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Biomedical subjects

S Lakshminarayan

Publications and source records attributed to S Lakshminarayan.

At least 55 records · Page 3Linked to original sources
PubMed1986

Hypoxia and hypercarbia increase bronchial blood flow through bronchopulmonary anastomoses in anesthetized dogs.

We studied the effect of systemic hypoxemia and hypercarbia on the bronchial blood flow in open-chested, anesthetized dogs. The pulmonary artery and vein of the left lower lobe (LLL) were isolated with cannulas and connected to reservoirs set at atmospheric pressure relative to the base of the LLL. That fraction of the bronchial arterial flow (Qbr) to the LLL, which flowed through the bronchopulmonary anastomoses into these reservoirs, was continuously measured. The LLL was inflated continuously with 6% CO2 and air at a constant alveolar pressure of 10 cm H2O. Systemic arterial O2 tension (PaO2) and arterial CO2 tension (PaCO2) were varied by separately ventilating the right lung through a bifurcated endotracheal tube. A 10-min period was allowed for stabilization after each change in experimental condition. Anastomotic Qbr was measured for 5 min during each experiment. In separate animals, similar studies were performed before and 30 min after intravenously administered indomethacin (6 mg/kg body weight). During normoxic conditions when PaO2 was 79 +/- 8 torr (mean +/- SEM), the mean anastomotic Qbr was 5.7 +/- 2.0 ml/min (n = 9). This flow increased to 8.3 +/- 2.5 ml/min (p less than 0.05) during hypoxemic conditions (PaO2, 38 +/- 3). The anastomotic Qbr increased from 5.8 +/- 1 to 9.0 +/- 2 ml/min (p less than 0.005) when PaCO2 was increased from 23 +/- 1 to 47 +/- 2 torr (n = 11). Pretreatment with intravenously administered indomethacin blocked both the hypoxemia-induced (n = 4) and hypercarbia-induced (n = 4) increases in anastomotic Qbr. We conclude that both hypoxemia and hypercarbia increased the anastomotic Qbr through a mechanism involving cyclooxygenase products of arachidonic acid.

Anesthesia, General↗
PubMed1985

Nifedipine dilates the pulmonary vasculature without producing symptomatic systemic hypotension in upright resting and exercising patients with pulmonary hypertension secondary to chronic obstructive pulmonary disease.

Vasodilator therapy may lower pulmonary vascular resistance in patients with chronic air-flow limitation. However, the effects of these agents on left ventricular afterload, cardiac output, and bronchial smooth muscle could lower the calculated pulmonary vascular resistance without specifically affecting pulmonary vascular tone. In addition, systemic hypotension in the upright position and worsening ventilation/perfusion heterogeneity could limit their use. We determined the pulmonary driving pressure (pulmonary arterial-pulmonary arterial wedge pressure) to flow relationship, as well as the transmural pulmonary arterial pressure in 9 patients with severe chronic air-flow limitation with pulmonary hypertension while in a clinically stable condition. Measurements were made at rest and during 3 stages of progressively increasing upright exercise on a bicycle before and after a single 20-mg dose of nifedipine. Nifedipine displaced both the driving pressure to flow and the pulmonary arterial transmural pressure to flow relationships towards higher flows in every subject, suggesting an active vasodilation. In the upright position, PaO2 did not change, and the systemic arterial pressure was only mildly reduced. In patients with pulmonary hypertension from chronic air-flow limitation, acute administration of nifedipine to upright patients causes pulmonary, as well as systemic vasodilation without causing symptomatic hypotension or reducing arterial oxygenation.

Adult↗
PubMed1985

Efficiency of air compressor-driven nebulizers.

Five different volumes of test solutions (1 to 3 ml) containing 15 mg of metaproterenol were placed in each of five different nebulizers. The time to complete nebulization and the amount of drug delivered varied considerably, depending upon the initial volume of solution placed in the nebulizer. Small volumes (1 ml) were almost totally retained in the nebulizer, whereas larger volumes (3 ml) took an unacceptably long time for nebulization. With vigorous agitation, a maximum of 53 to 72 percent of the dose left the nebulizer, but even less (34 to 59 percent) was delivered under simulated clinical conditions. When nebulization was synchronized with breathing, only 0.33 to 0.54 ml of solution (2 to 3.2 mg of metaproterenol) was delivered with 90 deep inhalations. If nebulization was continuous instead of intermittent during the time to take 90 breaths, the majority of the drug was nebulized to the atmosphere.

Aerosols↗
PubMed1985

Effects of accidental chlorine inhalation on pulmonary function.

In an industrial accident, 19 previously healthy workers were briefly exposed to high concentrations of chlorine gas. Pulmonary function tests were done at intervals for about two years but complete follow-up data were available in only 11 subjects. Immediately following the exposure, airway obstruction was detected in 10 of 19 patients; 700 days later this was found in only 3 of 11 patients. Two of these three patients had a history of smoking, however. The mean residual volume was 141% +/- 97 (mean +/- standard error of the mean) on day 1. In subsequent follow-up studies, the residual volume progressively fell in all patients, and 700 days later the mean residual volume was 90% +/- 5. In 5 of the 19 subjects, all pulmonary function test results were within normal limits on day 1. Apparently in some subjects acute exposure to chlorine gas may cause immediate changes in the lung functions, but these changes gradually resolve. Because of the small number of patients in our series, however, the long-term effects of chlorine are less apparent.

Accidents, Occupational↗
PubMed1984

Acute increase in anastomotic bronchial blood flow after pulmonary arterial obstruction.

We examined the acute changes in anastomotic bronchial blood flow (Qbr) serially for the 1st h after pulmonary arterial obstruction and subsequent reperfusion. We isolated and perfused the pulmonary circulation of the otherwise intact left lower lobe (LLL) with autologous blood in the widely opened chest of anesthetized dogs. Qbr was measured from the amount of blood overflowing from the closed pulmonary vascular circuit and the changes in the lobe weight. The right lung and the test lobe (LLL) were ventilated independently. The LLL, which was in zone 2 (mean pulmonary arterial pressure = 14.8 cm H2O, pulmonary venous pressure = 0, alveolar pressure = 5-15 cmH2O), was weighed continuously. The systemic blood pressure, gases, and acid-base status were kept constant. In control dogs without pulmonary arterial obstruction, the Qbr did not change for 2 h. Five minutes after pulmonary arterial obstruction, there was already a marked increase in Qbr, which then continued to increase for 1 h. After reperfusion, Qbr decreased. The increase in Qbr was greater after complete lobar than sublobar pulmonary arterial obstruction. It was unaltered when the downstream pulmonary venous pressure was increased to match the preobstruction pulmonary microvascular pressure. Thus, in zone 2, reduction in downstream pressure was not responsible for the increase in Qbr; neither was the decrease in alveolar PCO2, since ventilating the lobe with 10% CO2 instead of air did not change the Qbr. These findings suggest that there is an acute increase in Qbr after pulmonary arterial obstruction and that is not due to downstream pressure or local PCO2 changes.

Animals↗
PubMed1983

Extra-alveolar vessel contribution to hydrostatic pulmonary edema in in situ dog lungs.

We determined the relative contribution of larger extra-alveolar arteries and veins to hydrostatic edema in in situ dog lungs. Left lower lobe alveolar and vascular pressures were controlled in 24 open-chest, anesthetized, heparinized dogs. Zero pressure was at the lobe base. Normal blood gases were maintained by ventilating the right lung. The left lower lobe was inflated with 5% CO2 and air to an alveolar pressure of 10 or 25 cmH2O and suspended from a strain gauge, which allowed continual weight recording. Vascular pressures were raised to alveolar pressure plus lung height (zone III) before and after pulmonary arterial or venous embolization with 37- to 74-microns polystyrene beads, which isolated the larger extra-alveolar arteries or veins from alveolar vessels. The weight change occurring during the last 3 min of the 5-min hydrostatic stress was taken to represent transvascular fluid flux. At an alveolar pressure of 25 cmH2O (estimated transmural pressure 40 cmH2O), leakage from the larger extra-alveolar arteries and veins accounted for 41 and 32%, respectively, of the total transvascular fluid flux occurring after embolization. At an alveolar pressure of 10 cmH2O (estimated transmural pressure 22 cmH2O), no extra-alveolar vessel leakage occurred. However, when vascular pressures were raised to provide a transmural pressure similar to that present at the higher alveolar pressure, the same contribution from larger extra-alveolar vessels was observed.

Animals↗
PubMed1983

Factorial rating system for comparative efficacy of antiasthmatic medication: a multicentric study report.

Faced with 1-year daily medication diaries from over 300 patients, each documenting the use of from one to five medications a day, we found it was necessary to devise a system which would reduce this data into a form which would allow a meaningful interpretation of changes of medications in a single patient or group of patients. Since the medications were principally steroids, beta agonists, or xanthines, representative agents were chosen as the standard for each class and the other medications were rated against them. A conversion factor was then determined to allow comparison between classes. Each medication taken by a patient could now be expressed as a single number and the sum of all the medications would be the individual's Asthma Medication Index. The AMI allowed (i) evaluation of a single patient over time, (ii) comparison of different patients at any single point or over a period of time, and (iii) evaluation of entire groups of patients over time as was the case in our evaluation of Zaditen. Application of the system allowed the differentiation of two therapeutic agents versus placebo during a 1-year study, revealing excellent correlation with the physician's global assessment of the patient's improvement. With proper modification of the basic drug groups and intergroup factor relationship, the Index can be adapted to any disease state where a change in concomitant medication is an indicator of therapeutic effect.

Administration, Oral↗
PubMed1982

Inhaled atropine sulfate: dose-response characteristics in adult patients with chronic airflow obstruction.

Dose-response characteristics of inhaled atropine sulfate were examined in ten patients with chronic airflow obstruction using spirometric and plethysmographic measurements. Inhaled atropine in doses of 0.005, 0.01, 0.25, and 0.05 mg2kg of body weight and placebo were delivered by means of a precision metering device. All pulmonary function tests (FEV1, V50, and SGaw) improved progressively with increasing dose. There was a high degree of linear correlation between the peak response of each test and the logarithm of dose (r greater than or equal to 0.98). The highest dose studied (0.05 mg/kg) was found to have marginal benefit over 0.025 mg/kg, and had the highest incidence of adverse reactions. Duration of effect was dependent on dose. These results suggest that for adult patients with chronic airflow obstruction, 0.025 mg/kg delivered by a dosimeter approximates the optimally effective dose of inhaled atropine sulfate that can be given without unacceptable side effects.

Aerosols↗
PubMed1982

Venous air embolism.

Venous air embolism causes injury primarily by obstruction of blood flow from the right side of the heart to the left. This is due to mechanical obstruction of the right ventricular pulmonary outflow tract and pulmonary vasculature and to poorly understood pulmonary vasoconstrictive mechanisms. Venous air embolism can result in considerable hypoxemia from ventilation-perfusion maldistribution and shunt. With large emboli, systemic hypotension, myocardial ischemia, and arrhythmias can occur and result in death. One should be familiar with the clinical setting where embolism occurs, as prevention is the best treatment. When air embolism is suspected, placement of the patient in the left lateral decubitus position, initiating closed chest massage or, if possible, aspiration of air through a right atrial or Swan-Ganz catheter are all acceptable forms of treatment. The patient should also be given 100% oxygen.

Animals↗
PubMed1981

Tuberculosis in association with pregnancy.

A review was made of the records of 27 patients admitted to National Jewish Hospital who developed or experienced a reactivation of pulmonary tuberculosis during pregnancy or the first 12 month post partum. Sixteen patients had drug-resistant disease, and 11 had drug-susceptible disease. The drug-resistant group had more extensive radiographic abnormalities(p less than 0.01), longer sputum conversion times (p less than 0.05), and a higher incidence of pulmonary complications and death (p = 0.05). Patients with tuberculosis associated with pregnancy have the same clinical presentation as nonpregnant patients. Tuberculosis during pregnancy should be treated, and the drugs that appear to be safest for the fetus include isoniazid, para-aminosalicylic acid, ethambutol, and rifampin.

Adolescent↗
PubMed1981

Serum atropine concentrations after inhalation of atropine sulfate.

Six male subjects with chronic bronchitis were given a single aerosol dose of atropine sulfate (0.05 mg/kg). Spirometry and venous blood samples were obtained before and at 0.25, 0.5, 1.0, 1.5, 2.0, and 4.0 h after inhalation of drug. All subjects had a satisfactory bronchodilator response and detectable serum concentrations of atropine within 15 min. Measurable serum concentrations persisted for 4 h with apparent continued slow absorption occurring throughout the entire time interval. The maximal concentrations achieved ranged from 1.3 to 5.8 ng/ml in five subjects. A sixth subject achieved much higher concentrations (as high as 21 ng/ml) and experienced systemic side effects. This latter concentration is comparable to those achieved with doses of 1.5 to 2.0 mg of parenteral atropine. Significant systemic absorption may occur after inhalation of atropine sulfate, although the degree of absorption is variable.

Aerosols↗
PubMed1981

Atropine and terbutaline aerosols in chronic bronchitis: efficacy and sites of action.

To examine the additive properties and the sites of action of inhaled atropine sulfate (0.05 mg/kg of body weight) and terbutaline sulfate (0.005 mg/kg) in patients with chronic airflow obstruction, we tested these aerosols separately and together in a double-blind random sequence. Twelve patients with chronic bronchitis and perennial obstruction of airflow were studied by measuring three indices of efficacy (specific airway conductance [Gaw/VL], the forced expiratory volume in one second [FEV1] and the forced vital capacity [FVC]) and three indices of the site of action within the airway (delta [(Gaw/VL)/FEV1], the difference between the change in forced expiratory flow at 75 percent of vital capacity and the change in forced expiratory flow at 25 percent of vital capacity, and the change in density dependence of maximal airflow at 50 percent of vital capacity). Both atropine and the combination of atropine and terbutaline improved all indices of efficacy significantly more than did terbutaline. With individual exceptions, the addition of terbutaline to atropine improved Gaw/VL but not forced airflow. All measures of site of action suggested an advantage for atropine in relatively proximal airways. These results indicate that combined therapy with beta-adrenergic and anticholinergic bronchodilator drugs is marginally more effective than therapy with atropine alone in these patients and suggest that anticholinergic aerosols dilate larger airways more effectively than the beta-agonists.

Aerosols↗
PubMed1981

Allergy to aminophylline: lack of predictability by skin testing.

Problems with determining hypersensitivity to aminophylline, ethylenediamine, and theophylline with intradermal skin tests and patch tests are reported in three patients. Three patients were tested with intradermal injections of 0.9% sodium chloride, 1% aminophylline, 1% ethylenediamine, and 0.5% theophylline following apparent allergic reactions to aminophylline. Patch testing using hydrophilic ointment base, 1% aminophylline, 1% ethylenediamine, and 0.5% theophylline was also done. All three patients had no reaction to intradermal sodium chloride or theophylline; all patch tests were negative. The first patient reacted to ethylenediamine strongly and to aminophylline more weakly; punch biopsy of the ethylenediamine reaction site showed a direct toxic effect with no allergic component. Punch biopsy of the aminophylline site showed a typical hypersensitivity reaction. Two concentrations (0.5% and 1.0%) of ethylenediamine injection were used to test the second patient, and he reacted to both concentrations but not to any other injections. His positive reactions contained blisters rather than the typical wheal-and-flare reaction of hypersensitivity. The third patient had similar responses including reactions to 0.5% and 0.1% ethylenediamine (he was not tested with 1% ethylenediamine). Skin testing may be of value in predicting aminophylline or ethylenediamine allergy, but the nonspecific toxic effect of ethylenediamine makes interpretation difficult.

Aged↗
PubMed1980

Lung inflation can cause pulmonary edema in zone I of in situ dog lungs.

We investigated whether increases in lung water can occur due to lung inflation in zone I when alveolar vessels are collapsed. Static left lower lobe alveolar pressure, pulmonary arterial pressure, and pulmonary venous pressure were controlled in living, anesthetized, open-chested dogs. The lobe was inflated with 6% CO2 in air and suspended from a strain gauge, which allowed continual weight recording. The lung was held in zone I conditions. Arterial and venous pressures were equal at either 1 or 5 cmH2O, relative to the base of the 10- to 14-cm-high lobes. Weight changes were measured for 5 min after 5-cmH2O increments of alveolar pressure from 0 or 5 to 30 cmH2O. Lung weight gain due to edema occurred with inflation to alveolar pressures above 10 cmH2O. Greater lung distension resulted in greater rates of weight gain. Weight loss occurred on deflation. The fluid may have leaked from distended extra-alveolar vessels. This mechanism could explain the increased lung water seen with mechanical ventilation and/or positive end-expiratory pressure breathing.

Animals↗
PubMed1980

The effect of atropine inhalation in "irreversible" chronic bronchitis.

Fifteen patients with chronic bronchitis and airflow obstruction which was not improved by inhalation of isoproterenol (increase in forced expiratory volume in one second [FEV1] less than 15 percent) received an aerosol of atropine sulfate (0.05 mg/kg of body weight), in order to determine their response to an anticholinergic bronchodilator drug. The improvement over initial values for FEV1 at 15 minutes following inhalation of isoproterenol and at 90 minutres following inhalation of atropine averaged 5.9 percent and 19.2 percent, respectively (P less than 0.01). Eleven of 15 patients demonstrated a 15 percent or greater increase in FEV1 following inhalation of atropine, and six subjects demonstrated more than 25 percent improvement. The maximum effect of atropine was observed at or later than 90 minutes following inhalation in nine of 11 patients who were responsive to atropine. Minimal systemic toxic effects resulted from inhalation of atropine, although dryness of the mouth was frequent. In patients with chronic bronchitis, airflow obstruction resistant to isoproterenol may respond to inhalation of an aerosol of atropine sulfate.

Aged↗
PubMed1980

Pulmonary effects of topical timolol.

Timolol, a beta-adrenergic blocking agent, recently became available for the treatment of glaucoma. We report the occurrence of acute bronchospasm in a previously asymptomatic asthmatic patient following topical use of timolol. Therapy with the drug was discontinued, and four weeks later the patient was challenged with two drops of 0.5% timolol. A 25% decrease in forced expiratory volume at one second (FEV1) was demonstrated at one hour. The fall in FEV1 was even greater (47%) when the patient was rechallenged with four drops. We emphasize the need to avoid topical beta-adrenergic blocking agents in asthmatic patients.

Administration, Topical↗