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Biomedical subjects

S M Scharf

Publications and source records attributed to S M Scharf.

At least 19 recordsLinked to original sources
PubMed1995

Primary pulmonary hypertension and the human immunodeficiency virus. Report of two cases and a review of the literature.

We report two cases of human immunodeficiency virus (HIV) seropositivity and pulmonary hypertension seen at our institution and present a comprehensive literature review and available histopathologic findings of the association between HIV seropositivity and pulmonary hypertension. Studies and reviews pertaining to HIV seropositivity and pulmonary hypertension were identified through a MEDLINE search and reference citations. All studies and series found in the MEDLINE search were reviewed and are discussed in this article. Where data were available, comparisons and analyses were made between groups of reported cases of HIV seropositivity and pulmonary hypertension with regard to the following parameters: sex distribution, mode of acquiring HIV infection, presence or absence of the acquired immunodeficiency syndrome, CD4 cell counts, PO2 or oxygen saturation by pulse oximetry, concurrent lower respiratory tract infection, and histopathologic features. We conclude that there is strong evidence for pulmonary hypertension associated with HIV infection that is histologically indistinguishable from primary pulmonary hypertension. Consequently, HIV-seropositive patients with unexplained dyspnea should be evaluated for primary pulmonary hypertension. Prospective studies in HIV-positive patients are indicated.

Adult↗
PubMed1995

Effect of CPAP on pericardial pressure and respiratory system mechanics in pigs.

It has been postulated that increased cardiac surface pressure with continuous positive airway pressure (CPAP) results in decreased left-ventricular (LV) transmural pressure. We tested this hypothesis in seven sedated, unanesthetized, and previously instrumented pigs. We measured pericardial (Pperi), LV, airway (P(aw)), and esophageal (Pes) pressures at CPAP values of 0, 4, 8, and 12 cm H2O before and after blood-volume expansion. With normovolemia, CPAP resulted in an increase in Pperi (from -2.0 +/- 7.6 mm Hg at CPAP 0 to 2.3 +/- 5.6 mmHg at CPAP 12, p < 0.05). Baseline end-diastolic Pperi rose with volume expansion from -2.0 +/- 7.6 mm Hg to 5.4 +/- 5.4 mm Hg, p < 0.05. With hypervolemia, CPAP was associated with a decrease in Pperi (from 5.42 +/- 5.4 mm Hg to 2.3 +/- 5.6 mm Hg, p < 0.05). By contrast, Pes rose equally under both conditions with CPAP. LV transmural end-diastolic pressure (TMEDP) fell significantly under normovolemic conditions (from 16.5 +/- 7.4 mm Hg at CPAP 0 to 13.6 +/- 9.0 mm Hg at CPAP 12). The changes in FRC (pneumotachometry) with CPAP were similar under both conditions. We conclude that the CPAP-induced decrease in LV volume under hypervolemic conditions cannot be explained by an increase in cardiac surface pressure. We present a model to explain the decrease in cardiac surface pressure with CPAP.

Animals↗
PubMed1995

Effect of chronic resistive loading on ventilatory control in a rat model.

Acute resistive loading of the airway has been shown to activate the endogenous opioid system, with subsequent depression of ventilation. The present investigation was designed to assess the effect of chronic airway loading on ventilation and CO2 sensitivity, and to determine whether the endogenous opioid system contributes to long-term modulation of ventilatory control in this setting. A flow-resistive ventilatory load was imposed in 2-mo-old rats by surgical implantation of a circumferential tracheal band that approximately tripled tracheal resistance. Respiration and CO2 sensitivity were serially and noninvasively assessed by barometric plethysmography over a period of 21 wk. Ventilatory output was assessed as minute inspiratory effort, which was defined as the product of plethysmograph signal amplitude, inspiratory time, and respiratory rate (RR). CO2 sensitivity was calculated as the percent change in minute inspiratory effort from room air to CO2 exposure. The effect of naloxone administration on these parameters was also determine. Arterial blood gases demonstrated hypercapnia with maintenance of normoxia in loaded rats; these findings persisted for the duration of the study. Two days after surgery, rats with tracheal obstruction demonstrated a lower RR than controls during room air breathing and during CO2 stimulation. CO2 sensitivity was significantly depressed in obstructed animals at this time. Escape from suppression of RR and CO2 sensitivity was evident by 14 to 21 d after obstruction; however, suppression of these parameters reappeared and was maintained from 56 to 147 d after obstruction. Naloxone augmented minute inspiratory effort during CO2 stimulation at 2 d after obstruction but not thereafter; naloxone had no effect in control rats. These data indicate that chronic airway loading suppresses RR and CO2 sensitivity in a triphasic manner. The early suppression is partially reversible by naloxone; late-appearing suppression is unaffected by naloxone and is presumably mediated by mechanisms that do not involve endogenous opioids.

Airway Obstruction↗
PubMed1995

Intravenous magnesium sulfate as an adjunct in the treatment of acute asthma.

STUDY OBJECTIVE: This study was conducted to determine whether intravenous magnesium sulfate (MgSO4), when used as part of a standardized treatment protocol, can improve pulmonary function and decrease admission rate in patients presenting to the emergency department with exacerbations of asthma. DESIGN: In this randomized double-blind placebo-controlled study, patients with acute asthma were treated with inhaled beta-agonists at regular intervals and intravenous (IV) steroids. At 30 min after entry, patients received either 2 g IV MgSO4 or IV placebo. Patients were monitored for up to 4 h with regular measurements of pulmonary function. Patients who were discharged from the emergency department were contacted at 1 day and 7 days for follow-up. SETTING: Emergency departments of a university-affiliated, voluntary hospital and municipal hospital. PARTICIPANTS: Asthmatics aged 18 to 65 years during acute exacerbation with FEV1 less than 75% predicted both before and after a single albuterol treatment. INTERVENTIONS: Patients were given 2 g of MgSO4 or placebo as an adjunct to standardized emergency department procedure for acute asthma. MEASUREMENTS AND RESULTS: One hundred thirty-five patients were studied. Hospital admission rates were 35.3% for placebo-treated group and 25.4% for the magnesium-treated group (p = 0.21). FEV1 measured at 120 min was 56% predicted for the placebo-treated group and 55% predicted for the magnesium-treated group. (p = 0.92) For subgroup analysis, patients were divided into "severe" (baseline FEV1 < 25% predicted on presentation) or "moderate" (baseline FEV1, 25 to 75% predicted on presentation). For the severe group, admission rates were 78.6% (11/14) for the placebo-treated group and 33.3% (7/21) for the magnesium-treated group (p = 0.009). For the moderate patients, admission rates were 22.4% (11/49) for the placebo-treated group and 22.2% (10/25) for the magnesium-treated group (p = 0.98). There was no significant improvement in FEV1 in the moderate group for magnesium-treated patients. However, in the severe group, there was a significant improvement in FEV1 at 120 min and 240 min (p = 0.014 and 0.026, respectively). CONCLUSION: Intravenous MgSO4 decreased admission rate and improved FEV1 in patients with acute severe asthma but did not cause significant improvement in patients with moderate asthma.

Acute Disease↗
PubMed1994

Mechanisms of myocardial depression after bolus injection of sodium bicarbonate.

PURPOSE: The classic model for the effects of NaHCO3 on myocardial function predicts transient myocardial depression after an intravenous bolus of sodium bicarbonate in association with myocardial acidosis. METHODS: Five anesthetized, paralyzed, and ventilated dogs underwent midline sternotomy. Myocardial global function was assessed by cardiac output, left ventricular (LV) dp/dt, LV end-systolic, and LV end-diastolic pressures. Regional myocardial function assessed by measuring the LV regional end-systolic, LV end-diastolic lengths, and LAD coronary blood flow. Coronary sinus, intramyocardial and arterial pH were measured as was free serum Ca++. Animals were made acidemia by infusion of 0.3 N HCl and then given a bolus of sodium bicarbonate. This produced transient depression followed by recovery of myocardial function. RESULTS: During the depression phase there was no significant decrease in interstitial pH or an increase in A-VCO2 difference as predicted by the current model. However, there was a significant decrease in the serum free Ca++ that coincided with myocardial depression. CONCLUSION: We could not confirm the predictions of the classic model and hypothesize that myocardial depression may be caused by decreased availability of free Ca++ of decreased Ca++ flux rather than intracellular acidosis.

Acidosis↗
PubMed1994

Hemodynamic effects following injection of venom from the scorpion Leiurus quinquestriatus.

PURPOSE: The present study tested the hypothesis that scorpion sting induces left ventricular (LV) hypokinesia and myocardial ischemia shortly after injection due to reduction of coronary blood flow (CBF) and increased oxygen demand. METHODS: In 5 mechanically ventilated, open-chest dogs, we measured LV function following i.v. injection of venom (0.05 mg/kg) obtained from the scorpion Leiurus quinquestriatus. Hemodynamic responses to the venom were followed up for 90 minutes. RESULTS: The venom induced significant combined respiratory and metabolic acidosis (arterial pH progressed from 7.35 +/- 0.03 at baseline to 7.10 +/- 0.06 at 90 minutes). There were large increases in blood pressure, LV end systolic pressure, stroke work, and velocity of contraction. Twenty minutes following venom injection, cardiac output (CO) increased by 37% but then declined to 36% below baseline by 90 minutes (P < .05). CBF increased significantly in proportion to increased perfusion pressure; hence, there was no change in coronary vascular resistance. There was no evidence of myocardial ischemia or LV dysfunction because there was no change in myocardial pH, percentage fiber shortening, or LV end-diastolic pressure. Despite the fact that some variables returned to baseline at 90 minutes, they did not reach steady state; thus, the preparation would have continued to deteriorate. CONCLUSIONS: Myocardial ischemia does not occur in this dog model immediately following administration of scorpion venom. There are significant peripheral circulatory effects of the venom, which account for many of the hemodynamic changes.

Animals↗
PubMed1992

Ventilatory and P0.1 response to hypercapnia in quadriplegia.

Unlike individuals with comparable degrees of respiratory muscle weakness from other causes, quadriplegic patients have a blunted ventilatory and P0.1 response to hypercapnia. This suggests that the diminished response in quadriplegia is due, in part, to an alteration in respiratory drive. We measured the hypercapnic response in 9 subjects with chronic quadriplegia (Q) and 8 normal controls (N). Ventilatory muscle strength, maximum voluntary ventilation (MVV), and lung volumes were measured in all subjects. The ventilatory response (HCVR) in Q was significantly less than in N (0.73 +/- 0.37 vs 2.95 +/- 0.4 L.min-1.mmHg-1; P less than 0.001), even when normalized for indices of respiratory muscle performance (e.g., vital capacity, MVV). There was no significant change in the HCVR in Q after the administration of naloxone. We also serially studied 2 subjects with acute quadriplegia, and found that despite progressive improvement in respiratory muscle performance, there was no accompanying increase in the response to hypercapnia. These data suggest that muscle weakness alone cannot explain the blunted hypercapnic response in quadriplegia, and are consistent with the hypothesis that these subjects have a reduced ventilatory drive.

Adult↗
PubMed1992

Effects of inspiratory loading on left ventricular myocardial blood flow and metabolism.

With airways obstruction, mean pleural pressure decreases. It has been postulated that associated increases in left ventricular afterload increase myocardial O2 demand (MvO2) and coronary blood flow (CBF). We tested this hypothesis in 12 anesthetized mixed-breed dogs. Through a median sternotomy, dogs were instrumented for the measurement of mean arterial pressure, cardiac output, and left anterior descending CBF. A catheter placed in the coronary sinus allowed sampling of left ventricular venous blood. MvO2 was calculated as CBF x (arteriovenous content difference), and coronary resistance was calculated as (mean arterial pressure)/CBF. After closure of the thoracotomy, animals were studied before and during inspiratory threshold loading (IL) of -20 to -25 cmH2O while breathing 100% O2 before and after bilateral cervical vagotomy. During IL, heart rate fell [approximately 20 beats/min (NS prevagotomy, P less than 0.05 postvagotomy)], arterial PCO2 increased [45 to 66 Torr prevagotomy, 45 to 50 Torr postvagotomy (P less than 0.01)], and arterial O2 content was unchanged. CBF increased with IL:41% prevagotomy (P less than 0.01), 18% postvagotomy (P less than 0.02). However, with IL, MvO2 did not increase significantly either pre- or postvagotomy. Coronary resistance decreased with IL [30% prevagotomy, 24% postvagotomy (P less than 0.01)]. In eight dogs, PCO2 was increased by increasing dead space while the animals were mechanically ventilated and paralyzed. Although there was little change in CBF, heart rate fell by an amount equal to that with IL. We conclude that 1) IL causes coronary vasodilation not related to changes in MvO2, PCO2, or vagal tone; 2) MvO2 does not increase with IL; and 3) decreased heart rate with IL is related to hypercapnia and/or acidosis.

Airway Obstruction↗
PubMed1992

Oxygen cost of resistive-loaded breathing in quadriplegia.

We hypothesized that, in quadriplegia, chest wall distortion would increase the energy cost of ventilation. To assess this, we measured the oxygen cost of breathing (VO2 resp) and changes in chest wall configuration during inspiratory resistive-loaded breathing tasks in five quadriplegic and five normal subjects. Each subject performed three breathing tasks that spanned a range of work rates (Wtot). Configurational changes of the abdomen and upper, lower, and transverse rib cage were assessed with magnetometers. We found that 1) in both groups, VO2resp increased linearly with Wtot over the range of tasks performed, 2) the mean slope of the regression line of VO2resp vs. Wtot was greater for quadriplegic than for normal subjects (3.7 +/- 0.8 vs. 2.0 +/- 0.7 ml O2/J, P less than 0.01), 3) efficiency of breathing (Wtot/VO2resp) was less for quadriplegic than for normal subjects (1.9 +/- 0.6 vs. 3.5 +/- 1.4%, P less than 0.001), 4) during inhalation, upper and lower rib cages behaved similarly in the two groups, but the quadriplegic subjects had a decrease in transverse rib cage and a much greater increase in abdomen than normal subjects, and 5) functional residual capacity decreased in normal but not in quadriplegic subjects during the breathing tasks. We conclude that the lesser efficiency of breathing in quadriplegia may be related to the elastic work of chest wall distortion, shorter mean operational diaphragm length, and possibly differences between normal and quadriplegic subjects in mechanical advantage of available inspiratory muscles.

Adult↗
PubMed1992

Respiratory phasic effects of inspiratory loading on left ventricular hemodynamics in vagotomized dogs.

Exaggerated inspiratory swings in intrathoracic pressure have been postulated to increase left ventricular (LV) afterload. These predictions are based on measurements of LV afterload by use of esophageal or lateral pleural pressure. Using direct measurements of pericardial pressure, we reexamined respiratory changes in LV afterload. In 11 anesthetized vagotomized dogs, we measured arterial pressure, LV end-systolic (ES) and end-diastolic transmural (TM) pressures, stroke volume (SV), diastolic left anterior descending blood flow (CBF-D), and coronary resistance. Dogs were studied before and while breathing against an inspiratory threshold load of -20 to -25 cmH2O compared with end expiration. Relative to end expiration, SV and LVES TM pressures decreased during inspiration and increased during early expiration, effects exaggerated during inspiratory loading. In all cases, LV afterload (LVES TM pressure) changed in parallel with SV. LV end-diastolic TM pressure did not change. CBF-D paralleled arterial pressure, and there were no changes in coronary resistance. In two dogs, regional LVES segment length paralleled calculated changes in LVES TM pressure. We conclude that 1) LV afterload decreases during early inspiration and increases during early expiration, changes secondary to those in SV; 2) changes in CBF-D are secondary to changes in perfusion pressure during the respiratory cycle; and 3) the use of esophageal or lateral pleural pressure to estimate LV surface pressure overestimates changes in LV TM pressures during respiration.

Animals↗
PubMed1992

Cardiovascular effects of periodic occlusions of the upper airways in dogs.

Hypoxemia and decreased intrathoracic pressure have been postulated as contributing causes of cardiovascular morbidity in obstructive sleep apnea syndrome (OSAS). Because of the difficulty of manipulating experimental conditions in humans, we developed an anesthetized closed-chest dog model, simulating the periodic airway occlusions of OSAS by periodic occlusions of the endotracheal tube (PUO). Using a periodicity of 60 s occluded, followed by 60 s ventilation for five to seven cycles, we measured heart rate (HR), cardiac output (CO), arterial pressure (Pa); left ventricular (LV) end-diastolic and end-systolic transmural pressure; dp/dt of LV pressure; left anterior descending (LAD) coronary blood flow (CBF), and regional myocardial contractility and intramyocardial pH. Four experimental conditions were studied: room air (RA) breathing (PO2 = 40); 100% O2 breathing (O2), and RA and O2 breathing with critical LAD stenosis (CS). Under all conditions PUO produced decreases in CO (10 to 30%) and proportional decreases in Pa. HR decreased, and in all but RA conditions stroke volume was unchanged. During the obstructed phase, indices of LV preload decreased. Indices of LV afterload also decreased except for LAD-perfused myocardium under RACS conditions. This latter was shown to be associated with regional ischemia (decreased regional pH and shortening). Regional ischemia was also demonstrated in two of nine dogs even under O2CS conditions. Among our major conclusions: (1) decreased Pa during PUO is due to decreased CO; (2) LV afterload does not increase during PUO; (3) with limited coronary flow reserve (CS), PUO can lead to myocardial ischemia. This is mostly but not solely due to hypoxia.

Animals↗
PubMed1991

Cardiovascular effects of airways obstruction.

Airways obstruction is usually associated with substantial decreases in inspiratory and mean intrathoracic pressure (ITP). The change in ITP is correlated with the degree of inspiratory fall in arterial pressure, pulsus paradoxus. The factors influencing the degree of pulsus include venous return, afterload effects on the left ventricle (LV), diastolic ventricular interdependence, lung volume, and circulatory reflexes. I have reviewed these factors and attempted to demonstrate that their relative importance changes under different circumstances. I have discussed the importance of measuring transmural pressures to assess ventricular performance, and pointed out some possible pitfalls in the use of esophageal or pleural pressure to estimate LV surface pressure. During normal and loaded inspiration, decreased LV preload, probably related to right ventricle (RV)-LV diastolic interdependence, appears to be the primary mechanism responsible for decreased stroke volume during inspiration. During Mueller maneuvers, and possibly with severe decreases in ITP. LV afterload may be more important. When lung volume increases, as with asthma, venous return from the lower body may be a more important determinant of pulsus paradoxus. Although previous predictions that decreased ITP would lead to increased myocardial O2 consumption were not borne out, coronary blood flow did increase with inspiratory loading. This appears to be due to a nonvagally mediated change in autonomic tone with loaded breathing. This and other reflex-mediated effects deserve more attention in future studies of stressed or abnormal inspiration. As a final point, pericardial tamponade probably leads to pulsus paradoxus by exaggerating normal diastolic right-left interactions.

Blood Pressure↗
PubMed1991

Effect of chronic resistive loading on inspiratory muscles in rats.

The development of animal models of respiratory muscle training would be useful in studying the physiological effects of training. Hence, we studied the effects of chronic resistive loading (CRL) for 5 wk on mass, composition, and mechanics of inspiratory muscles in laboratory rats. CRL was produced by means of a tracheal cannula (loaded animals) and results were compared with sham-operated controls. Acutely, upper airway obstruction led to a doubling of inspiratory pleural pressure excursion and 25% decrease in respiratory rate. We observed no changes in lung pressure-volume curves, nor in the geometry of the respiratory system in loaded compared with control animals. Muscle mass normalized for body mass increased in the diaphragm (DI) and the wet weight-to-dry weight ratio increased in the sternomastoid (SM) in loaded compared with control animals. Loaded animals demonstrated a decrease in ether extractable (fat) content of the DI and SM muscles but not the gastrocnemius. For the DI there was no change in length at which active tension was maximal (Lo), but there was an increase in maximum tension at lengths close to Lo in loaded compared with control rats. Endurance did not change, although twitch tensions remained higher in loaded compared with control rats. We conclude that 1) alteration of inspiratory muscle structure and function occurs in rats with CRL; 2) the DI and SM demonstrate different adaptive responses to CRL; and 3) although maximum tension increases, endurance does not.

Animals↗
PubMed1990

Screening for subclinical sleep-disordered breathing.

We evaluated self-administered questionnaires and short sleep studies in screening for sleep-disordered breathing (SDB) in 40 hypertensive men ages 36-66 unselected for symptoms. Each subject completed a questionnaire including questions on sleep-related symptoms and underwent overnight polysomnography in which we evaluated the apnea-hypopnea index (AHI) and the percentage of time during which arterial O2 saturation was less than 90% (T90). The first 90 min of overnight study was evaluated separately, and 10 subjects with an AHI greater than or equal to 10 also underwent late afternoon nap study. By overnight polysomnography, 48% of the cohort had an AHI greater than or equal to 10, and 35% had a T90 greater than or equal to 10%. Using linear regression, we found no features of the symptom questionnaire that strongly predicted AHI. Only self-reported snoring and baseline arterial Po2 significantly predicted T90. The AHI and T90 were not significantly correlated. Considering an AHI greater than or equal to 10 in the overnight study as "abnormal" and an AHI greater than or equal to 10 on the short study as a "positive" test, the specificity of the AHI in the first 90 min was 100% (21/21), and the sensitivity was 42% (8/19). The sensitivity of the nap study was 60% (6/10). We conclude that in a cohort unselected for symptoms, the ability of self-administered questionnaires to predict SDB was low; short studies were only moderately sensitive for detecting an AHI greater than or equal to 10, and the AHI was not a major determinant of nocturnal desaturation.

Adult↗
PubMed1989

Intrathoracic pressures and left ventricular configuration with respiratory maneuvers.

In 12 dogs, we examined the correspondence between esophageal (Pes) and pericardial pressures over the anterior, lateral, and inferior left ventricular (LV) surfaces. Pleural pressure was decreased by spontaneous inspiration, Mueller maneuver, and phrenic stimulation and increased by intermittent positive pressure ventilation (IPPV) and positive end-expiratory pressure (PEEP). To separate effects due to blood flow, we analyzed beating and nonbeating hearts. In beating hearts, there were no significant differences between changes in Pes and pericardial pressures. In arrested hearts, increasing LV pressure by 8 Torr increased pericardial pressures by only 3.6 Torr. With IPPV and PEEP, increases in Pes and pericardial pressures were equal in live hearts and in low-volume arrested hearts (LV pressure = 4 Torr). In high-volume arrested hearts (LV pressure = 12 Torr), the increase in pericardial pressure over the anterior LV surface was less than Pes, whereas that over the lateral and inferior LV surfaces was the same as Pes. At high LV volume, in arrested hearts pericardial pressures decreased less than Pes during negative pressure maneuvers. In another six dogs, external LV configuration and volume were measured. In beating hearts during spontaneous inspiration, Mueller maneuver, and phrenic stimulation (endotracheal tube open), septal-lateral dimension and LV volume decreased by approximately 3% (P less than 0.05). This was also true for PEEP. In arrested hearts, septal-lateral dimension and LV volume decreased only with PEEP. We conclude that 1) the relationship between Pes and pericardial pressures is complex and depends on LV volume, local pericardial compliance, and the means by which Pes is changed, 2) changes in measured pericardial pressures did not completely explain changes in LV configuration, and 3) during different respiratory maneuvers, different forces account for the same observed changes in LV volume and configuration.

Animals↗
PubMed1989

Diaphragm metabolism during supramaximal phrenic nerve stimulation.

The metabolic changes accompanying diaphragm fatigue caused by supramaximal stimulation of the phrenic nerves are incompletely described. In particular, we wished to determine whether the occurrence of anaerobic metabolism correlated with fatigue as defined by decline in force generation. In 10 anesthetized mechanically ventilated mongrel dogs we measured arterial pressure, transdiaphragmatic pressure (Pdi), phrenic arterial flow (Qdi-Doppler flow probe), arterial and phrenic venous blood gases, and lactate levels. From these we derived indexes of diaphragm O2 consumption (VO2) and lactate production. Bilateral phrenic nerve pacing was carried out (50 Hz, duty cycle 0.4, 24 contractions/min) for two 15-min pacing periods separated by a 45-min rest period. Over each pacing period Pdi decreased from approximately 16 to approximately 10 cmH2O (P less than 0.01, no significant difference between periods). Initially, during pacing, Qdi and VO2 each increased fivefold over prepacing base line. Qdi remained elevated at this level whereas VO2 decreased over the pacing period by approximately 25%. Hence, the change in VO2 over the pacing period was due primarily to changes in O2 extraction. During the first pacing period lactate production was observed early and declined throughout the pacing period. No lactate production was observed during the second pacing period, although Pdi, VO2, and Qdi responses were the same for both pacing periods. Phrenic venous PO2 remained greater than 30 Torr throughout both pacing periods.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Correlation of left phrenic arterial flow with regional diaphragmatic blood flow.

Previous work has assumed that left phrenic arterial blood flow (Qpa) reflects diaphragmatic blood flow. We have tested this assumption in four anesthetized mechanically ventilated dogs by measuring Qpa with a Doppler flow probe and regional diaphragmatic blood flow with radiolabeled microspheres. Flows were examined during control 1 (diaphragm at rest), pacing (phrenic pacing: rate 20/min, duty cycle 0.33), control 2, hypotension (rest with mean arterial pressure reduced by 45% of the control 1 value), and hypotension and pacing. As a percent of the control 1 value, Qpa was 511 +/- 107% during pacing, 139 +/- 12% during control 2, 40 +/- 13% during hypotension, and finally 347 +/- 31% during hypotension and pacing. Similarly, percent left hemidiaphragmatic blood flow (Qlh) was 362 +/- 91% during pacing, 91 +/- 10% during control 2, 14 +/- 2% during hypotension, and finally 213 +/- 50% during hypotension and pacing. The changes in flow to the left costal and crural diaphragm were similar to those recorded for Qlh. We conclude that Qpa correlates with total and regional diaphragmatic blood flow (r = 0.77-0.81, P less than 0.001) under conditions of supramaximal phrenic nerve stimulation in which the metabolic demands of the region perfused by the phrenic artery are presumed to be similar to the metabolic demands of the rest of the diaphragm.

Animals↗