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Biomedical subjects

S Lakshminarayan

Publications and source records attributed to S Lakshminarayan.

At least 37 records · Page 2Linked to original sources
PubMed1992

Influence of lung volume and alveolar pressure on reverse pulmonary venous blood flow.

We have reported that left atrial blood refluxes through the pulmonary veins to gas-exchanging tissue after pulmonary artery ligation. This reverse pulmonary venous flow (Qrpv) was observed only when lung volume was changed by ventilation. This was believed to drive Qrpv by alternately distending and compressing the alveolar and extra-alveolar vessels. Because lung and pulmonary vascular compliances change with lung volume, we studied the effect of positive end-expiratory pressure (PEEP) on the magnitude of Qrpv during constant-volume ventilation. In prone anesthetized goats (n = 8), using the right lung to maintain normal blood gases, we ligated the pulmonary and bronchial arterial inflow to the left lung and ventilated each lung separately. A solution of SF6, an inert gas, was infused into the left atrium. SF6 clearance from the left lung was determined by the Fick principle at 0, 5, 10, and 15 and again at 0 cmH2O PEEP and was used to measure Qrpv. Left atrial pressure remained nearly constant at 20 cmH2O because the increasing levels of PEEP were applied to the left lung only. Qrpv was three- to fourfold greater at 10 and 15 than at 0 cmH2O PEEP. At these higher levels of PEEP, there were greater excursions in alveolar pressure for the same ventilatory volume. We believe that larger excursions in transpulmonary pressure during tidal ventilation at higher levels of PEEP, which compressed alveolar vessels, resulted in the reflux of greater volumes of left atrial blood, through relatively noncompliant extra-alveolar veins into alveolar corner vessels, and more compliant extra-alveolar arteries.

Animals↗
PubMed1991

Comparison of estimates of cardiac output by indicator dilution and freon 22 uptake during gas mixing in dogs.

STUDY OBJECTIVE: The aim was to measure cardiac output while rebreathing tidal volumes, by correction of soluble gas uptake for gaseous mixing. DESIGN: Simultaneous measurements of cardiac output by indocyanin green and freon 22 uptake during rebreathing were made. Mixing for a hypothetical gas of identical gaseous diffusivity to freon 22 was calculated by interpolation between concentrations of two insoluble gases, helium and sulphur hexafluoride. Mixing efficiency was estimated by the number of breaths for helium to become 99% equilibrated with lung gas (n99-He). EXPERIMENTAL MATERIAL: Five anaesthetised dogs rebreathed at intervals with 300 ml of test gas. MEASUREMENTS AND MAIN RESULTS: 63 comparisons of cardiac output using indocyanin green and freon 22 uptake (over breaths 7-13 using the mean mixed volume of distribution), gave a mean (95% confidence interval) underestimation of 0.345 (0.093-0.597) litre.min-1 (14%). Exclusion of 12 points in which n99-He was greater than 15 resulted in a mean underestimation of 0.052(-0.163-0.267) litre.min-1 (2%). Without correction for gaseous mixing, freon 22 uptake for these data overestimated blood flow by a mean of 1.31 litre.min-1 (overestimation = 2.7 over breaths 5-11). Use of the equilibrium volume of distribution resulted in an overestimation of blood flow relative to green dye of 1.2 litre.min-1 (breaths 5-11) and 0.76 litre.min-1 (breaths 7-13). CONCLUSIONS: Estimates of cardiac output by soluble gas uptake are optimal when correction is made for mixing of gas of identical diffusivity. The mean mixed gas volume gives the best correlation with the reference method, implying a selective distribution of blood flow to the better ventilated areas.

Animals↗
PubMed1991

Influence of lung volume and left atrial pressure on reverse pulmonary venous blood flow.

Infarction of the lung is uncommon even when both the pulmonary and the bronchial blood supplies are interrupted. We studied the possibility that a tidal reverse pulmonary venous flow is driven by the alternating distension and compression of alveolar and extra-alveolar vessels with the lung volume changes of breathing and also that a pulsatile reverse flow is caused by left atrial pressure transients. We infused SF6, a relatively insoluble inert gas, into the left atrium of anesthetized goats in which we had interrupted the left pulmonary artery and the bronchial circulation. SF6 was measured in the left lung exhalate as a reflection of the reverse pulmonary venous flow. No SF6 was exhaled when the pulmonary veins were occluded. SF6 was exhaled in increasing amounts as left atrial pressure, tidal volume, and ventilatory rates rose during mechanical ventilation. SF6 was not excreted when we increased left atrial pressure transients by causing mitral insufficiency in the absence of lung volume changes (continuous flow ventilation). Markers injected into the left atrial blood reached the alveolar capillaries. We conclude that reverse pulmonary venous flow is driven by tidal ventilation but not by left atrial pressure transients. It reaches the alveoli and could nourish the alveolar tissues when there is no inflow of arterial blood.

Animals↗
PubMed1990

The drainage routes of the bronchial blood flow in anesthetized dogs.

It is generally accepted that the bronchial blood flow from extrapulmonary airways drains to the systemic veins through the bronchial veins, while that from the intrapulmonary airways drains into the pulmonary vasculature and eventually the left heart. This concept has not been confirmed by physiologic studies in live animals. We measured the routes taken by radionuclide-labeled Diethylenetriamine pentaacetate (DTPA) deposited in the extrapulmonary and the intrapulmonary airways in dogs. In living, anesthetized open chest animals, the pulmonary circulation of the left lower lobe was isolated and perfused with autologous heparinized blood. 99mTc DTPA was deposited on the mucosa of the extrapulmonary left mainstem bronchus just beyond the main carina (extrapulmonary deposition) and 111In DTPA on that of an intrapulmonary left lower lobe segmental bronchus (intrapulmonary deposition). Sequential blood samples from the right heart and from the isolated left lower lobe pulmonary circuit were counted for radioactivity, corrected for the volume in which they were distributed and for the bronchial blood that flowed into the isolated left lower lobe circuit, and expressed as the ratio of systemic to pulmonary drainage from each deposition site. The extrapulmonary tracer drained mostly to the systemic veins (84% of total) but also into the pulmonary circulation (16% of total). The intrapulmonary tracer drained mostly into the pulmonary circulation (70% of total) but also into the right heart (30% of total). Since tracers from both deposition sites drained to both circulations, the bronchial vasculature is continuous between the systemic (right heart) and the pulmonary circulation. Thus, it may provide a pathway for blood flow between the right and left heart.

Anesthesia↗
PubMed1990

The effect of bronchial venous pressure on pulmonary edema in the dog.

We examined the effect of elevating systemic venous pressure on the rate of edema formation in the left lower lobes (LLL) of anesthetized, open-chested dogs. The pulmonary circulation of the LLL was isolated using cannulae in the artery and vein which were attached to blood-filled reservoirs. The LLL was distended to an alveolar pressure of 25 cm H2O with 5% CO2 and air, and suspended from a strain gauge which allowed continuous weight recording. The pulmonary vascular pressures were raised so all of the LLL was in zone III. The rate of weight change occurring over the last 4 minutes of a 6 minute period of this pulmonary vascular pressure rise was taken to represent the control transvascular fluid flux. The rate of weight gain of the LLL was then determined with the same pulmonary vascular pressure elevation only when downstream bronchial venous pressure alone, downstream lymphatic pressure alone, or when both downstream lymphatic and bronchial venous pressures were elevated. The transvascular fluid flux was increased when downstream bronchial venous pressure was elevated. When only downstream lymphatic pressure was elevated there was no augmentation of transvascular fluid flux. These findings suggest that when a lung is already subjected to raised pulmonary vascular pressure sufficient to cause edema, acute elevation of bronchial systemic venous pressure augments the net rate of outward fluid flux, while downstream lymphatic pressure elevation does not.

Animals↗
PubMed1990

Vagal cooling and positive end-expiratory pressure reduce systemic to pulmonary bronchial blood flow in dogs.

Positive end-expiratory pressure (PEEP) reduces systemic to pulmonary bronchial blood flow [Qbr(s-p)] presumably because it increases bronchial vascular resistance. Since PEEP increases lung volume and thus could stimulate pulmonary stretch receptors, we investigated the hypothesis that the PEEP-related decrease in bronchial blood flow was due to a reflex mediated by the vagus. In open-chest dogs the left lower lobe (LLL) was isolated, independently ventilated, perfused in situ with a closed pulmonary vascular circuit and weighed continuously. Qbr(s-p) was measured as LLL vascular circuit overflow and changes in LLL weight. When LLL PEEP was increased from 5 to 15 cm H2O in a group of 11 dogs Qbr(s-p) was reduced by half from 60.8 +/- 10.5 to 31.6 +/- 6.1 ml/min/100 g dry lobe weight. In another group of 7 dogs Qbr(s-p) was 46.5 +/- 6.9 with PEEP = 5 cm H2O; it decreased to 28.3 +/- 6.8 with bilateral cervical vagal cooling (0-1.5 degrees C) and did not decrease further after increasing PEEP to 15 cm H2O. We conclude that the effect of resting vagal tone is to increase Qbr(s-p) and that the effect of PEEP on Qbr(s-p) may be mediated at least partially by vagal influences.

Animals↗
PubMed1990

The pulmonary sequelae associated with accidental inhalation of chlorine gas.

Twenty previously healthy individuals were accidentally exposed to high concentrations of chlorine gas in 1975. Pulmonary function tests were performed on these individuals on several occasions over the next 12 years. On average, each subject was followed up for 8.5 years and 13 of the 20 exposed persons were tested 12 years following the exposure. Pulmonary function tests obtained one day following the accident were most notable for the high prevalence of airflow obstruction and air trapping. Over the ensuing years, the airflow obstruction persisted; however, the high prevalence of air trapping resolved. Of note, the prevalence of a low residual volume consistently increased during the follow-up period (p less than 0.001) and at year 12, 67 percent of those tested had residual volumes below 80 percent of their predicted value. We also found that five of 13 subjects tested at year 12 had an increase in airway reactivity (greater than 15 percent decline in FEV1) to inhaled methacholine. Those individuals with reactive airways were older (p = 0.004) and had more marked airflow obstruction (p = 0.03) and air trapping (p = 0.03) immediately following the exposure. These data suggest that exposure to high concentrations of chlorine gas may result in long-term pulmonary complications that are characterized by a reduced residual volume. Unfortunately, these data preclude us from determining whether the chlorine exposure led to the development of airway reactivity or the presence of reactive airways accounted for the air trapping that was observed following the exposure to chlorine gas.

Accidents, Occupational↗
PubMed1990

The effect of diet or exercise on plasma norepinephrine kinetics in moderately obese young men.

An increase in sympathetic nervous system (SNS) activity in the obese has been described by some but not all investigators. It is possible that an increase in SNS tone may play a role in the predisposition to atherosclerotic cardiovascular disease noted in the obese. The effect of dietary weight loss or exercise training on resting SNS activity in moderately obese subjects has not been extensively studied and the results of previous studies are conflicting. Therefore, we prospectively evaluated resting SNS activity in healthy moderately obese subjects randomized to either a three month dietary weight loss (n = 13) or endurance exercise training (n = 18). All subjects were weight stabilized on a constant composition diet for 10 days prior to study both before and after the interventions. Although both groups lost weight, weight loss was greater in the diet group (-13.6 +/- 6.7 vs -2.3 +/- 3.4 kg, P less than 0.001). The composition of weight loss was also different with 32 percent of total weight loss as fat free mass (FFM) in the dieters compared to no significant change in FFM in the exercisers. The caloric requirement for weight stabilization declined after the diet but increased following exercise training (-247 vs + 202 kcal/day, P less than 0.001). No significant changes in blood pressure occurred in either group, and neither group had a significant change in resting plasma norepinephrine concentration. Plasma epinephrine concentrations were also unchanged. However, SNS activity as reflected by arterialized plasma NE kinetics revealed that NE appearance rate declined by 17 percent after dietary weight loss (P less than 0.01), but was not significantly changed after exercise training. These results suggest that dietary weight loss is more effective than exercise training in reducing overall resting SNS activity in normotensive subjects. Since exercise training is known to reduce the SNS response to a given submaximal workload, a combination of diet plus exercise might be the most effective way to reduce overall SNS activity and its possible role in the premature atherosclerosis associated with obesity.

Adolescent↗
PubMed1990

Reflux pulmonary vein flow prevents pulmonary infarction after pulmonary artery obstruction.

Küttner showed in 1874 that simultaneous ligation of the pulmonary veins increased the frequency and severity of lung infarctions after pulmonary artery obstruction. The authors studied the possibility that a tidal pulmonary venous blood flow reflux from the left atrium could nourish the alveolar tissue. This could be driven by left atrial pressure transients and alternate expansion and compression of alveolar and extra alveolar vessels due to tidal lung volume changes. 5 anesthetized, closed chest goats were studied in the prone position after left pulmonary artery ligation and the obstruction of all bronchial blood flow to the left lung, checked by systemic microsphere injection. The inert, insoluble gas SF6 was infused into the left atrium and the exhaled gas from left and right lungs was collected separately. SF6 was found in the gas exhaled from the left lung, showing that left atrial blood had reached the alveolar tissues. The effective reflux blood flow was increased from control levels (no ventilation, normal left atrial pulses) by tidal volume changes, and by increased left atrial pressure transients (balloon induced mitral insufficiency). This venous reflux flow could explain why alveolar tissues do not suffer more severe injury when the pulmonary artery is obstructed.

Animals↗
PubMed1989

Pulmonary artery infusion of prostacyclin increases lobar bronchial blood flow.

Intrapulmonary systemic to pulmonary bronchial blood flow [Qbr (s-p)] decreases with administration of cyclooxygenase inhibitors. This effect may be due to a decrease in the production of vasodilating prostaglandins and reflect either a decrease in the total intrapulmonary bronchial blood flow (Qbr), or a redistribution of the intrapulmonary systemic venous return. In nine open chested dogs the left lower lobe (LLL) was isolated and perfused in situ. Blood flow to the extrapulmonary airways (Qep), and Qbr were measured by the reference flow technique. Qbr (s-p) was measured as the overflow from the closed LLL perfusion circuit. After ibuprofen, PG-I2 was infused into the LLL PA and the Qbr (s-p) was continuously monitored. Qbr, and Qep were measured before and after ibuprofen, and during and after the PG-I2 infusion. The upstream pressure for Qbr (s-p) was estimated with and without PG-I2 infusion. After ibuprofen the Qep, Qbr, and Qbr (s-p) fell to 45, 22, and 17%, respectively, of the pre-ibuprofen values (P less than 0.05). PG-I2 increased the Qbr (s-p) and Qbr (P less than 0.05), while Qep was unchanged. During all experimental conditions the simultaneous measurements of Qbr and Qbr (s-p) were not different from each other (P less than 0.001). The upstream pressure for Qbr (s-p) increased from 30 to 50 cm H2O (P less than 0.05). Intralobar bronchial blood flow is drained almost entirely through the pulmonary circulation, and PG-I2 in the LLL pulmonary circulation increases systemic blood flow to the LLL, probably acting at the level of a systemic arteriole.

Animals↗
PubMed1987

Comparison of inhaled albuterol powder and aerosol in asthma.

In this multicenter, randomized, double-blind study comparing the efficacy and safety of aerosolized albuterol with the dry powder formulation, 231 patients with chronic reversible obstructive airway disease were randomly allocated to receive either placebo albuterol aerosol followed immediately by active albuterol powder (200 micrograms) or active albuterol aerosol (two puffs, 180 micrograms) followed immediately by placebo lactose powder four times a day for a period of 12 weeks. No statistically significant differences were found between the powder and aerosol formulations with respect to pulmonary function, length of time mean FEV1 remained greater than or equal to 15% above baseline, physicians' assessments of patients' clinical response, or patients' subjective symptom scores. There were also no significant differences between treatment groups in cardiovascular effects, laboratory values, or adverse events. Among patients who expressed a preference for one of the delivery systems, half preferred using the powder. Results of this study demonstrate that 200 micrograms of albuterol powder is as safe and effective as 180 micrograms of albuterol aerosol.

Administration, Inhalation↗
PubMed1987

Acute increases in anastomotic bronchial systemic to pulmonary blood flow due to generalized lung injury.

Since pulmonary blood flow to regions involved in adult respiratory disease syndrome (ARDS) is reduced by hypoxic vasoconstriction, compression by cuffs of edema, and local thromboses, we postulated that the bronchial circulation must enlarge to provide for the inflammatory response. We measured anastomotic bronchial systemic to pulmonary blood flow [QBr(s-p)] serially in a lung lobe in 31 open-chest dogs following a generalized lobar injury simulating ARDS. The pulmonary circulation of the weighed left lower lobe (LLL) was isolated and perfused (zone 2) with autologous blood in anesthetized dogs. QBr(s-p) was measured from the amount of blood which overflowed from this closed vascular circuit corrected by any changes in the lobe weight. The LLL was ventilated with 5% CO2 in air. The systemic blood pressure (volume infusion), gases, and acid-base status (right lung ventilation) were kept constant. We injured the LLL via the airway by instilling either 0.1 N HCl or a mixture of glucose and glucose oxidase or via the pulmonary vessels by injecting either alpha-naphthylthiourea or oleic acid into the LLL pulmonary artery. In both types of injury, there was a prompt rise in QBr(s-p) (mean rise = 247% compared with control), which was sustained for the 2 h of observation. The cause of this increase in flow was studied. Control instillation of normal saline into the airways or into the pulmonary vessels did not change QBr(s-p) nor did a similar increase in lobar fluid (weight) due to hydrostatic edema. Neither cardiac output nor systemic blood pressure increased.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Upstream pressure for systemic to pulmonary flow from bronchial circulation in dogs.

Systemic to pulmonary flow from bronchial circulation, important in perfusing potentially ischemic regions distal to pulmonary vascular obstructions, depends on driving pressure between an upstream site in intrathoracic systemic arterial network and pulmonary vascular bed. The reported increase of pulmonary infarctions in heart failure may be due to a reduction of this driving pressure. We measured upstream element for driving pressure for systemic to pulmonary flow from bronchial circulation by raising pulmonary venous pressure (Ppv) until the systemic to pulmonary flow from bronchial circulation ceased. We assumed that this was the same as upstream pressure when there was flow. Systemic to pulmonary flow from bronchial circulation was measured in left lower lobes (LLL) of 21 anesthetized open-chest dogs from volume of blood that overflowed from pump-perfused (90-110 ml/min) pulmonary vascular circuit of LLL and was corrected by any changes of LLL fluid volume (wt). Systemic to pulmonary flow from bronchial circulation upstream pressure was linearly related to systemic arterial pressure (slope = 0.24, R = 0.845). Increasing Ppv caused a progressive reduction of systemic to pulmonary flow from bronchial circulation, which stopped when Ppv was 44 +/- 6 cmH2O and pulmonary arterial pressure was 46 +/- 7 cmH2O. A further increase in Ppv reversed systemic to pulmonary flow from bronchial circulation with blood flowing back into the dog. When net systemic to pulmonary flow from bronchial circulation by the overflow and weight change technique was zero a small bidirectional flow (3.7 +/- 2.9 ml.min-1 X 100 g dry lobe wt-1) was detected by dispersion of tagged red blood cells that had been injected.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Bronchial circulation and cyclooxygenase products in acute lung injury.

The role of cyclooxygenase products in the response of the bronchial circulation to acute lung injury was examined in 30 dogs. By use of an open-chest preparation the left lower lobe (LLL) pulmonary circulation was isolated, continuously weighed, and perfused in situ. The anastomotic bronchial blood flow [Qbr(s-p)] was measured as the rate of increase in the volume of the LLL-perfusion circuit. Four groups of dogs were studied. In group A, six dogs received cyclooxygenase inhibition (COI) with either indomethacin (2 mg/kg) or ibuprofen (10 mg/kg). In group B (n = 10) lung injury caused by airway instillation of glucose (15 mg) with glucose oxidase (500 micrograms/kg) (G/GO) or LLL pulmonary arterial infusion of alpha-napthyl thiourea (ANTU, 2 mg/kg). Group C (n = 10) received COI, and 30 min later injury was induced as above with either ANTU or G/GO. Group D (n = 4) received COI immediately after anesthesia; then, 30 min after completion of the surgical preparation, injury was induced with ANTU or G/GO. After COI, Qbr(s-p) decreased to 35 +/- 9% of the basal values (P less than 0.05). After administration of ANTU or G/GO, Qbr(s-p) increased irrespective of whether COI was present. 6-Ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane B2 (TxB2) were measured by radioimmunoassay in the LLL pulmonary artery and systemic venous blood, demonstrating an increase in 6-keto-PGF1 alpha due to surgical preparation and confirming complete COI in those animals receiving COI immediately after anesthesia. These findings demonstrate that 1) the bronchial circulation is capable of a sevenfold increase in flow in response to acute lung injury.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Ipratropium bromide in chronic bronchitis/emphysema. A review of the literature.

Many studies have evaluated the efficacy of ipratropium bromide in chronic obstructive pulmonary disease (COPD). Single-agent studies have shown ipratropium to be both safe and effective in COPD. Several studies have compared ipratropium with sympathomimetic agents or methylxanthines in patients with chronic bronchitis or emphysema; all of these studies have shown at least an equal, and in most instances a superior, bronchodilator action with ipratropium in terms of duration of action as well as peak bronchodilator effect in patients with COPD. In some patients with COPD, beta agonists, theophylline, or corticosteroids may have some additive, but not synergistic, bronchodilator effects when given with ipratropium.

Atropine Derivatives↗
PubMed1986

Factors affecting bronchial blood flow through bronchopulmonary anastomoses in dogs.

Most of the bronchial arterial blood flow (Qbr) drains through bronchopulmonary anastomoses into the pulmonary circulation, and the remainder goes into the systemic venous system via the bronchial veins. We studied the relationship between blood flow through bronchopulmonary anastomoses, and alveolar pressure and pulmonary vascular pressures as well as hydrostatic pressure in the bronchial veins in 10 adult dogs. The pulmonary artery and vein of the experimental left lower lobes (LLL) of open-chested, anesthetized dogs were isolated and connected to reservoirs. That part of the Qbr that flowed through bronchopulmonary anastomoses into the reservoirs was continuously measured at constant pulmonary vascular pressures of 0 cm H2O relative to the lung base. Any bronchial blood volume that retained within the LLL was estimated from changes in lobe weight. The lobe was distended with 5% CO2 and air, at alveolar pressures of 5, 10, or 20 cm H2O in a random sequence. Because bronchial veins drain into the azygos vein, the bronchial venous pressure was elevated by snaring the azygos vein. The mean anastomotic Qbr was 4.4 +/- 1.1 (mean +/- SEM) ml/min and it decreased by 23 and 39% when alveolar pressure was raised from 5 cm H2O to 10 and 20 cm H2O respectively (p less than 0.05). Approximately 75% of the total anastomotic Qbr was collected from the pulmonary venous reservoir at all alveolar pressures. When both pulmonary artery and venous pressures were increased higher than the alveolar pressure (zone III), azygos snaring increased the anastomotic Qbr by 13 and 31% at alveolar pressures of 10 and 20 cm H2O, respectively (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗