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Biomedical subjects

C M Alexander

Publications and source records attributed to C M Alexander.

At least 55 records · Page 3Linked to original sources
PubMed1989

New discharge criteria decrease recovery room time after subarachnoid block.

The authors completed a two-phase study to determine criteria that might predict hemodynamic stability during recovery from subarachnoid block (SAB). Patients' supine and sitting (2 min) blood pressures were determined at 30-min intervals in the recovery room (RR). In the first group of 26 patients, retrospective analysis revealed that the orthostatic decrease in mean arterial pressure (MAP) never exceeded 15% following two successive orthostatic decreases of 10% or less. This finding was validated prospectively in a second group of 26 patients. Following two successive orthostatic MAP decreases of 10% or less, none of 65 orthostatic challenges resulted in an MAP decrease of more than 15%; conversely, in the absence of two successive MAP decreases of less than 10%, 5 of 51 orthostatic challenges resulted in an MAP decrease of greater than 15% (P less than 0.02). Had patients been discharged from the RR based on two successive MAP decreases of less than 10%, 35 of 52 patients could have been discharged from the RR 76 +/- 6 min (mean +/- SE) sooner than they would have under usual empirical discharge criteria of supine hemodynamic stability, regression of sensory level to T10, and return of toe movement. Following SAB, hemodynamic stability may return before sensory and motor function; for many patients, orthostatic testing following SAB may safely decrease the amount of time spent in the RR.

Aged↗
PubMed1988

Isolation of an abundantly expressed sequence from the human X chromosome by differential screening.

A cDNA library was constructed from poly(A)+ RNA derived from MP2H4, a mouse-human somatic cell hybrid, containing as its only human contribution an X-6 translocation chromosome. This library was screened with [32P] c-DNA derived from MP2H4 and counterscreened with a phenotypically similar mouse cell line. From a screen of 4000 recombinants, seven clones were isolated which hybridized more strongly with cDNA derived from the mouse-human hybrid than with the mouse only cell line. Southern blot analysis showed that four of the seven clones originate from the human genome, three of these contain repeat sequences, and one, SCR10, is devoid of repeats. SCR10 identifies a 1-kb mRNA transcribed from the human X chromosome mapping to the region Xq13-q13.3 or Xq21.3-q22 and is an abundantly and ubiquitously expressed gene. A near, or full-length clone of SCR10, SCAR, was isolated and sequenced; the conceptional translation of this sequence encodes a basic protein of 27.5 kd. Sequences homologous to SCAR were detected in primates, rodents, avians, and Xenopus.

Animals↗
PubMed1988

Awakening concentrations of isoflurane are not affected by analgesic doses of morphine.

A randomized, double-blind study was performed to determine how morphine 0.1 mg/kg IV, or placebo administered 80 +/- 11 (means +/- SE) minutes before the end of surgery affect recovery from isoflurane/oxygen anesthesia. End-tidal isoflurane remained constant at 1.10 +/- 0.02% (means +/- SE) in both groups intraoperatively, and no other anesthetics were given after the administration of the morphine or placebo. Duration of anesthesia did not differ significantly between the morphine (172 +/- 7 minutes) and placebo (163 +/- 18 minutes) groups. Times from discontinuation of isoflurane until eye-opening in response to verbal command were similar in the morphine (19 +/- 2 minutes) and placebo (22 +/- 3 minutes) groups. At the time of eye-opening, end-tidal isoflurane concentrations did not differ between subjects receiving morphine (0.20 +/- 0.02%) and placebo (0.18 +/- 0.01%). It is concluded that the awakening concentration (MAC-awake) during recovery from isoflurane anesthesia is approximately 0.19% and is not affected by analgesic doses or morphine.

Adult↗
PubMed1988

Sedative doses of midazolam depress hypoxic ventilatory responses in humans.

The effect of midazolam on the hypoxic ventilatory response of eight healthy volunteers was examined during isocapnic rebreathing. The magnitude of the slope of the ventilatory response to hypoxia (VE vs SaO2) decreased from 1.48 +/- 0.24 to 0.70 +/- 0.13 L.min-1.%SaO2(-1) (means +/- SE, P less than 0.005) after midazolam 0.1 mg/kg IV. The calculated ventilation at an arterial saturation of 90% also decreased from 28.6 +/- 4.4 to 19.9 +/- 2.7 L/min (P less than 0.05). Before midazolam, hypoxia to an SaO2 of 75 +/- 2% was associated with a 23 +/- 3 beats/min increase in heart rate; after midazolam, the increase in heart rate with hypoxia was only 4 +/- 2 beats/min (P less than 0.001). Additionally, a double-blind crossover study evaluated the effect of physostigmine on awareness and hypoxic ventilatory response after midazolam. The change in hypoxic response slope after physostigmine 2.0 mg IV (an increase of 0.28 +/- 0.34 L.min-1.%SaO2(-1] did not differ significantly from that after placebo (an increase of 0.03 +/- 0.22 L.min-1.%SaO2(-1], although physostigmine significantly increased awareness. It is concluded that a sedative dose of midazolam depresses hypoxic ventilatory response and attenuates the hyperpnea and tachycardia associated with hypoxemia. Furthermore, physostigmine-glycopyrrolate reversal of midazolam-induced sedation was associated with nausea (five subjects), vomiting (three subjects), and tachycardia without reversal of the depressed hypoxic ventilatory response.

Adult↗
PubMed1988

The effect of pleural pressure on the hypoxic pulmonary vasoconstrictor response in closed chest dogs.

The effect of intrapleural pressure on the hypoxic pulmonary vasoconstrictor (HPV) responses to atelectasis and hypoxia were measured in two groups of anesthetized closed chest dogs. The right lung was continuously ventilated with 100% O2. The left lung was initially ventilated with 100% O2 (hyperoxia) but subsequently underwent either reabsorption atelectasis (atelectasis; group I) or ventilation with a hypoxic gas mixture (hypoxia; group II). The mean intrapleural pressure in the left hemithorax was 5.4 cm H2O during hyperoxia, but with left lung atelectasis decreased significantly to -3.8 cm H2O by 15 minutes and to -4.2 cm H2O by 90 minutes. Venous admixture (% VA) increased significantly from 10.3% during hyperoxia to 33.2% at 15 minutes of left lung atelectasis and to 34.6% at 90 minutes. However, after sternotomy with the left lung still atelectatic, the %VA decreased significantly to 25.4% For the hypoxia group, %VA increased significantly from 9.2% during hyperoxia to 29.9% at 15 minutes of left lung hypoxia and 25.1% at 90 minutes. HPV diverted blood flow away from both atelectatic lung and hypoxic lung. However, due to the negative intrapleural pressure generated during left lung resorption atelectasis when the chest was closed, HPV was less effective during atelectasis than during hypoxia.

Animals↗
PubMed1987

The effect of changes in arterial CO2 tension on plasma lidocaine concentration.

The authors studied the effect of changes in arterial carbon dioxide tension on plasma lidocaine concentrations during a constant lidocaine infusion in eight healthy volunteers. With a PaCO2 of 41.4 +/- 0.9 mmHg (mean +/- SE), total plasma lidocaine concentrations were 3.97 +/- 0.20 microgram X ml-1. There was no significant change associated with hypercarbia (PaCO2 = 55.7 +/- 1.5 mmHg, lidocaine = 3.93 +/- 0.18 microgram X ml-1) or hypocarbia (PaCO2 = 19.5 +/- 1.4 mmHg, lidocaine = 4.29 +/- 0.25 microgram X ml-1), despite the known effects of changes in CO2 tension on hepatic blood flow and lidocaine protein binding. During hypercarbia, plasma lidocaine binding decreases while total plasma lidocaine remains essentially constant; therefore, increased CO2 tensions could cause toxicity if total lidocaine concentrations were in the high therapeutic range (5 micrograms X ml-1). Four subjects experienced transient symptoms of mild lidocaine toxicity during acute increases in carbon dioxide tension.

Adult↗
PubMed1987

Evaluation of the Ohmeda 3700 pulse oximeter: steady-state and transient response characteristics.

The authors determined the accuracy of the Ohmeda 3700 (version J) pulse oximeter in healthy volunteers rendered hypoxic (SaO2 from 60-98%) by breathing mixtures of O2 in N2. When equipped with an ear probe, the pulse oximeter reading (y) reliably predicted arterial saturation (x) under steady-state conditions (y = 1.05x - 4.66, r = 0.98) as well as when oxygen saturation was rapidly decreasing (y = 1.05x - 6.38, r = 0.96). Conversely, when equipped with a finger probe, the oximeter tended to significantly underestimate steady-state arterial saturation (y = 1.21x - 19.1, r = 0.98, P less than 0.001). In response to this information, the manufacturer modified the oximeter's software (version XJ1), resulting in improved agreement between oximeter readings and arterial values (y = 0.96x + 4.59, r = 0.99). Despite the close correlation between steady-state oximeter readings and arterial saturation, the 99% prediction limits for both the ear and finger probes (version XJ1) were +/- 8%. Finger probe readings did not reliably reflect radial arterial oxygenation during rapid desaturation (y = 0.55x + 45.2, r = 0.78). This may be related to the time required to "arterialize" the blood in the finger; during acute resaturation, we found that the ear- to finger-probe delay was 24.0 +/- 2.3 s (means +/- SE, P less than 0.001).

Adult↗
PubMed1986

Influence of isoflurane on hypoxic pulmonary vasoconstriction in dogs.

The authors studied the influence of locally administered isoflurane anesthesia on the pulmonary vascular response to regional alveolar hypoxia (hypoxic pulmonary vasoconstriction [HPV]) over a range of cardiac outputs (COs) in seven mechanically ventilated, closed-chest dogs. The right lung was ventilated with 100% O2 throughout the study. The left lung was ventilated with either 100% O2 (normoxia) or an hypoxic gas mixture (hypoxia). Different alveolar concentrations of isoflurane (0, 1, and 2.5 MAC) were administered to the left lung in a randomized sequence. The CO was altered by opening and closing surgically produced arteriovenous fistulae, at all isoflurane concentrations, and by hemorrhage at 0 MAC isoflurane. The magnitude of the HPV response was measured by differential CO2 elimination in the absence of isoflurane and by venous admixtures in all phases. During normoxia, the left lung effective flow (QL%) measured from differential CO2 excretion was 39.9 +/- 1.2% of the total blood flow and decreased to 18.8 +/- 2.6% when ventilated with the hypoxic gas mixture. Venous admixture (QVA/QT%) was significantly correlated with QL% during hypoxic ventilation in the absence of isoflurane. QVA/QT% was 22.3 +/- 2.7% during hypoxia with normal CO, and it increased significantly to 27.7 +/- 1.1% when the CO was increased 43%. It was not significantly altered (23.6 +/- 3.6%) when the CO was decreased by 54%. Isoflurane 2.5 MAC significantly increased QVA/QT% during hypoxic ventilation of the left lung to 33.9 +/- 2.6% with low CO and 35.4 +/- 1.7% with normal CO. Isoflurane 1 MAC increased QVA/QT% to 27.2 +/- 2.7% with normal CO and 28.1 +/- 2.6% with high CO.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

The influence of halothane and isoflurane on pulmonary collateral ventilation.

The effects of halothane and isoflurane on hypocapnic increases in pulmonary collateral resistance were studied in dogs. A bronchoscope with a double lumen catheter in the suction port obstructed a peripheral airway and allowed gas to flow out of the isolated segment of lung only via collateral channels. The collateral gas flow (Vcoll) was measured with a flowmeter and delivered through one lumen of the catheter, while the other lumen measured distal pressure (Pb). At FRC, the resistance to collateral ventilation (Rcoll) was calculated as Rcoll = Pb/Vcoll. The rest of the lung was ventilated with air, while air (hypocapnia), 10% CO2 in air, or air and halothane or isoflurane were delivered to the isolated segment. A measurement of resistance was made after 4 min of test gas flow. For each segment, when air replaced 10% CO2, the average increase in Rcoll was calculated and called Rmax. When 10% CO2 in air was infused into segments the mean Rcoll (n = 50) was 0.0196 +/- 0.0022 cmH2O X ml-1 X min. This increased to 0.0285 +/- 0.0031 cmH2O X ml-1 X min (mean +/- E) when air was infused, a mean increase in resistance of 52 +/- 3%. When halothane or isoflurane was added to air the hypocapnic increase in Rcoll was attenuated with a 50% decrease at 1.3% (1.4 MAC and 0.8 MAC, respectively). These two inhalational anesthetics reduce active changes in the flow resistance to collateral ventilation. When collateral resistance acts to adjust ventilation perfusion deviations, this action of halothane and isoflurane may make this regulation less effective.

Airway Resistance↗
PubMed1985

Hypoxic pulmonary vasoconstriction is not potentiated by repeated intermittent hypoxia in closed chest dogs.

Hypoxic pulmonary vasoconstrictor (HPV) responses were measured with repeated intermittent hypoxic challenges in eight non-traumatized closed chest dogs anesthetized with pentobarbital. The right lung was ventilated continuously with 100% O2 while the left lung was either ventilated with 100% O2 (control) or ventilated with a gas mixture containing 3-4% O2 (hypoxia). Mean per cent left lung blood flow for all four normoxic periods was 43.1 +/- 1.5% (mean +/- SE) of the total blood flow by the SF6 excretion method and 40.8 +/- 1.1% by the differential CO2 excretion method, corrected for the Haldane effect. With hypoxic ventilation, flow diversion from the hypoxic lung was maximal with the first exposure and did not change subsequently with a total of four alternating exposures to normoxia and hypoxia. Flow diversion during hypoxia was approximately 50.5 +/- 2.4% by the SF6 method and 50.3 +/- 3.5% by the VCO2 method. This result contrasts with the increasing flow diversion response with intermittant hypoxic exposure that has been reported in animals exposed first to thoracotomy and surgical dissection. It is concluded that in the absence of surgical trauma the initial response to hypoxia is maximal and is not potentiated by repeated hypoxic stimulation.

Anesthesia, Intravenous↗
PubMed1984

Oral triiodothyronine administration lowers plasma fibronectin levels in humans.

It has been shown that both serum triiodothyronine (T3) and plasma fibronectin values decline with fasting and increase with treatment of diabetic ketoacidosis in a paralles manner. To evaluate the mechanism responsible for these changes, we examined the effects of both oral T3 administration and fasting in six healthy, adult subjects. Initial plasma fibronectin values were normal in four subjects (group 1) and decreased in two subjects (group 2). Initial serum T3 and thyroxine (T4) values were normal in both groups. Despite a substantial rise in serum T3 values with oral T3 administration, plasma fibronectin fell in group 1 subjects. Fasting caused a significant decline in serum T3 levels, but only a small further decline of plasma fibronectin concentrations. Serum T3 levels rose after 1 week of refeeding, whereas plasma fibronectin levels in group 1 did not return toward normal. Plasma fibronectin values did not change in group 2 subjects with oral T3, fasting, or refeeding. In conclusion, there is no simple cause-and-effect relationship between previously observed changes in plasma fibronectin and serum T3 concentrations. High doses of oral T3 will lower plasma fibronectin levels in subjects with initially normal plasma fibronectin values and a normal caloric intake.

Administration, Oral↗
PubMed1984

Time course and responses of sustained hypoxic pulmonary vasoconstriction in the dog.

The stability of the pulmonary blood pressure and flow response to alveolar hypoxia (hypoxic pulmonary vasoconstriction or HPV) was studied in six pentobarbital anesthetized, mechanically ventilated open-chested dogs. Aortic and left pulmonary artery blood flows; systemic and pulmonary arterial, central venous, left atrial, and airway pressures; hemoglobin; arterial and mixed venous blood gases were measured. The right lung was ventilated continuously with 100% oxygen, while the left lung was ventilated alternately with 100% O2 ( prehypoxia control phase), an hypoxic gas mixture containing 4% O2, 3% CO2, balance N2 for 4 h, or 100% O2 (post-hypoxia control phase). Hypoxic ventilation of the left lung resulted in an immediate and sustained decrease in left lung blood flow (QL%) from 39.0 +/- 1.8% (mean +/- SE) to 9.9 +/- 3.6% at 15 min of hypoxic ventilation. QL% remained decreased and did not vary significantly during the 4 h of hypoxia. Venous admixture correspondingly was increased and PaO2 decreased by hypoxic ventilation and did not vary significantly during the 4 h of hypoxia. All variables returned to control levels upon reestablishing ventilation with 100% O2. While the maximal reduction in QL% with left lung hypoxic ventilation was identical to that observed during atelectasis previously in our laboratory, the time course of the response was different. The response to hypoxia was maximal by 15 min, however, QL% decreased more slowly during atelectasis, where the maximal reduction was observed by 60 min. The present study therefore demonstrated that hypoxic ventilation of the left lung yielded an immediate and sustained decrease in left lung blood flow for 4 h. The stability of the HPV response probably was accounted for by the lack of such confounding factors as respiratory alkalosis, severe systemic hypoxemia, and increased cardiac output.

Analysis of Variance↗
PubMed1984

Influence of the method of re-expansion of atelectatic lung upon the development of pulmonary edema in dogs.

An endobronchial tube was used to separately ventilate each lung in anesthetized dogs, and absorption atelectasis was then induced in the left lung and maintained for 3 1/2 h. The left lung was partially re-expanded by ventilation at normal tidal volumes for 10 min, and then completely re-expanded by manual hyperinflation. This delayed re-expansion was associated with an extravascular water content significantly greater than that of the right lung. A previous study demonstrated no increase in the ratio of left to right lung water content after 3 h of atelectasis alone and a significant increase after immediate hyperinflation. Delayed re-expansion produces significantly different results, and it is therefore concluded that the method of lung re-expansion influences the development of pulmonary edema after atelectasis.

Animals↗
PubMed1983

Rapid increase in both plasma fibronectin and serum triiodothyromine associated with treatment of diabetic ketoacidosis.

Plasma fibronectin and serum thyroid parameters were determined in 6 hyperglycemic nonketoacidotic patients (HNK) and 12 subjects with diabetic ketoacidosis (DKA). The DKA patients showed a marked increase in both plasma fibronectin and serum T3 over 5 days of insulin treatment [175.2 +/- 18.1% (+/- SEM) and 208.7 +/- 17.6% of initial values respectively], while these parameters did not change in the HNK patients despite equivalent control of diabetes. Serum rT3 levels declined, as expected, to 65.8 +/- 10.9% of the initial values in the DKA patients, but did not change in the HNK patients. There was a significant positive correlation between changes in plasma fibronectin and serum T3 values in the DKA patients (r = 0.5; P less than 0.005). Other reports have shown a decrease in plasma fibronectin concentrations in fasted patients, a well known low T3 state; therefore, the association between changes in plasma fibronectin and serum T3 values may be a widely observed phenomenon. The parallel changes in fibronectin and T3 may reflect alterations in the metabolic state of these patients. The precise nature of the relationship between changes in fibronectin and T3 concentrations requires additional investigations.

Adult↗
PubMed1983

Immunoreactivity of human insulin of recombinant DNA origin.

To evaluate possible advantages of human insulin of recombinant DNA origin (HI) in the treatment of diabetic patients, we compared cellular and humoral immunoreactivities of HI and porcine insulin (PI). Anti-insulin IgE bound equal amounts of 125I-HI and 125I-PI. There was no difference between HI- and PI-stimulated lymphocyte transformation indices. The binding of 125I-HI with circulating anti-insulin IgG was lower compared with 125I-PI binding (12.1 +/- 1% versus 15.4 +/- 1.5%, P less than 0.001) in 60 insulin-treated cases. Thirteen sera were selected for high antibody titers and analyzed in detail. In the competitive inhibition assays, a 50% displacement of 125I-PI required a fourfold higher concentration of HI than PI. Although total insulin binding capacities were almost equal, 63 +/- 11 nM/L for PI and 60 +/- 12 nM/L for HI, the high-affinity antibodies had significantly reduced avidity for HI compared with PI. These differences in avidities suggest that HI may be useful in treatment of immune-type insulin resistance.

Adolescent↗