Search PubMedSearch

Biomedical subjects

S F Sullivan

Publications and source records attributed to S F Sullivan.

At least 19 recordsLinked to original sources

Lack of arrhythmogenicity of isoflurane following administration of aminophylline in dogs.

Induction of halothane anesthesia after aminophylline administration may cause ventricular arrhythmias. Isoflurane may be as effective a bronchodilator as halothane. This study was designed to determine whether induction of isoflurane anesthesia after intravenous aminophylline is arrhythmogenic in dogs. One group of six dogs was anesthetized with 1.5% isoflurane in the absence of aminophylline. Three additional groups of six dogs were given intravenous aminophylline 10, 25, or 50 mg/kg, respectively, followed 3 min later by 1.5% isoflurane. No arrhythmias occurred after aminophylline and isoflurane at any time in any animal. In contrast to halothane, induction of isoflurane anesthesia after aminophylline is safe and does not cause cardiac arrhythmias.

Aminophylline

Enflurane, halothane, and aminophylline--uptake and pharmacokinetics.

This study was designed to evaluate the effects of induction of enflurane or halothane anesthesia on the distribution and elimination of previously administered intravenous aminophylline, and to evaluate the effect of previously administered intravenous aminophylline on the uptake of enflurane or halothane. Fifty-four dogs were studied: 6 received no anesthetic, 24 received enflurane, and 24 halothane. The six animals receiving no anesthetic were given 10 mg/kg of aminophylline. In each of the two groups of 24 animals, six animals served as controls and received no aminophylline. Of the other 18 animals in each group, six received 10 mg/kg of aminophylline, six received 25 mg/kg of aminophylline, and six received 50 mg/kg of aminophylline intravenously before induction of enflurane or halothane anesthesia. The redistribution (alpha) phase of theophylline was similar when anesthesia was induced with either enflurane or halothane and slightly more rapid when no anesthetic was given following aminophylline administration. The elimination (beta) phase of theophylline in the presence of either anesthetic was not significantly different than when no anesthetic was administered. The uptake of enflurane or halothane was unaffected by prior administration of aminophylline. Differences in arrhythmogenicity between enflurane and halothane after aminophylline administration are not related to alterations in theophylline pharmacokinetics or anesthetic uptake.

Aminophylline

Increasing myocardial oxygen demand during prolonged halothane anesthesia in dogs.

The effect of prolonged halothane anesthesia on myocardial oxygen uptake and coronary blood flow is unknown. This 5.5-hr study was undertaken to determine whether myocardial changes occur in dogs during prolonged steady-state halothane anesthesia. Hourly data were collected beginning 1.5 hr after induction of steady-state anesthesia. When compared to values obtained at 1.5 hr of halothane anesthesia, no significant myocardial changes were observed during the initial 3.5 hr. However, after 4.5 hr, mean arterial blood pressure increased 14% (P less than 0.01), coronary sinus flow increased 22% (P less than 0.05), and myocardial oxygen uptake increased 19% (P less than 0.05). At 5.5 hr mean arterial pressure was 18% (P less than 0.01), coronary sinus flow 31% (P less than 0.01), and myocardial oxygen uptake 21% (P less than 0.05) above levels measured at 1.5 hr. At 5.5 hr whole body oxygen uptake was 6% (P less than 0.01) above the 1.5 hr value. Cardiac output, heart rate, and systemic and coronary vascular resistances did not change significantly. This study demonstrates that duration of anesthesia is an important factor in determining the metabolic oxygen requirements of the heart. During prolonged anesthesia, the increase in myocardial oxygen demands may have an unfavorable effect on the myocardial oxygen supply-demand relationship.

Anesthesia, Inhalation

Cardiovascular effects of ketamine following administration of aminophylline in dogs.

The induction of halothane anesthesia following intravenous administration of aminophylline may cause ventricular arrhythmias. Ketamine has been recommended for anesthesia induction and maintenance in patients with asthma. This study was designed to determine whether induction and maintenance of ketamine anesthesia following intravenous aminophylline is arrhythmogenic in dogs. One group of six dogs was anesthetized with intravenous ketamine, 5 mg/kg, followed by infusion of 5 mg/kg/hr. Three additional groups of six dogs were given intravenous aminophylline, 10, 25, and 50 mg/kg, respectively, followed 3 minutes later by intravenous ketamine, 5 mg/kg, and a 5 mg/kg/hr ketamine infusion. No arrhythmias occurred at any time in any animal. Ketamine use following aminophylline would appear to lack arrhythmogenic potential and may be advantageous in the clinical setting.

Aminophylline

Oxygen stores.

Explore the source record for details and available documents.

Anemia

Hypoxemia and pulmonary gas exchange during hemodialysis.

With measured values of arterial blood gas tensions, of expired respiratory gas fractions, and volume of the expired ventilation, the determinants of alveolar oxygen tension (PAO2) were used to evaluate their influence on the development of the arterial hypoxemia that occurs in spontaneously breathing patients undergoing hemodialysis using an acetate dialysate. Dialysis produced no significant changes in the alveolar-arterial O2 tension gradient (AaDO2). The extracorporeal dialyzer removed an average of 30 ml.m-2.min-1 of CO2. Accordingly the pulmonary gas exchange ratio (R) dropped from a mean predialysis value of 0.81 to 0.62 (P less than 0.001). The arterial CO2 tension remained constant throughout, whereas the minute ventilation, both total (P less than 0.01) and alveolar (P less than 0.01), decreased during dialysis. This decrease in ventilation accounts for more than 80% of the fall in PAO2. During dialysis there was a decrease (P less than 0.001) in arterial oxygen tension (PaO2), which varied among the individuals from 9 to 23% of control. During the postdialysis hour PaO2 returns to control values concomitant with increase in ventilation. The quantitative gas exchange relationships among R, alveolar ventilation, and AaDO2 predict the PaO2 values actually measured.

Adult

Aminophylline.

Explore the source record for details and available documents.

Adult

Halothane-induced cardiac arrhythmias following administration of aminophylline in experimental animals.

Cardiac arrhythmias often occur when patients receiving aminophylline are anesthetized with halothane. This animal study was designed to define what constitute arrhythmogenic doses of aminophylline when administered before halothane anesthesia. One group of six dogs was given aminophylline, 10 mg/kg IV, followed in 3 minutes by inhalation of 1% halothane. In two additional groups of dogs the same experimental protocols were used except that aminophylline doses were 25 mg/kg and 50 mg/kg. In the first group, two of six dogs developed ventricular arrhythmias during induction of halothane anesthesia. One of six dogs given 25 mg/kg of aminophylline developed a ventricular arrhythmia. Three of six dogs given 50 mg/kg of aminophylline developed ventricular arrhythmias. Sustained ventricular arrhythmias occurred in 33% of the animals with "therapeutic" serum theophylline levels and in 33% of the animals with "toxic" levels. Induction of halothane anesthesia within 15 minutes of aminophylline administration may be dangerous and is likely to result in severe and persistent ventricular arrhythmias.

Aminophylline

Safety of enflurane following administration of aminophylline in experimental animals.

The induction of halothane anesthesia following intravenous administration of aminophylline may cause ventricular arrhythmias. This study was designed to determine whether induction of enflurane anesthesia following intravenous aminophylline is arrhythmogenic in dogs. One group of six dogs was anesthetized with 2% enflurane in the absence of aminophylline. Three additional groups of six dogs were given intravenous aminophylline, 10, 25, or 50 mg/kg, respectively, followed 3 minutes later by 2% enflurane. No arrhythmias occurred at any time in any animal. In contrast to halothane induction of enflurane anesthesia following aminophylline appears to be safe and does not cause cardiac arrhythmias.

Aminophylline

Cardiorespiratory effects of hypothermia and bicarbonate alkalosis.

The cardiorespiratory effects of reducing body temperature to 30 degrees C (by packing in ice) and subsequent metabolic alkalosis (by infusion of NaHCO3) were studied in six anesthetized, paralyzed, and artificially ventilated (FIO2 = 0.4) dogs. Heart rate decreased from 135 +/- 6 beats/min (mean +/- S.E.) at 37 degrees C to 84 +/- 4 at 30 degrees C; it increased to 96 +/- 4 after 2 h alkalosis. Cardiac output decreased from 1.84 +/- 0.14 to 0.66 +/- 0.08 l/min and then increased to 0.83 +/- 0.07. pHa increased, as expected on cooling, from 7.41 +/- 0.07 to 7.49 +/- 0.03; with bicarbonate it increased to 7.79 +/- 0.03. PaCO2 decreased on cooling from 32.9 +/- 1.4 to 21.7 +/- 1.2 torr, increasing with bicarbonate to 27.9 +/- 1.4 torr. VO2 decreased from 104.9 +/- 5.1 ml . min-1 . m-2 at 37 degrees C to 51.3 +/- 2.0 at 30 degrees C; with alkalosis it increased by 16.2% to 59.6 +/- 3.3 ml . ml-1 . m-2, an increase identical to that seen in normothermic alkalosis. Thus, the mechanism of the alkalosis-induced increase in oxygen consumption is not suppressed by the decrease in VO2 seen in hypothermia, and the increase in VO2 appears to be a consequence of the change in relative alkalinity rather than the increase in pH.

Alkalosis

Aminophylline pharmacokinetics and cardiorespiratory effects during halothane anesthesia in experimental animals.

The pharmacokinetics and cardiorespiratory effects of aminophylline during halothane anesthesia are not well established and are the subject of this study. Eleven dogs were anesthetized with 1% halothane in air and given 10 mg/kg of intravenous aminophylline (theophylline ethylenediamine) over 5 minutes. Serum theophylline levels were measured over the next 60 minutes and were found to be in the therapeutic range (10-20 mg/L). Theophylline levels decayed according to a two-component exponential function. The half-time for the fast component was 4.5 minutes, while the slow component half-time was 134.5 minutes. Heart rate increased significantly (p less than 0.05) within 2 minutes following aminophylline, and remained significantly elevated for 60 minutes. Pulmonary capillary wedge pressure and systemic vascular resistance decreased 2 minutes after aminophylline, as did the arterial-mixed venous oxygen content difference. Cardiac index increased 2 minutes following aminophylline. All these changes were transient, and values returned to near control values within 10 minutes after aminophylline. Arterial oxygenation, venous admixture, and physiologic dead space were not significantly (p less than 0.05) altered by aminophylline. No cardiac arrhythmias occurred. Other than a sustained 12% increase in heart rate, and transient hemodynamic changes immediately following its administration, aminophylline in therapeutic doses did not have adverse effects on cardiorespiratory function during prolonged 1% halothane anesthesia in normoxic, eucapnic dogs.

Aminophylline

Arrhythmogenic effects of aminophylline during halothane anesthesia in experimental animals.

Arrhythmogenic effects of aminophylline (theophylline ethylenediamine) during halothane anesthesia have been reported but have not been related to serum theophylline levels. This study was designed to determine the arrhythmogenicity of therapeutic and toxic serum theophylline levels during halothane anesthesia. The study consisted of three parts. In part 1 (induction) six dogs were anesthetized for 15 minutes with 1% halothane in air and then given intravenous aminophylline, 50 mg/kg. In part 2 (maintenance) eight dogs were anesthetized for 2 hours with 1% halothane and then given intravenous aminophylline, 10 mg/kg. In part 3, after four additional hours of steady-state 1% halothane anesthesia, additional intravenous aminophylline, 25 mg/kg, was given to these eight animals. Three of six dogs in part 1 had arrhythmias following aminophylline, with serum theophylline levels ranging from 48 to 66 mg/L. No dog in part 2 had arthythmias following the 10 mg/kg dose of aminophylline, with serum theophylline levels of 14 to 23 mg/L. Six of eight dogs in part 3 had arrhythmias shortly after aminophylline, 25 mg/kg, with serum theophylline levels of 36 to 72 mg/L. Aminophylline administration after prolonger 1% halothane anesthesia appears free from arrhythmogenic effects if serum theophylline levels remain near the therapeutic range (10 to 20 mg/L). Aminophylline administration resulting in high serum theophylline levels (above 36 mg/L) causes ventricular arrhythmias when aminophylline is given during induction or maintenance of 1% halothane anesthesia. Arrhythmias usually (89%) begin with 5 minutes of aminophylline administration, and these arrhythmias always resolve spontaneously within 2 minutes of onset.

Aminophylline

Pulmonary shunting and lung volume during hypotension induced with trimetaphan.

In 10 dogs anaesthetized with pentobarbitone mean Pa02 decreased from the control value of 13.5 kPa to 10.2 kPa, cardiac output decreased by 33%, and right-to-left shunt doubled during hypotension induced with trimetaphan. There was no signficant change in functional residual capacity during the period of hypotension or recovery. The hypoxaemia resulted from an increase in ventilation/perfusion inequality, with a decrease in arterial saturation consequent upon a decrease in cardiac output with a constant shunt. During the recovery period, right-to-left shunting remained greater than the values obtained before induction of hypotension.

Animals

Determinants of oxygen uptake during sodium bicarbonate infusion.

Steady-state passive hyperventilation alkalosis produces a predictable increase in oxygen uptake (VO2) proportional to the change in arterial pH (pHa) while variable changes in VO2 have been reported during alkali infusion. To compare metabolic with respiratory alkalosis 17 dogs were anesthetized with halothane and their VO2 response to respiratory alkalosis evaluated by hyperventilation. The pHa measured during this phase was duplicated during the later continuous infusion of NaHCO3 at which time either 1) ventilation was held constant at the control level, allowing arterial carbon dioxide tension (PaCO2) to rise as a consequence of the bicarbonate dissociation, or 2) PaCO2 was held constant by servo control of ventilation. Hyperventilation (pHa 7.6, PaCO2 13 Torr) produced an average increase in VO2 of 24%. During the bicarbonate infusion at constant ventilation (pHa 7.6, PaCO2 45 Torr) VO2 increased only 7%; however, when PACO2 was held constant by servo ventilation VO2 increased 21% above control. We conclude that respiratory and metabolic alkalosis produce similar increases in VO2 when steady-state acid-base conditions are achieved.

Alkalosis

Intraocular reticulum cell sarcoma: its dramatic response to systemic chemotherapy and its angiogenic potential.

A 77-year-old woman with reticulum cell sarcoma in apparent remission presented with neovascular glaucoma. Ultrasonography demonstrated a 360 degree ring tumor of the ciliary body which totally regressed in 3 weeks after reinsitution of systemic chemotherapy. This appears to be a ring reticulum cell sarcoma of the ciliary body and is apparently the first reported case of an intraocular reticulum cell sarcoma which has undergone such a dramatic response to combined chemotherapy. A review of the English literature of all published cases of ocular reticulum cell sarcoma (16 cases) discloses no similar case, and emphasizes for the first time the angiogenic potential of this tumor. Secondary glaucoma was found to be associated with intraocular reticulum cell sarcoma in approximately two-thirds of the reported cases, and neovascular glaucoma in about one-quarter of these cases.

Aged

Acute clinical hypocalcemic myocardial depression during rapid blood transfusion and postoperative hemodialysis: a preventable complication.

Despite experimental evidence that myocardial depression resulting from rapid transfusion of ACD blood (citrate binds ionic calcium) is avoidable by simultaneous calcium administration, most hypovolemic patients receive calcium either after transfusion or not at all. Similar iatrogenic hypocalcemic myocardial depression occurs in normovolemic patients with known myocardial damage who are dialyzed for acute uremia when ACD blood prime is used at high initial flow rates (350 c.c. per minute) and when dialysis is performed against low calcium dialysate (2.5 mEq. per liter or less). This study tests the hypotheses that (1) rapid transfusion of as little as one unit of CPD blood causes a significant reduction in ionized calcium, (2) the depressive effect of CPD blood is significant and similar to that of ACD blood, (3) rapid blood transfusion (ACD or CPD) is safe if calcium is given simultaneously, (4) addition of calcium to the extracorporeal heparinized blood prime used in dialysis prevents initial depression, and (5) hemodynamic instability during dialysis is prevented when the dialysate is normocalcemic. From the results of our study, we made the following conclusions: (1) Ionized calcium is reduced significantly by rapid transfusion of CPD blood; (2) acute myocardial depression noted with CPD blood is similar to that previously observed with ACD blood and is prevented during transfusion of either type of blood by simultaneous calcium administration; and (3) hemodialysis in patients who have had cardiac surgery is safe if calcium is added to blood prime and dialysate is made normocalcemic.

Blood Preservation

Pulmonary shunting during anaesthesia in man.

Qs/Qt was determined during halothane and oxygen anaesthesia in 22 patients. All were believed to have no pulmonary dysfunction. A surgical operation was in progress and respiration was controlled. Qs/Qt was minimal in 15 of these patients (means 3.9 plus or minus 0.3%), indicating that anaesthesia and operation can be conducted in man without a significant increase of pulmonary shunting. The level of shunting was increased in the other seven patients. In neither group was Qs/Qt altered by the passage of time. Age varied between 23 and 61 years and was directly and significantly correlated to Qs/Qt (r=0.57,P less than0.01).

Adult