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Biomedical subjects

A H Idris

Publications and source records attributed to A H Idris.

13 recordsLinked to original sources
PubMed1995

The tumor suppressor gene WT1 inhibits ras-mediated transformation.

Wilms' tumor belongs to a small group of pediatric neoplasms that have served as paradigms of human cancers in which recessive mutations play a primary role in tumorigenesis. WT1 is a candidate tumor suppressor gene that is mutationally inactivated in a proportion of both familial and sporadic Wilms' tumors. Recent studies demonstrated that WT1 can partially suppress growth of a Wilms' tumor cell line in vitro and in vivo. We investigated the ability of WT1 to inhibit the expression of the transformed phenotype in non-Wilms' tumor cells. The expression of WT1 cDNA in ras-transformed NIH3T3 cells yielded large, flat cells that exhibited complete contact-inhibition. These morphologic changes were associated with decreased proliferation, suppression of clonogenicity in soft agar and inhibition of tumor growth in nude mice. Moreover, expression of WT1 in non-transformed NIH3T3 cells resulted in similar morphologic changes and profound resistance to transformation by an activated ras oncogene. These studies suggest that tumor inhibition by WT1 in these cells may be achieved by interference with the ras-mediated signalling pathway.

3T3 Cells↗
PubMed1995

Automatic mechanical device to standardize active compression-decompression CPR.

STUDY OBJECTIVE: To develop an automatic mechanical device capable of performing active compression-decompression (ACD) CPR in laboratory animals. DESIGN: A swine model was used to study standard and ACD CPR. One-minute periods of standard mechanical chest compressions were alternated with mechanical ACD CPR. SETTING: University hospital laboratory. INTERVENTIONS: A commercially available device that provided standard chest compressions only was modified to deliver ACD CPR. RESULTS: The absolute difference in intrapleural pressure and tidal volume almost doubled during ACD CPR compared with that with standard CPR. CONCLUSION: The presence of a greater negative change in intrapleural pressure confirmed that active decompression of the chest had occurred and that the device was capable of performing ACD CPR. The device provides consistent rate, depth, force, and duty cycle.

Animals↗
PubMed1995

Does hypoxia or hypercarbia independently affect resuscitation from cardiac arrest?

STUDY OBJECTIVE: In a previous cardiopulmonary resuscitation (CPR) study in swine, ventilation was associated with improved rate of return of spontaneous circulation (ROSC) compared with nonventilated animals, which had greater hypoxia and hypercarbic acidosis. We used the same model to determine the independent effect of hypoxia and hypercarbic acidosis on ROSC after cardiac arrest. DESIGN: Laboratory model of cardiac arrest. SETTING: University teaching hospital laboratory. PARTICIPANTS: Domestic swine (23 to 61 kg). INTERVENTIONS: Twenty-four swine were randomly assigned to three groups receiving ventilation during CPR with 85% O2/15% N2 (control), 95% O2/5% CO2 (hypercarbia), or 10% O2/90% N2 (hypoxia). All animals had ventricular fibrillation for 6 min without CPR, then CPR with one of the ventilation gases for 10 min, then defibrillation. Animals without ROSC received epinephrine, 85% O2, CPR for another 3 min, and defibrillation. MEASUREMENTS AND RESULTS: During the tenth minute of CPR, the hypercarbic group had more mean (SD) arterial hypercarbia than the control group (PCO2, 47 +/- 6, compared with 34 +/- 6; p < 0.01), and greater mixed venous hypercarbia (PCO2, 72 +/- 14, compared with 59 +/- 8; p < 0.05), while mean arterial and mixed venous PO2 was not significantly different. The hypoxic group had significantly less mean arterial (43 +/- 9 compared with 228 +/- 103 mm Hg) and mixed venous (22 +/- 5 compared with 35 +/- 7 mm Hg) PO2 when compared with the control group (p < 0.01), while mean arterial and mixed venous PCO2 were not significantly different. Thus, the model succeeded in producing isolated hypercarbia without hypoxia in the hypercarbic group and isolated hypoxia without hypercarbia in the hypoxic group. The rate of ROSC was 6/8 (75%) for the control group, 1/8 (13%) for the hypercarbic group, and 1/8 (13%) for the hypoxic group (p < 0.02). CONCLUSIONS: Both hypoxia and hypercarbia independently had an adverse effect on resuscitation from cardiac arrest. In this model with a prolonged interval of untreated cardiac arrest, adequate ventilation was important for resuscitation.

Analysis of Variance↗
PubMed1994

Changes in arterial and mixed venous blood gases during untreated ventricular fibrillation and cardiopulmonary resuscitation.

This investigation was designed to evaluate the changes in arterial and mixed venous acid-base conditions during untreated ventricular fibrillation and after institution of cardiopulmonary resuscitation (CPR). Fifty-two swine (weight: 25-40 kg) were studied after induction of ventricular fibrillation. In a subgroup of 10 animals, 10-min CPR trials were performed. Arterial and mixed venous blood gases were monitored at baseline, after 5 min of untreated ventricular fibrillation (nonintervention interval) and after 10 min of mechanical CPR. Standard CPR was performed at compression rates of 100/min with a 60% duty cycle. Arterial pH, Pco2, and HCO3 were unchanged when baseline values were compared with those obtained after 5 min of untreated ventricular fibrillation, while arterial Po2 decreased from 81 to 69 torr. Mixed venous pH decreased from 7.41 to 7.35, Pco2 increased from 43 to 48 torr, Po2 decreased from 40 to 38 torr and HCO3 decreased from 28 to 26 mEq/l (P < 0.05). Although these changes were statistically significant, many remain in the normal range. Both arterial and mixed venous pH and HCO3 fell further after 9 min of CPR and Pco2 increased (P < 0.05). Alterations in mixed venous pH and Pco2 were more apparent than corresponding changes in arterial blood gas composition. We conclude that untreated cardiac arrest may be accompanied by normal arterial and mixed venous blood gas levels. Tissue acidosis is only revealed after tissue perfusion is restored and is most accurately reflected in the mixed venous blood gas composition. This apparent paradox provides insight into the relationship between tissue perfusion and arterial and mixed venous acid-based composition.

Acid-Base Equilibrium↗
PubMed1994

Ventilation caused by external chest compression is unable to sustain effective gas exchange during CPR: a comparison with mechanical ventilation.

OBJECTIVE: To compare the tidal volume, minute ventilation, and gas exchange caused by mechanical chest compression with and without mechanical ventilatory support during cardiopulmonary resuscitation (CPR) in a laboratory model of cardiac arrest. DESIGN: A laboratory swine model of CPR was used. Eight animals with and eight animals without mechanical ventilation received chest compression (100/min) for 10 min. Coronary perfusion pressure, tidal volume, and minute ventilation were recorded continuously. INTERVENTIONS: Ventricular fibrillation for 6 min without CPR, then mechanical chest compression for 10 min. RESULTS: During the first minute of chest compression, mean (+/- S.D.) minute ventilation was 11.2 +/- 5.9 l/min in the mechanically ventilated group and 4.5 +/- 2.8 l/min in the group without mechanical ventilation (P = 0.01). Minute ventilation gradually declined to 5.8 +/- 1.4 l/min and 1.7 +/- 1.6 l/min, respectively, during the last minute of chest compression (P < 0.0001). After 10 min of chest compression, mean arterial pH was significantly more acidemic in the group without mechanical ventilation (7.16 +/- 0.13 compared with 7.30 +/- 0.07 units) and PCO2 was higher (62 +/- 19 compared with 35 +/- 9 mmHg). Mixed venous PCO2 was also higher (76 +/- 15 compared with 61 +/- 8 mmHg). CONCLUSION: Standard chest compression alone produced measurable tidal volume and minute ventilation. However, after 10 min of chest compression following 6 min of untreated ventricular fibrillation, it failed to sustain pulmonary gas exchange as indicated by significantly greater arterial and mixed venous hypercarbic acidosis when compared with a group receiving mechanical ventilation.

Acid-Base Equilibrium↗
PubMed1994

Lack of uniform definitions and reporting in laboratory models of cardiac arrest: a review of the literature and a proposal for guidelines.

BACKGROUND: Researchers are interested in improved uniformity of definitions and standards of reporting data for human CPR studies, and international guidelines (Utstein style) have been developed. However, no guidelines exist for animal CPR investigations. OBJECTIVE: To assess published animal CPR studies for adequacy of reporting and uniformity of methods and definitions regarding such important factors as the interval from the onset of ventricular fibrillation to the start of CPR (the nonintervention interval), ventilation, chest compression, coronary perfusion pressure, and return of spontaneous circulation. DESIGN: A blinded review of the methodology described in 42 articles concerned with animal CPR research published during the last ten years. An article had to report cardiac arrest and CPR as part of the protocol and return of spontaneous circulation as one of the outcome variables in order to be included in this study. We excluded abstracts, nonresuscitation models, and human CPR studies. MEASUREMENTS AND MAIN RESULTS: There was wide variation in the experimental methods reported in the studies. The nonintervention interval ranged from 0 to 15 minutes. The majority of studies initiated CPR within three minutes after the onset of ventricular fibrillation. Twenty-two percent of studies reported tidal volume, and 18% reported minute ventilation. Of the 14 studies that used blood pressure or coronary perfusion pressure as a target for titration of chest compression force, 12 used different target blood pressure values. We found 29 different definitions of return of spontaneous circulation. The duration of return of spontaneous circulation ranged from 30 seconds to 60 minutes; however, 52% of studies did not report a duration. CONCLUSION: Important differences exist in animal CPR research methodology among laboratories. Failure to define or report minute ventilation, coronary perfusion pressure, and return of spontaneous circulation made it difficult to compare studies. In order to make valid comparisons of studies, blood flow and ventilation should be measured and controlled when they are not experimental variables. Uniform definitions and guidelines for reporting should be developed for laboratory CPR research.

Animals↗
PubMed1994

End-tidal carbon dioxide during extremely low cardiac output.

STUDY OBJECTIVE: A number of studies have shown that expired CO2 concentration is closely related to cardiac output, but that cardiac output was not controlled as an independent variable. In addition, the partial pressure of end-tidal CO2 (PETCO2) during extremely low cardiac output has not been reported. The objective of the present study was to measure PETCO2 during well-controlled, very low blood flow rates under conditions of constant minute ventilation. DESIGN: Ten anesthetized, intubated, and mechanically ventilated swine (weight, 43 to 102 kg) were placed on two ventricular assist devices in order to control cardiac output. Minute ventilation was measured and kept constant. Ventricular assist device output (measured with an ultrasonic flow probe); PETCO2; and aortic, pulmonary artery, and central venous pressures were recorded continuously. INTERVENTIONS: After electrical induction of ventricular fibrillation, pump output was decreased in steps. MEASUREMENTS AND MAIN RESULTS: Cardiac index ranged from 0 to 5,371 mL/min/m2; 59% of PETCO2 measurements were made at cardiac indexes of less than 1,313 mL/min/m2 (30 mL/min/kg). The relationship of PETCO2 levels to cardiac index was determined with linear regression analysis; P < .05 was statistically significant. PETCO2 correlated significantly with cardiac index (P < .0001). The best-fit line by least-squares analysis produced the equation: PETCO2 = 4.98 + 0.012 [cardiac index] (r2 = .82). CONCLUSION: Under conditions of constant minute ventilation, PETCO2 correlated closely with cardiac index over a large range of blood flow rates, including extremely low rates.

Animals↗
PubMed1994

Effect of ventilation on resuscitation in an animal model of cardiac arrest.

BACKGROUND: The need for ventilation during the initial management of cardiac arrest is an important public health problem that is being debated. The present study was designed to determine whether ventilation affects return of spontaneous circulation from cardiac arrest in a swine model with an interval of untreated ventricular fibrillation of 6 minutes, as reported in witnessed out-of-hospital human cardiac arrest. METHODS AND RESULTS: Twenty-four animals were randomly assigned to two groups: one that received ventilation during the first 10 minutes of chest compression and one that did not. Coronary perfusion pressure and minute ventilation were continuously recorded. Arterial and mixed venous blood gases were measured at intervals. Return of spontaneous circulation was defined prospectively as an aortic systolic blood pressure of > 80 mm Hg for > 5 minutes and was the primary outcome variable. All animals were anesthetized, paralyzed, and intubated. Ventricular fibrillation was induced and persisted for 6 minutes without chest compression, followed by mechanical chest compression for 10 minutes and then attempted defibrillation. Animals without return of spontaneous circulation were given epinephrine, ventilation, and chest compression for an additional 3 minutes. Defibrillation was again attempted, and animals were assessed for return of spontaneous circulation. There were no significant differences between the two groups in baseline prearrest mean cardiac index, coronary perfusion pressure, or arterial and mixed venous blood gases. However, after 9 minutes of chest compression, significant differences were noted between the ventilated and nonventilated groups. The nonventilated group had significantly (P < .05) lower mean arterial PO2 (38 +/- 17 mm Hg compared with 216 +/- 104 mm Hg) and higher PCO2 (62 +/- 16 mm Hg compared with 35 +/- 8 mm Hg), lower mixed venous PO2 (15 +/- 7 mm Hg compared with 60 +/- 7 mm Hg). Nine of 12 (75%) of the ventilated animals, and only 1 of 12 (8%) of the nonventilated animals had return of spontaneous circulation after cardiac arrest (P < .002). CONCLUSIONS: In this animal model of cardiac arrest, ventilation was important for resuscitation. The importance of ventilation could be related to the prolonged duration of untreated ventricular fibrillation and the significantly greater hypoxia and hypercarbic acidosis found in the nonventilated animals.

Animals↗
PubMed1994

The composition of gas given by mouth-to-mouth ventilation during CPR.

STUDY OBJECTIVE: To compare the concentration of a rescuer's exhaled O2 and CO2 during mouth-to-mouth ventilation with or without chest compression. DESIGN: Prospective repeated measures study. Simulated one- and two-rescuer cardiopulmonary resuscitation (CPR) was performed as recommended by the American Heart Association. SETTING: University laboratory. PARTICIPANTS: Fifty-five healthcare professionals certified in basic and advanced cardiac life support volunteered as rescuers in this study. MEASUREMENTS AND RESULTS: Thirty-three volunteers performed one-rescuer CPR, and 22 volunteers performed two-rescuer CPR. Minute ventilation for both groups increased 50% to 130% during CPR (p < 0.05). During the performance of CPR, the concentration of exhaled O2 increased from 16.4 +/- 0.7% to 16.9 +/- 0.5% in the one-rescuer CPR group and from 16.5 +/- 0.9% to 17.8 +/- 0.6% in the two-rescuer CPR group (p < 0.05). The concentration of exhaled CO2 in the one-rescuer CPR group did not change significantly throughout the entire experiment, but decreased in the two-rescuer CPR group from a baseline measurement of 4.0 +/- 0.6% to 3.5 +/- 0.4% (p < 0.05). During CPR, the concentration of exhaled CO2 was 4.0 +/- 0.4% in the one-rescuer CPR group compared with 3.5 +/- 0.4% in the two-rescuer CPR group (p < 0.05). CONCLUSIONS: The gas given by mouth-to-mouth ventilation is a hypercarbic and hypoxic mixture compared with room air. Mouth-to-mouth ventilation is the only circumstance in which a hypercarbic and hypoxic gas is given as therapy. Further laboratory and clinical studies are necessary to determine the effect of mouth-to-mouth ventilation during CPR.

Carbon Dioxide↗
PubMed1994

Effect of ventilation on acid-base balance and oxygenation in low blood-flow states.

OBJECTIVES: To investigate how minute ventilation affects the partial pressure of end-tidal CO2 and arterial and mixed venous pH, PCO2, PO2, and the concentration of bicarbonate during low blood-flow states. We tested the null hypothesis that acid-base conditions during low rates of blood flow are not significantly different when minute ventilation is doubled or halved. DESIGN: Prospective, experimental, animal study. SETTING: University hospital laboratory. SUBJECTS: Domestic swine. INTERVENTIONS: We studied ten anesthetized and mechanically ventilated swine (weight, 43 to 102 kg) in a new model of controlled systemic and pulmonary blood flow in which each animal was maintained on ventricular assist devices. After electrical induction of ventricular fibrillation, ventricular assist device blood flow was decreased in steps. At each decrease, control minute ventilation, two times the control minute ventilation (hyperventilation), and one-half the control minute ventilation (hypoventilation) were administered; each ventilatory change was maintained for 6 mins. MEASUREMENTS AND MAIN RESULTS: Aortic, pulmonary arterial and central venous pressures, ventricular assist device blood flow, and end-tidal CO2 were recorded continuously. Acid-base conditions were studied at three different mean blood flow rates: 49%, 30%, and 12% of baseline prearrest cardiac index. Arterial pH and PaO2 and mixed venous pH varied directly (p < .003) with minute ventilation, while PaCO2 and mixed venous PCO2, and end-tidal CO2 varied inversely (p < .0001) with minute ventilation. Mixed venous PO2 was not significantly related to minute ventilation (p = .6). PaCO2 and arterial bicarbonate; mixed venous pH, mixed venous PO2, and mixed venous bicarbonate, and end-tidal CO2 varied directly (p < .001) with blood flow, while mixed venous PCO2 varied inversely with blood flow (p < .05). Arterial pH was not significantly related to blood flow (p = .3). When minute ventilation changed from hyperventilation to hypoventilation at a mean blood flow rate of 49%, mean arterial pH decreased 0.22 +/- 0.06 (p < .05), mean PaCO2 increased 28 +/- 6 torr (3.7 +/- 0.8 kPa) (p < .05), and mean PaO2 decreased 99 +/- 77 torr (13.2 +/- 10 kPa); mean mixed venous pH decreased 0.11 +/- 0.02, mean mixed venous PCO2 increased 16 +/- 2.2 torr (2.1 +/- 0.3 kPa) (p < .05), and mean mixed venous PO2 did not change; mean end-tidal CO2 increased 18 +/- 2 torr (2.4 +/- 0.3 kPa) (p < .05). The effect of changes in minute ventilation on blood gases and end-tidal CO2 was similar for mean blood flow rates of 30% and 12% of baseline cardiac index. CONCLUSIONS: During low rates of blood flow similar to those rates found in shock and cardiopulmonary resuscitation, alterations in minute ventilation significantly influenced end-tidal CO2 and both arterial and mixed venous pH and PCO2. These findings may have clinical importance in improving the treatment of shock and cardiac arrest.

Acid-Base Equilibrium↗
PubMed1992

High-flow sheaths for pediatric fluid resuscitation: a comparison of flow rates with standard pediatric catheters.

We evaluated high-flow intravenous devices designed specifically for fluid resuscitation of infants and children. Fluid flow rates with 4-, 5-, and 6-Fr high-flow sheaths and 18-, 20-, and 22-gauge catheters were measured and compared. Flow rate is significantly faster with the 4-Fr sheath (P less than 0.0001) than with the 18-, 20-, or 22-gauge catheter. The high flow rates possible with the sheaths make them ideal for use in patients who require rapid fluid resuscitation.

Catheterization↗
PubMed1986

Transfers to a public hospital. A prospective study of 467 patients.

In recent years there has been a dramatic increase in the number of patients transferred to public hospitals in the United States. We prospectively studied 467 medical and surgical patients who were transferred from the emergency departments of other hospitals in the Chicago area to Cook County Hospital and subsequently admitted. Eighty-nine percent of the transferred patients were black or Hispanic, and 81 percent were unemployed. Most (87 percent) were transferred because they lacked adequate medical insurance. Only 6 percent of the patients had given written informed consent for transfer. Twenty-two percent required admission to an intensive care unit, usually within 24 hours of arrival. Twenty-four percent were in an unstable clinical condition at the transferring hospital. The proportion of transferred medical-service patients who died was 9.4 percent, which was significantly higher than the proportion of medical-service patients who were not transferred (3.8 percent, P less than 0.01). There was no significant difference in the proportion of deaths on the surgical service between patients who were transferred and those who were not (1.5 vs. 2.4 percent). We conclude that patients are transferred to public hospitals predominantly for economic reasons, in spite of the fact that many of them are in an unstable condition at the time of transfer.

Adult↗