall in QS/QT to 7.9% (P less than 0.005), QL to 5.0 ml/hr (P less than 0.05), and L/P QL to 2.9 ml/hr (P less than 0.05). During hemorrhage, plasma TxB2 rose to 2.18 ng/ml (P less than 0.005) and lymph TxB2 to 2.32 ng/ml (P less than 0.001). Infusion of ZAP during hemorrhagic shock was followed by a fall in WBC to 2,300/microliter (P less than 0.001); but QS/QT, PaO2, QL, and L/P.QL remained unchanged. After indomethacin and ZAP, WBC fell to 3,210/microliter (P less than 0.001), Ppa rose to 27.0 torr (P less than 0.05), QL rose to 8.3 ml/hr (P less than 0.05), and L/P.QL rose to 5.2 ml/hr (P less than 0.05). PaO2 fell to 75.0 torr (P less than 0.05) and QS/QT increased to 17.1% (P less than 0.005). The protective effect of hemorrhagic shock on ZAP-induced pulmonary dysfunction was not reversed by indomethacin. It is concluded that hemorrhagic shock prevents hypoxemia and increased pulmonary permeability induced by activation of the complement system by ZAP.

Animals↗