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Biomedical subjects

M R Salem

Publications and source records attributed to M R Salem.

At least 37 records · Page 2Linked to original sources
PubMed1997

Role of adenosine triphosphate-sensitive potassium channels in coronary vasodilation by halothane, isoflurane, and enflurane.

BACKGROUND: Halothane, isoflurane, and enflurane cause coronary vasodilation and cardiac depression. This study was performed to assess the role of adenosine triphosphate (ATP)-sensitive potassium channels (KATP channels) in these effects. METHODS: Twenty-five thoracotomized dogs were anesthetized with fentanyl and midazolam. The left anterior descending coronary artery was perfused via either of two pressurized (80 mmHg) reservoirs. One reservoir was supplied with arterial blood free of a volatile anesthetic, and the second reservoir was supplied with arterial blood equilibrated in an oxygenator with a 1 minimum alveolar concentration of either halothane (0.9%, n = 10), isoflurane (1.4%, n = 8), or enflurane (2.2%, n = 7). Coronary blood flow (CBF) was measured using a Doppler flow transducer, and segmental shortening (SS) was measured with ultrasonic crystals. Responses to the volatile anesthetics were assessed under control conditions, during intracoronary infusion of the KATP channel inhibitor glibenclamide (100 micrograms/min), and after cessation of glibenclamide (recovery). The effectiveness of glibenclamide was verified from inhibition of coronary vasodilator responses to the KATP channel opener cromakalim without effect on those to the KATP channel-independent vasodilators, sodium nitroprusside and acetylcholine. RESULTS: Under control conditions, the volatile anesthetics caused pronounced increases in CBF (isoflurane > halothane = enflurane), and decreases in SS (enflurane > halothane = isoflurane). Glibenclamide blunted significantly (and reversibly) the increases in CBF, but it had no effect on the decreases in SS. CONCLUSIONS: The KATP channels play an important role in coronary vasodilation but apparently are not involved in cardiac depression caused by halothane, isoflurane, and enflurane in canine hearts in situ.

Adenosine Triphosphate↗
PubMed1996

Isoflurane-induced coronary vasodilation is preserved in reperfused myocardium.

Isoflurane causes vasodilation in the coronary circulation. The present study evaluated whether this action is preserved after a brief coronary occlusion followed by reperfusion. Fourteen open-chest dogs anesthetized with fentanyl and midazolam were studied. The left anterior descending coronary artery was perfused via an extracorporeal system with normal arterial blood or with arterial blood equilibrated with 1.4% (1 minimum alveolar anesthetic concentration [MAC]) isoflurane. Coronary perfusion pressure was maintained at 90 mm Hg. Coronary blood flow (CBF) was measured with a Doppler flow transducer. Steady-state changes in CBF during isoflurane, and during intracoronary infusions of acetylcholine (Ach; 20 micrograms/min), an endothelium-dependent vasodilator, and sodium nitroprusside (SNP; 80 micrograms/min), an endothelium-independent vasodilator, were compared in normal myocardium and in myocardium subjected to 15 min of ischemia (due to cessation of perfusion) followed by 30 min of reperfusion. Ischemia-reperfusion had no significant effect on the increases in CBF by isoflurane (421% +/- 88% vs 388% +/- 84%) or SNP (115% +/- 18% vs 135% +/- 19%), whereas it attenuated these increases in CBF by Ach (232% +/- 38% vs 143% +/- 21%). In conclusion, a brief period of myocardial ischemia followed by reperfusion did not affect the coronary vasodilating effects of isoflurane and SNP, although it blunted these effects of Ach. The present findings provide further evidence suggesting that the ability of isoflurane to relax coronary vascular smooth muscle is independent of the nitric oxide-cyclic guanosine monophosphate pathway.

Acetylcholine↗
PubMed1996

The direct effects of enflurane on coronary blood flow, myocardial oxygen consumption, and myocardial segmental shortening in in situ canine hearts.

This study evaluated changes in coronary blood flow (CBF), myocardial oxygen consumption (MVo2), and myocardial segmental shortening (SS) during intracoronary administrations of enflurane in in situ canine hearts. The left anterior descending coronary artery (LAD) of 11 anesthetized and mechanically ventilated dogs was perfused at constant perfusion pressure (80 mm Hg) with enflurane-free blood or with blood equilibrated in an extracorporeal oxygenator with enflurane (1.1%, 2.2%, 4.4%). CBF (measured with a Doppler flow transducer) was multiplied by the local arteriovenous (A-V) O2 difference to calculate MVo2. SS was measured with ultrasonic crystals. Myocardial lactate uptake was assessed. Peak CBF responses during enflurane were compared with those during maximum coronary vasodilation with adenosine. Enflurane caused concentration-dependent increases in CBF, and decreases in MVo2 and SS. The greatest increase in CBF during enflurane (4.4%) was similar to that achievable with adenosine. Myocardial lactate uptake was not affected by enflurane. In conclusion, enflurane has a direct coronary vasodilating effect. The potency of this effect is underscored by the ability of enflurane to cause marked increases in CBF, while appreciably reducing myocardial O2 demand. Since the enflurane-induced reduction in myocardial contractility was not due to ischemia, it likely reflected a direct negative inotropic effect. When the direct effects of enflurane are compared with those of equianesthetic concentrations of halothane and isoflurane previously shown in the same model, enflurane has a coronary vasodilating effect similar to that of halothane but less than that of isoflurane, and it has a negative inotropic effect greater than that of both isoflurane and halothane.

Anesthetics, Inhalation↗
PubMed1996

Efficacy of the self-inflating bulb in confirming tracheal intubation in the morbidly obese.

BACKGROUND: This study was designed to determine the incidence of false-negative and false-positive results when the self-inflating bulb (SIB) is used to differentiate tracheal from esophageal intubation in morbidly obese patients using two techniques. In technique 1, the SIB is compressed before it is connected to the tube; in technique 2, the SIB is compressed after connection to the tube. METHODS: With institutional review board approval, 54 consenting adult morbidly obese patients (body mass index > 35) undergoing elective surgical procedures were included in the study. After anesthetic induction and muscle relaxation, both the trachea and esophagus were intubated under direct vision with identical cuffed tubes. The efficacy of the SIB in verifying the position of both tubes was tested by a second anesthesiologist. The speed of reinflation was graded as rapid ( < 4 s) or none ( > 4 s), using both techniques. In the case of tracheal intubation, the absence of reinflation was recorded as a false-negative, whereas in cases of esophageal intubation, rapid reinflation was recorded as a false-positive. Identification of tube location by the second anesthesiologist was based on SIB reinflation results from techniques 1 and 2, as well as the presence of a flatuslike sound elicited by technique 2 in esophageally placed tubes. All patients were retested by the SIB after receiving three breaths of 400-500 ml each. In all patients exhibiting false-negative results, six obese patients exhibiting true-positive results, and four nonobese patients exhibiting true-positive results, tracheal responses to the SIB maneuvers were observed directly by a flexible fiberoptic bronchoscope incorporating an airtight system, 15-20 min after mechanical ventilation was instituted. RESULTS: The incidence of false-negative results was initially 30% with technique 1 and 11% with technique 2, but decreased to 4% when technique 2 was used after the delivery of three breaths. The second anesthesiologist initially identified tube location in 92.5% of patients correctly. After the delivery of three breaths, tube location was correctly identified in 96.3% of patients. Fiberoptic bronchoscopic examination of the patients exhibiting false-negative results revealed exaggerated inward bulging of the posterior tracheal membrane during reinflation of the SIB when technique 1 was used. CONCLUSIONS: Contrary to previous investigations in healthy patients, the current study demonstrates a high incidence of false-negative results when the SIB is used to confirm tracheal intubation in morbidly obese patients. If the SIB is used, the technique should include compression of the SIB after connection to the tube and should be used in conjunction with other clinical signs and technical aids. The mechanism of false-negative results in these patients seems to be related to reduction of caliber of airways secondary to a marked decrease in functional residual capacity, and collapse of large airways due to invagination of the posterior tracheal wall when sub-atmospheric pressure is generated by the SIB.

Adolescent↗
PubMed1996

Investigations into the mechanisms of coronary vasodilation by contrast media in dogs.

RATIONALE AND OBJECTIVES: The study was performed to clarify the mechanisms underlying contrast-induced coronary vasodilation. METHODS: The left anterior descending coronary artery of 14 open-chest dogs was perfused at constant pressure. Coronary blood flow (CBF) was measured electromagnetically and used to calculate myocardial oxygen consumption (MVO2). Responses were evaluated during intracoronary infusions (2 mL/ minute) of the ionic contrast medium, Hypaque-76, and the nonionic contrast medium, Isovue-370, and compared with those caused by hypertonic saline solutions with comparable osmolarities. Studies also were conducted using Isovist-300, which is a new nonionic and iso-osmolar contrast medium. RESULTS: Hypaque-76 and Isovue-370 caused initial peak increases in CBF (reflecting decreases in coronary vascular resistance), which waned rapidly to achieve more modest steady-state increases within 2 to 3 minutes. Both the peak and steady-state increases in CBF were greater during Hypaque-76 than during Isovue-370. The increases in CBF caused by the contrast medium were greater than those caused by the corresponding saline solution. Neither Hypaque-76 nor Isovue-370 changed MVO2-Isovist-300 had no effect on CBF or MVO2. CONCLUSIONS: The coronary vasodilation by contrast media is the result of a direct vasorelaxing effect rather than secondary to a metabolic mechanism. Hyperosmolarity can account only in part for contrast-induced coronary vasodilation.

Animals↗
PubMed1995

Effectiveness of the self-inflating bulb for verification of proper placement of the Esophageal Tracheal Combitube.

The esophageal tracheal Combitube (ETC; Sheridan Catheter Corporation, Argyle, NY) is a twin-lumen tube used to establish emergency ventilation. After blind placement, ventilation is performed via the proximal lumen if it is in the esophagus or via the distal lumen if it is in the trachea. This investigation was designed to test the reliability of the self-inflating bulb (SIB) in identifying the location of the ETC and facilitating its proper positioning in anesthetized patients. In Group 1 (n = 26), the ETC was introduced blindly. In Group 2 (n = 20), the tube was placed in the trachea (eight patients) or once in the trachea and once in the esophagus, randomly (12 patients) under direct vision rigid laryngoscopy by the anesthesiologist performing the intubation. In both groups, the efficacy of the SIB in identifying the location of the ETC was tested by a second blinded anesthesiologist. In Group 1, blind insertion of the ETC resulted in esophageal placement in all patients, and in each case was correctly identified. The second anesthesiologist reported no reinflation when the compressed SIB was connected to the distal lumen. When the compressed SIB was connected to the proximal lumen, instantaneous reinflation was observed in 23 patients, delayed reinflation (2-4 s) in two and no reinflation (> 4 s) in one patient. Instantaneous reinflation occurred in these three patients after repositioning of the ETC. In Group 2, the second anesthesiologist correctly identified the location of the ETC in all cases. The results confirm previous findings that blind introduction of the ETC leads to esophageal placement and yields adequate ventilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1995

Direct effects of halothane on coronary blood flow, myocardial oxygen consumption, and myocardial segmental shortening in in situ canine hearts.

Previous in vivo studies of the coronary vascular effects of halothane (HAL) were complicated by varying hemodynamic conditions and global cardiac work demands. Accordingly, the current study evaluated changes in coronary blood flow (CBF) and associated variables during selective intracoronary administrations of HAL in in situ canine hearts using an extracorporeal-controlled pressure perfusion system. Findings during HAL were compared to those during isoflurane (ISO). The left anterior descending coronary artery (LAD) of 8 open-chest dogs anesthetized with fentanyl and midazolam was perfused at constant pressure (109 +/- 2 mm Hg) with HAL-free arterial blood or with blood equilibrated in an extracorporeal oxygenator with HAL (0.5%, 1.0%, 2.0% in 95% O2-5.0% CO2). In the LAD bed, measurements of CBF were obtained with an electromagnetic flowmeter and used to calculate myocardial oxygen consumption (MVO2). Percent segmental shortening (%SS) was measured with ultrasonic crystals. Changes in CBF by HAL were compared to those during maximal vasodilation with adenosine. Separate studies (n = 5) were performed using 1.4% [1 minimum alveolar anesthetic concentration (MAC)] ISO and the findings compared to those during an equianesthetic (1.0%) concentration of HAL. HAL caused concentration-dependent increases in CBF, and decreases in MVO2 and %SS. With 2.0% HAL, the level of CBF was 50% of the maximal adenosine-induced response. At equianesthetic concentrations, HAL caused increases in CBF that were one-third of those caused by ISO, while the decreases in MVO2 and %SS caused by the drugs were not significantly different.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1995

Hemodilution impairs hypocapnia-induced vasoconstrictor responses in the brain and spinal cord in dogs.

Despite the increasing use of plasma expanders in the perioperative period, there have been few studies of cerebrovascular responsiveness during hemodilution. The present study was performed to evaluate the influence of isovolemic hemodilution on vasoconstrictor responses in the brain and spinal cord during hypocapnia. Sixteen mechanically ventilated, halothane-anesthetized dogs were randomly divided into two equal groups: Group 1, control group (hematocrit [Hct], 42% +/- 2%); Group 2, isovolemic hemodilution with 5% dextran 40 (Hct, 19% +/- 2%). Hypocapnia (22 +/- 1 mm Hg) was induced in both groups by removal of dead space tubing without altering mechanical ventilation. Regional blood flow in the brain and spinal cord was measured with 15-microns radioactive microspheres and used to calculate regional vascular resistance (RVR). In Group 1, hypocapnia caused increases in RVR (ranging from 44% +/- 10% in the cerebral cortex to 93% +/- 17% in the thoracic spinal cord). In Group 2, hemodilution itself decreased RVR relatively uniformly throughout the brain and spinal cord. After hemodilution, hypocapnia had no significant effect on RVR in the cerebral cortex, cerebellum, pons, and medulla, and caused less pronounced increases in RVR within the spinal cord. We conclude that hemodilution either attenuated or completely abolished vasoconstrictor responses within the brain and spinal cord during hypocapnia. Furthermore, the present findings suggest that induced hypocapnia may be less effective as a clinical maneuver to reduce increased intracranial pressure during hemodilution.

Animals↗
PubMed1995

Coronary vasodilation by isoflurane. Abrupt versus gradual administration.

BACKGROUND: Under certain circumstances, isoflurane is associated with coronary artery vasodilation. The objective of the current study was to ascertain whether the rate of administration of isoflurane influences its vasodilating effect in the coronary circulation. METHODS: Seven open-chest dogs anesthetized with fentanyl and midazolam were studied. The left anterior descending coronary artery was perfused via either of two pressurized (80 mmHg) reservoirs; reservoir 1 (control) was supplied with arterial blood free of isoflurane, and reservoir 2 was supplied with blood from an extracorporeal oxygenator, which was provided with 95% O2/5% CO2 gas that passed through calibrated vaporizer. Coronary blood flow (CBF) was measured with Doppler flow transducer. In each dog, isoflurane was administered according to two protocols; abrupt (isoflurane-A) or gradual (isoflurane-G). In isoflurane-A, the left anterior descending coronary artery was switched from reservoir 1 to reservoir 2 after the latter was filled with blood previously equilibrated with 1.4% (1 MAC) isoflurane. In isoflurane-G, the left anterior descending coronary artery was switched to reservoir 2 with vaporizer set at 0% isoflurane; then the vaporizer was adjusted to 1.4% isoflurane, which produced a gradual increase in isoflurane concentration within reservoir 2 that reached a level equivalent to that in isoflurane-A (as evaluated by gas chromatography) by 30 min. CBF during maximally dilating, intracoronary infusion of adenosine served as a reference to assess effects of isoflurane. RESULTS: Isoflurane-A caused marked increases in CBF, which, at constant perfusion pressure, reflected pronounced reductions in vascular resistance. These increases in CBF were 80% of those with adenosine. Although isoflurane-G also caused increases in CBF, the increases were only 45% of those caused by isoflurane-A. CONCLUSIONS: The current findings demonstrate that the extent of coronary vasodilation by isoflurane was not dependent only on its blood concentration but also on the rate at which this blood concentration was achieved; a gradual increase in blood concentration blunted the vasodilator effect. Differences in the rate of administration of isoflurane likely contributed to its widely variable coronary vasodilating effects in previous studies.

Adenosine↗
PubMed1995

Preoperative pregnancy testing in ambulatory surgery. Incidence and impact of positive results.

BACKGROUND: The incidence of unrecognized early pregnancy and its influence on the surgical and anesthetic course in patients presenting for elective ambulatory surgery have not been previously determined. The current study was designed to determine the incidence of unrecognized pregnancy in women presenting for ambulatory surgery. In addition, it examined how discovery of the pregnancy altered the anesthetic or surgical course. METHODS: In a prospective study over a 1-yr period, all women of childbearing potential (defined as menstruating women without prior hysterectomy or tubal ligation) were preoperatively evaluated and tested for urine or serum human chorionic gonadotropin, to determine unrecognized pregnancy. If a pregnancy was detected, the disposition of the surgical procedure and the effect on the surgical and anesthetic management was recorded. RESULTS: Of 2,056 women of childbearing potential presenting for ambulatory surgery, testing revealed 7 previously unrecognized pregnancies, an incidence of 0.3%. Included among these patients were two patients scheduled to undergo fertility procedures. On learning the test result and even before being advised of available options, all patients elected to cancel or postpone the surgical procedure. CONCLUSIONS: The incidence of previously unrecognized pregnancy in menstruating women presenting for ambulatory, nonobstetric surgery was 0.3%. The knowledge of a positive test resulted in cancellation or postponement of the operative procedure. Patient desire for cancellation was the main determining factor in each case.

Ambulatory Surgical Procedures↗
PubMed1995

Contribution of nitric oxide to coronary vasodilation during hypercapnic acidosis.

The present study was performed to evaluate the role of nitric oxide (NO) in coronary vasodilation during hypercapnic acidosis (HC). The left anterior descending coronary arteries of 17 anesthetized, open-chest dogs were perfused with normal arterial blood or with arterial blood equilibrated in an extracorporeal circuit with 90% O2-10% CO2 [arterial carbon dioxide tension (PaCO2) 72 +/- 3 mmHg, arterial pH 7.16 +/- 0.02]. Coronary perfusion pressure (CPP) was initially set at 100 mmHg. Coronary blood flow (CBF) was measured with a Doppler transducer. Studies were conducted under constant-pressure (variable CBF; n = 13) and constant-flow (variable CPP) conditions (n = 4). Steady-state changes in CBF (or CPP) during HC and during intracoronary infusions of acetylcholine (ACh, 20 micrograms/min), an endothelium-dependent vasodilator, and sodium nitroprusside (SNP, 80 micrograms/min), an endothelium-independent vasodilator, were compared before and after intracoronary infusion of a NO synthase inhibitor, either NG-nitro-L-arginine methyl ester (L-NAME, 4.5 mg) or NG-monomethyl-L-arginine (L-NMMA, 30 mg). Under constant pressure, L-NAME blunted increases in CBF by HC (274 +/- 32 vs. 113 +/- 24%) and ACh (400 +/- 43 vs. 68 +/- 17%), whereas increases in CBF by SNP were not significantly affected (207 +/- 34 vs. 186 +/- 18%). Results with L-NMMA were similar. Under constant flow, L-NAME attenuated decreases in CPP by HC and ACh, whereas it had no significant effect on decreases in CPP by SNP. In conclusion, HC elicits release of NO from coronary vascular endothelium via a direct effect rather than secondary to an increased flow rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1994

Efficacy of the self-inflating bulb in detecting esophageal intubation. Does the presence of a nasogastric tube or cuff deflation make a difference?

BACKGROUND: The principle underlying the use of the self-inflating bulb in differentiating esophageal from tracheal intubation is that the trachea is held open by rigid cartilaginous rings, whereas the esophagus collapses when a negative pressure is applied to its lumen. This investigation was designed to test the efficacy of the bulb in detecting esophageal intubation in the presence of a nasogastric tube and after tracheal tube cuff deflation. METHODS: In anesthetized patients, the trachea and esophagus were intubated with identical tubes. The efficacy of the bulb was tested after a nasogastric tube was placed (group 1, n = 70) and after cuff deflation (group 2, n = 60) by a second anesthesiologist. RESULTS: In patients with nasogastric tubes (group 1), the anesthesiologists reported no reinflation of the compressed bulbs connected to tubes placed in the esophagus and immediate reinflation when connected to tracheally placed tubes in every case. In group 2, the determination of tube placement was correct in every case after cuff deflation. Mean (+/- SEM) negative pressures generated when compressed bulbs were connected to esophageally placed tubes were 57.8 +/- 0.48 mmHg (group 1) and 55.3 +/- 0.52 mmHg (group 2) and remained unchanged after the introduction of nasogastric tubes or after cuff deflation. CONCLUSIONS: These results confirm that a nasogastric tube or cuff deflation does not interfere with the reliability of the self-inflating bulb in detecting esophageal intubation and thus does not contribute to false positive results. Confirmation of tracheal tube placement by this simple method makes it ideal for use with other recognized methods both in and outside the operating rooms and enables physicians and emergency personnel to proceed with other resuscitative measures.

Adolescent↗
PubMed1994

Nitric oxide does not mediate coronary vasodilation by isoflurane.

BACKGROUND: Isoflurane causes vasodilation in the coronary circulation. The current study employed a canine model permitting selective intracoronary administrations of isoflurane (1) to test the hypothesis that coronary vasodilation by isoflurane is mediated by nitric oxide and (2) to evaluate the persistence of coronary vasodilation during an extended exposure to isoflurane. METHODS: Open-chest dogs anesthetized with fentanyl and midazolam were studied. The left anterior descending coronary artery (LAD) was perfused via extracorporeal system with normal arterial blood or with arterial blood equilibrated with 1.4% (1 MAC) isoflurane. In the LAD bed, coronary blood flow (CBF) was measured with an electromagnetic flowmeter and used to calculate myocardial oxygen consumption (MVO2). In series 1, performed at constant coronary perfusion pressure (CPP), the LAD was exposed to 3 h of isoflurane in two groups of eight dogs: control group, normal coronary endothelium; and experimental group, intracoronary infusion of the nitric oxide synthase inhibitor L-NAME (0.15 mg/min for 30 min). Series 2 was performed with CBF constant; thus, CPP varied directly with coronary vascular resistance. In this series, initial steady-state changes in CPP by isoflurane were evaluated in the same four dogs before and after L-NAME. RESULTS: In the control group of series 1, isoflurane caused a maximal, initial increase in CBF of 444%; however, CBF decreased progressively reaching a value not significantly different from baseline after 3 h of isoflurane. Isoflurane caused a significant (approximately 35%) decrease in MVO2, which persisted during the 3-h administration. Findings after L-NAME (experimental group) were not significantly different from those in control group. In series 2, isoflurane caused significant decreases in CPP that were not affected by L-NAME. CONCLUSIONS: The lack of effect of L-NAME on isoflurane-induced coronary vasodilation suggests that nitric oxide does not mediate this response. The increase in CBF during prolonged isoflurane waned over time, perhaps because of tachyphylaxis or emergence of a competitive vasoconstrictor mechanism, e.g., metabolic factors secondary to reduced oxygen demands.

Animals↗