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Biomedical subjects

A Sidi

Publications and source records attributed to A Sidi.

At least 37 records · Page 2Linked to original sources
PubMed1994

Cardiovascular effects of a non-xanthine-selective antagonist of the A1 adenosine receptor in the anaesthetised pig: pharmacological and therapeutic implications.

OBJECTIVE: To study antagonism of A1 adenosine receptors in an anaesthetised open chest swine model, the selective A1 receptor antagonist, N6-endonorbornan-2-yl-9-methyladenine (N-0861), was examined to see if it attenuates bradycardia, augments reflex tachycardia associated with adenosine infusion, or both. Its effects were compared with those of the non-selective antagonist of adenosine A1 and A2 receptors, 8-(p-sulphophenyl)-theophylline (8-pST). METHODS: Twenty nine pigs were studied. The prolongation of P-R interval mediated by A1 receptors, the increase in left anterior descending coronary artery blood flow mediated by A2 receptors, and decreases in systemic and left ventricular pressures and first derivative of left ventricular pressure (dP/dt) were monitored in each animal assigned to one of three protocols. (1) Adenosine, 40 to 180 micrograms.kg-1.min-1, was infused for more than 6 min before and immediately after rapid infusion of 8-pST, 5 mg.kg-1 intravenously, or a solvent that did or did not contain N-0861, 0.2 mg.kg-1 intravenously (n = 14). (2) In the same animal, we compared N-0861 and 8-pST in reversing responses mediated by A1 and A2 receptors during two 10 min infusions of adenosine separated by a 1 h washout period (n = 7). (3) N-0861 with adenosine (mean dose, 0.4 mg.kg-1) was infused with or without complete autonomic blockade with atropine (2.5 mg.kg-1) and propranolol (2 mg.kg-1) (n = 8). RESULTS: Adenosine prolonged P-R interval (and cycle length in non-paced hearts), increased coronary flow, and decreased calculated coronary resistance. N-0861 alone did not affect any variable, but N-0861 with adenosine prevented or reversed A1 receptor mediated prolongation of P-R interval in paced hearts and cycle length in non-paced hearts and enhanced A2 receptor mediated coronary vasodilatation. Left ventricular dP/dt and rate-pressure product were maintained with N-0861 and adenosine, and N-0861 unmasked a postadenosine reflex tachycardia. Prolonged PR interval, decreased heart rate, and increased coronary flow were prevented or reversed by the non-selective antagonist 8-pST. CONCLUSIONS: Selectivity of N-0861 for the adenosine A1 receptor may, without reducing coronary blood flow, ameliorate bradyarrhythmia and maintain the positive inotropic response when exogenous adenosine is given or when interstitial myocardial adenosine is increased.

Adenine↗
PubMed1993

Early administration of amrinone does not impair regional metabolism of O2 or lactate and, by improving myocardial performance, preserves myocardial blood flow in the ischemic canine heart.

The inotropic and vasodilating effects of amrinone can upset the balance of O2 supply and demand by changing those components in opposite directions simultaneously. We used a canine model of acute coronary artery occlusion to test our hypothesis that early administration of amrinone (before failure of the heart) would have beneficial effects on hemodynamic status and regional metabolism during ischemia, even before heart failure. Twenty dogs anesthetized with thiamylal were subjected to 50%, 75%, and 100% occlusion of the left anterior descending coronary artery. Half of the dogs were given a bolus injection of amrinone (0.75 mg/kg) 1-2 min before each occlusion, immediately followed by continuous infusion (10 micrograms.kg-1 x min-1) during occlusion; the other half did not receive amrinone (control). Hemodynamic and metabolic variables were measured in the ischemic area (the left anterior descending coronary artery) and in a nonischemic area (the circumflex vein). Amrinone not only decreased heart rate, left ventricular systolic and end-diastolic pressures, and mean pulmonary arterial pressure during constrictions but also maintained contractility, stroke volume index, and stroke volume index/left ventricular end-diastolic pressure before and during constrictions. Regional myocardial blood flow in ischemic areas decreased with amrinone during constrictions but was still higher than in untreated animals. Regional ischemic and nonischemic metabolic variables (metabolism of intracoronary potassium, CO2, O2, glucose, and lactate) were similar for both groups and changed to the same extent. Amrinone appears to improve left ventricular performance and increase blood flow to ischemic myocardium while not worsening regional metabolic effects during various grades of ischemia in the dog.

Amrinone↗
PubMed1992

Adenosine for controlled hypotension: systemic compared with intracoronary infusion in dogs.

We hypothesized that either through local myocardial or systemic effects, adenosine could be used to control hypotension during ischemia. Therefore, we compared the effects of systemic with intracoronary infusion of adenosine on myocardial hemodynamics and metabolism during ischemia in 27 dogs. Left anterior descending artery (LADa) flow was measured and the LADa constricted by a micrometer to restrict resting flow by 50%, 75%, and 100%. Adenosine was infused either systemically (n = 9), to maintain mean aortic pressure at 50-60 mm Hg, or directly into the LADa (n = 9), to create maximal coronary hyperperfusion; no adenosine was infused in the control group (n = 9). With systemic adenosine, during each constriction aortic pressure, left ventricular first derivative (LV dP/dt), and heart rate (HR) decreased: aortic pressure by 56.1% +/- 2.9% (mean +/- SEM), LV dP/dt by 36.2% +/- 2.2%, systemic resistance by 42.7% +/- 5%, and HR by 38.7% +/- 3% during 50% constriction (P less than 0.05 for each variable). Intracoronary adenosine decreased only aortic pressure, LV dP/dt, and HR, all to a lesser extent: aortic pressure by 5% +/- 2.8%, LV dP/dt by 15% +/- 1.2%, and HR by 4.6% +/- 1.7% (P less than 0.05, compared with systemic adenosine for each variable). With systemic adenosine only in the nonischemic area, regional myocardial blood flow increased and remained high, from 224.6 +/- 65.2 to 342 +/- 46.2 mL.min-1.100 g-1 during 50% constriction (P less than 0.05); with intracoronary adenosine, ischemic zone regional myocardial blood flow increased, but not consistently. In the ischemic area, O2 consumption was less with than without systemic adenosine; also, lactate flux production was less positive (-60.2 +/- 37.6 compared with 80.3 +/- 20.2 mmol.min-1.100 g-1 x 10(-3) during 50% constriction; P less than 0.05). Systemic infusion of adenosine during coronary hypoperfusion improves regional metabolism during ischemia and, thus, may mitigate myocardial ischemia. The mechanism by which systemic infusion improves metabolic status may be by decreases in both systemic pressure and systemic vascular resistance.

Adenosine↗
PubMed1991

Decreased regional lactate production and output due to intracoronary continuous infusion of esmolol during acute coronary occlusion in dogs.

This study was designed to test the hypothesis that intracoronary administration of esmolol can confer metabolic protection during coronary constriction or occlusion, without affecting hemodynamic parameters, in a canine model. Seventeen anesthetized open-chest dogs underwent direct cannulation of the left anterior descending coronary artery (LADa), its companion vein (LADv), and the distal circumflex vein (CFXv). LADa flow was measured with an electromagnetic flowmeter. Using a micrometer-driven snare around the LADa, flow was reduced by 50%, 75%, and 100% for 15 minutes, with 1 hour of normal flow before each constriction. In 7 dogs (group 1) chosen randomly, esmolol, 15 to 20 micrograms/kg/min, was infused continuously into the LADa; the rate was adjusted to maintain baseline hemodynamic values. The second group (10 dogs) was not treated with esmolol. Heart rate (HR), electrocardiogram (ECG), LADa flow, LV dP/dt, and aorta (Ao), pulmonary artery (PA), LADa, and left ventricular (LV) pressures were recorded continuously. Cardiac output (CO) (thermodilution) was measured and blood was sampled from all catheters before and after constrictions for analysis of glucose, lactate, sodium, potassium, and blood gases. Flow and pressure in the LADa in both groups decreased similarly during each corresponding constriction. Systolic LV pressure, LV dP/dt, and LV stroke work index were affected in both groups only during 100% constriction. HR, Ao, and PA pressures, and total and peripheral pulmonary resistances were affected similarly in both groups during each constriction. Myocardial lactate extraction and consumption were less negative (negative = net production and output) in the LAD perfusion bed during corresponding constrictions with esmolol than without it.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1990

Prolonged neuromuscular blockade and ventilatory failure after renal transplantation and cyclosporine.

In a retrospective one-year study, we documented respiratory failure or prolonged neuromuscular blockade in eight of 65 patients with chronic renal failure who had received either vecuronium (four of 29 patients) or atracurium (four of 36 patients) during anaesthesia for kidney transplantation. We reviewed the charts of the patients and recorded all aspects of medication and anaesthesia to try to determine whether there might be a single factor associated with this high incidence (12 per cent) of respiratory failure. Anaesthesia for all patients was induced with thiopentone, isoflurane, and N2O/O2. Tracheal intubation was facilitated with muscle relaxants in a single bolus of vecuronium, 0.07 to 0.1 mg.kg-1, or atracurium, 0.3 to 0.5 mg.kg-1. Additional doses were given according to neuromuscular activity, which was monitored visually by response to train-of-four and tetanic stimulation. Anaesthesia was maintained with fentanyl/isoflurane and N2O/O2. After induction of anaesthesia, each patient received methylprednisolone, cefazolin, mannitol infusion for 24 hr beginning at the start of renal artery anatomosis, and either azathioprine (n = 57) or cyclosporine (n = 8). Relaxation was evaluated toward the end of the operation by train-of-four stimulation. Neuromuscular blockade was reversed with edrophonium (0.75-1 mg.kg-1) or neostigmine (0.06-0.08 mg.kg-1). The eight patients with prolonged neuromuscular blockade received ventilatory support for one to three hours after operation. Respiratory failure was significantly more frequent in patients who received cyclosporine (P less than 0.05).

Adult↗
PubMed1989

Direct cannulation of myocardial blood vessels without interfering with regional blood flow distribution, resting blood flow, or reactive hyperemia.

An in vivo technique of directly cannulating coronary arteries and veins for sampling blood and measuring hemodynamic parameters is described. The cannulation procedure was evaluated for its effects on regional myocardial blood flow (RMBF), transmural RMBF distribution, and reactive hyperemia. In a group of ten dogs, RMBF was measured by using radionuclide microspheres. Values for left anterior descending (LAD) perfusion zone (with catheter) and circumflex (CX) zone (no catheter) did not differ significantly (119 +/- 14 mL/min/100 g v 123 +/- 14 mL/min/100 g, respectively). Likewise, endocardial-to-epicardial RMBF ratio was similar for the two areas (0.99 +/- 0.06 and 1.04 +/- 0.06, respectively). In five dogs, aortic and left ventricular pressures agreed closely with the LAD coronary artery pressure measured with the described catheter system. Arterial flow during rest and reactive hyperemia was measured in five additional dogs by using electromagnetic flow probes placed around the LAD and CX coronary arteries. During both rest and reactive hyperemia, flow was greater in the CX than in the LAD (65.46 +/- 4.12 and 169.62 +/- 9.04 in the CX v 30.24 +/- 0.78 and 102.28 +/- 5.38 in the LAD; P less than 0.05 for both); however, the percentage change from rest to reactive hyperemia was similar for both vessels. In each perfusion zone, flow during rest and reactive hyperemia and the percentage change were not affected by cannulation. The effects of an infusion of adenosine (20 to 40 micrograms/min) into the pulmonary artery with and without the LAD coronary catheters (artery and vein) were tested in six other dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1989

Lactate extraction fails to accurately reflect regional lactate production in ischemic myocardium.

Lactate extraction (defined as arteriovenous lactate concentration difference divided by arterial concentration and expressed as a percent) is often reported as the indicator of anaerobic cardiac metabolism in studies dealing with myocardial ischemia. However, lactate extraction ignores the effect of regional blood flow and, therefore, fails to consider the total mass of lactate consumed or produced (lactate flux). This study examined the relationship between lactate flux and calculated lactate extraction. Fourteen anesthetized dogs were instrumented to allow sampling of blood from the left anterior descending coronary artery (LADa) and vein (LADv) and a circumflex coronary vein (CFXv), as well as measurement of regional myocardial blood flow (RMBF) using microspheres, and measurement of systemic hemodynamic variables. Complete data sets (before LADa occlusion, after 15 minutes of LAD occlusion, and after 1 hour of reperfusion) were obtained in nine dogs. Only minor systemic hemodynamic changes occurred during LADa occlusion when compared with "before" and "after" values. Likewise, LADa occlusion produced only minor alterations in blood gas tensions, pH, concentrations of glucose, lactate, and RMBF in samples from the CFX perfusion zone. In contrast, LAD occlusion decreased RMBF in the LADa perfusion zone and produced significant hypercarbia and acidemia, as well as an increased LADv lactate concentration. In the LAD zone, lactate extraction decreased significantly from 15.9% +/- 7.0% before LAD occlusion to -77.4% +/- 21.8% during LAD occlusion (P less than 0.05). However, lactate flux (arteriovenous concentration difference x RMBF) in the LAD zone before and during LAD occlusion was not statistically significantly different (1.3 +/- 0.8 mg/min/100 g and -1.5 +/- 0.8 mg/min/100 g, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Effect of isoflurane on the extent of myocardial necrosis and on systemic hemodynamics, regional myocardial blood flow, and regional myocardial metabolism in dogs after coronary artery occlusion.

Anesthetized dogs were studied in two protocols to determine the effect of isoflurane on the extent of myocardial injury resulting from left anterior descending coronary artery (LAD) occlusion. In 22 dogs (11 treated with isoflurane 1% inspired, beginning 1 hr after LAD occlusion, and 11 control) myocardial infarct size measured postmortem after 6 hr of LAD occlusion was significantly less with isoflurane than without it, 23.4 +/- 3.8% vs 36.2 +/- 2.4% of left ventricle; regional myocardial blood flow (RMBF) did not differ between groups and hemodynamic differences were slight. Fifty-two other dogs underwent two 15-min periods of LAD occlusion separated by 1 hr of reperfusion. Without isoflurane (n = 12), hemodynamic, RMBF, and regional metabolic data did not differ between the two occlusion periods. When isoflurane 1.3% inspired was administered during one of the two occlusion periods by random assignment, coronary perfusion pressure, left ventricular stroke work index, and systolic left ventricular pressure decreased more than when isoflurane was not administered. Both oxygen (O2) consumption and supply in ischemic myocardium decreased proportionately during LAD occlusion, but more so with isoflurane. Neither lactate production, potassium release, glucose extraction, nor coronary venous carbon dioxide (CO2) or O2 content differed between LAD occlusion periods with and without isoflurane. Thus, isoflurane decreased the extent of myocardial necrosis produced by LAD occlusion but neither RMBF nor metabolic indications were improved during transitory ischemia.

Animals↗
PubMed1988

Regional myocardial metabolism and electrolyte balance during acute ischemia in dogs.

The relationships among regional (ischemic and nonischemic) myocardial extracellular (coronary venous) potassium concentration, potassium-sodium concentration ratio, acid-base balance, and metabolism of glucose and lactate were evaluated in 14 anesthetized dogs in which ischemia was produced by transitory left anterior descending coronary artery (LAD) occlusion. Coronary blood samples were obtained from the specific regions by using coronary arterial and venous catheters placed directly into the vessel supplying (or draining) that region. During ischemia, in coronary venous blood sampled from the ischemic area, pH decreased, and PCO2, base deficit, potassium concentration, and the potassium-sodium ratio increased. In LAD venous blood samples obtained during LAD occlusion, the percentage change in potassium concentration was inversely related to the percentage change in PCO2 (r = -0.634, P < 0.05), but not to the percentage change in hydrogen ion concentration (r = -0.339, P > 0.05). During ischemia, arteriovenous O2 content difference in the LAD region increased from 8.54 +/- 0.73 vol % to 10.71 +/- 0.73 vol %; lactate extraction became negative (indicating net production), values decreasing from 27.76 +/- 4.49% to -138.10 +/- 16.81% (P < 0.05); and glucose extraction increased from 14.57 +/- 2.88% to 19.01 +/- 6.06% (0.05 < P < 0.1). These observations indicate that efflux of potassium from the myocardium during ischemia is linked to tissue hypoxia, increased glucose extraction, lactate production, and extracellular acidosis. A further contributor to potassium release, failure of the normal membrane-bound, energy-requiring ion pump, cannot be excluded by these data. With the model used in this study, blood can be sampled from discrete regions of the heart, which enables the study of interactions between pharmacologic agents, such as anesthetics, and the metabolic abnormalities produced by acute ischemia.

Acid-Base Equilibrium↗
PubMed1988

Experimental closed head injury in rats: mechanical, pathophysiologic, and neurologic properties.

A model of closed head injury in rats was developed using a calibrated weight-drop device. The development of edema was studied in various brain regions (cerebral hemispheres, brain stem, cerebellum) using a linear specific gravity gradient column. Regional brain tissue density was measured within 1 min, at 15 and 60 min, 18 h, 4 and 10 days after injury to the left cerebral hemisphere, and was compared with values in sham-operated and control rats. Significant edema (i.e., reduced specific gravity) occurred only in the traumatized hemisphere and was maximal at 18 h. A neurologic severity score (NSS) was developed to evaluate the status of the rat after injury. Specific gravity was significantly correlated with NSS at 18 h after injury. The affected hemisphere displayed hemorrhagic lesions as early as one hour post head trauma (HT), which evolved into hemorrhagic necrosis at 18 h. A pathologic score, evaluated 18 h post HT based on size and severity of the lesion, was correlated with the NSS and evaluated for each rat at one hour and 18 h postimpact. This correlation was found to be highly significant. This model of brain injury may be useful in future studies on the effects of therapeutic agents.

Animals↗
PubMed1988

Esmolol decreases the adverse effects of acute coronary artery occlusion on myocardial metabolism and regional myocardial blood flow in dogs.

This study was designed to test the hypothesis that beta-adrenergic receptor blockade with esmolol would decrease the hemodynamic and myocardial metabolic impairment produced by left anterior descending coronary artery (LADa) occlusion. Twenty-three anesthetized open-chest dogs underwent direct cannulation of the LADa, its companion vein (LADv), and a distal circumflex vein (CFXv) for blood sampling. All dogs were subjected to two consecutive 15-minute periods of total LADa occlusion; group 1 (n = 11) received an infusion of esmolol (150 micrograms.kg-1.min-1) during either occlusion period (randomly assigned) and group 2 (n = 12) received no intervention during either occlusion period. One hour of reperfusion was interposed between the two periods of LADa occlusion. Hemodynamic measurements were made and blood was sampled from the aorta, CFXv, LADa, and LADv before and during both periods of LADa occlusion. Without esmolol infusion, LADa occlusion was associated with decreases in stroke index, coronary perfusion pressure, and left ventricular stroke work index; with esmolol infusion these hemodynamic decrements did not occur. During both LADa occlusion periods in both groups, lactate extraction became negative, i.e., there was net lactate production. Despite this, the magnitude of lactate production was less with esmolol than without it. Finally, average endocardial-to-epicardial blood flow ratio in the LAD perfusion area was decreased during each LAD occlusion period except when esmolol was infused, during which the baseline value was maintained. Thus, infusion of esmolol during temporary LADa occlusion preserved certain hemodynamic variables, preserved the ratio of endocardial-to-epicardial blood flow, and decreased the apparent magnitude of lactate production.

Analysis of Variance↗
PubMed1987

Methylene blue and indocyanine green artifactually lower pulse oximetry readings of oxygen saturation. Studies in dogs.

The effects of fluorescein, methylene blue, and indocyanine green on hemodynamic variables and on pulse oximetry and co-oximetry measurements of arterial hemoglobin oxygen saturation (SaO2) and oxyhemoglobin percentage (% HbO2) were evaluated in 16 anesthetized dogs in vitro by co-oximetry (% HbO2) and in vivo by pulse oximetry (SaO2). The light absorbance (optical density) in plasma (range 500 to 800 nm) was measured by a spectrophotometer. Fluorescein did not affect oximetry measurements, plasma light absorbance in the range measured, or hemodynamic variables. Methylene blue caused dose-dependent decreases in measurements made with both forms of oximetry for up to 30 minutes, the decrease being greater and longer lasting with pulse oximetry (P less than 0.05). Hemodynamic measurements in 5 dogs showed that methylene blue (1 to 5 mg/kg) increased arterial pressure transiently, after which cardiac output, stroke index, and left ventricular stroke work index decreased and left ventricular end-diastolic pressure and systemic and pulmonary vascular resistances increased (P less than 0.05 with 5 mg/kg). Methemoglobin concentration measured by co-oximetry increased significantly (to 19.9 +/- 1.4%, P less than 0.05) 1 minute after 5 mg/kg of methylene blue was injected. Methylene blue had a dose- and time-dependent effect on plasma light absorbance, and this effect peaked in the 660- to 670-nm range. The data do not distinguish the relative contributions of physiology (hemodynamic change), chemistry (methemoglobin production), and physics (optical properties) to the decrease in pulse oximetry and co-oximetry measurements that follows injection of methylene blue. Indocyanine green affected neither hemodynamic variables nor co-oximetry readings but decreased pulse oximetry readings for up to 10 minutes dose dependently.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Pulse oximetry fails to accurately detect low levels of arterial hemoglobin oxygen saturation in dogs.

The accuracy of two commercially available pulse oximeters (the Ohmeda Biox 3700, software version "J," and the Nellcor N-100) in detecting low levels of arterial hemoglobin oxygen saturation (SaO2) was evaluated in 10 dogs in which hypoxia was induced by stopping the fresh gas flow into the anesthesia machine circle system. Measurements made in vivo with the pulse oximeters, with detectors placed on the tongue, were compared with measurements made in vitro using an IL 282 CO-Oximeter as SaO2 decreased toward zero. Measurements from the two oximeters correlated poorly over the range from 0 to 100% SaO2 (r = 0.69). In this range, the correlation between Nellcor N-100 measurements and those of the CO-Oximeter had an r of 0.82, a regression line slope of 0.82, and a y intercept of 14.8; the correlation between the Ohmeda Biox 3700 and the CO-Oximeter had an r of 0.83, a regression line slope of 0.66, and a y intercept of 32.7. The correlation with the CO-Oximeter was similar for both the Ohmeda and the Nellcor pulse oximeters at an SaO2 of 80% or more. However, when SaO2 was less than 80%, measurements by pulse oximetry correlated less well with CO-Oximeter measurements (r = 0.62, slope = 0.64, and y intercept = 21.0 for Nellcor; r = 0.71, slope = 0.67, and y intercept = 32.4 for Ohmeda). When SaO2 was less than 60%, both oximeters inaccurately indicated the co-oximetry values (r = 0.36 and y intercept = 26.1 for the Nellcor; r = 0.48 and y intercept = 33.2 for the Ohmeda).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

The use of mechanical stimulation to obtain the sacral reflex latency: a new technique.

We determined sacral reflex latencies and morphologies in 18 neurologically normal patients and 83 with neurological disease by stimulating the glans penis or clitoris using electrical and a new technique of mechanical stimulation, and recording from the external urethral sphincter. The results with both stimulation techniques were compared among various diagnostic groups. In normal patients the mean sacral reflex latencies were 35.3 +/- 2.5 (standard deviation) msec. with electrical stimulation, and 39.1 +/- 4.0 msec. with mechanical stimulation. The mean reflex latencies in patients with lower motor neuron lesions studied by both methods were statistically longer than in normal subjects, and the mean reflex latencies in patients with upper motor neuron impairment studied by both methods were not statistically different from those in normal subjects. The morphological findings of the reflex tracings suggest that both types of evoked responses follow the same general anatomical pathway and both resemble a special human flexor reflex. The mechanical technique has advantages over the electrical technique because it is less painful and in certain instances it is easier to obtain.

Adult↗
PubMed1987

Head injury induces increased prostaglandin synthesis in rat brain.

Head injury was induced in the left hemisphere of rats. The rats were killed at various time intervals after trauma (immediately, 15 min, 1 and 18 h, and 4 and 10 days), and the rates of synthesis and release of prostaglandin PGE2, 6-keto-PGF1 alpha, and thromboxane TXB2 from cortical slices of both hemispheres were studied. The rate of synthesis of PGE2 after 18 h was six and four times higher than control in the contused and contralateral hemispheres, respectively. By 10 days post-trauma, both hemispheres had normal rate of PGE2 release. TXB2 and 6-keto-PGF1 alpha synthetases were affected already 15 min after the injury, and a similarly elevated rate of synthesis was found in both hemispheres. The maximal effect was detected after 1 or 18 h with return to normal after 4 or 10 days for TXB2 and 6-keto-PGF1 alpha, respectively. Tissue specific gravity was determined for both hemispheres using linear gradient columns. The results of these determinations indicate that development of edema occurs in the contused hemisphere as early as 15 min post trauma; it reaches its maximal level at 18 h and returns to normal at 10 days. Arterial pressure was monitored, and a transient increase was found at 10 min post trauma. We suggest that the production of edema after brain injury may be related to the increased rate of PGE2 and PGI2 synthesis, which occurs at similar time intervals after injury.

6-Ketoprostaglandin F1 alpha↗