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S M Scharf

Publications and source records attributed to S M Scharf.

At least 37 records · Page 2Linked to original sources
PubMed1998

Systemic and myocardial hemodynamics during periodic obstructive apneas in sedated pigs.

The effects of periodic obstructive apneas on systemic and myocardial hemodynamics were studied in nine preinstrumented sedated pigs under four conditions: breathing room air (RA), breathing 100% O2, breathing RA after critical coronary stenosis (CS) of the left anterior descending coronary artery, and breathing RA after autonomic blockade with hexamethonium (Hex). Apneas with RA increased mean arterial pressure (MAP; from baseline 103.0 +/- 3.5 to late apnea 123.6 +/- 7.0 Torr, P < 0.001) and coronary blood flow (CBF; late apnea 193.9 +/- 22.9% of baseline, P < 0.001) but decreased cardiac output (CO; from baseline 2.97 +/- 0.15 to late apnea 2.39 +/- 0.19 l/min, P < 0.001). Apneas with O2 increased MAP (from baseline 105.1 +/- 4.6 to late apnea 110.7 +/- 4.8 Torr, P < 0. 001). Apneas with CS produced similar increases in MAP as apneas with RA but greater decreases in CO (from baseline 3.03 +/- 0.19 to late apnea 2.1 +/- 0.15 l/min, P < 0.001). In LAD-perfused myocardium, there was decreased segmental shortening (baseline 11.0 +/- 1.5 to late apnea 7.6 +/- 2.0%, P < 0.01) and regional intramyocardial pH (baseline 7.05 +/- 0.03 to late apnea 6.72 +/- 0. 11, P < 0.001) during apneas with CS but under no other conditions. Apneas with Hex increased to the same extent as apneas with RA. Myocardial O2 demand remained unchanged during apnea relative to baseline. We conclude that obstructive apnea-induced changes in left ventricular afterload and CO are secondary to autonomic-mediated responses to hypoxemia. Increased CBF during apneas is related to regional metabolic effects of hypoxia and not to autonomic factors. In the presence of limited coronary flow reserve, decreased O2 supply during apneas can lead to myocardial ischemia, which in turn adversely affects left ventricular function.

Animals↗
PubMed1998

A "closed" medical intensive care unit (MICU) improves resource utilization when compared with an "open" MICU.

We hypothesized that a "closed" intensive care unit (ICU) was more efficient that an "open" one. ICU admissions were retrospectively analyzed before and after ICU closure at one hospital; prospective analysis in that ICU with an open ICU nearby was done. Illness severity was gauged by the Mortality Prediction Model (MPM0). Outcomes included mortality, ICU length of stay (LOS), hospital LOS, and mechanical ventilation (MV). There were no differences in age, MPM0, and use of MV. ICU and hospital LOS were lower when "closed" (ICU LOS: prospective 6.1 versus 12.6 d, p < 0.0001; retrospective 6.1 versus 9.3 d, p < 0.05; hospital LOS: prospective 19.2 versus 33.2 d, p < 0.008; retrospective 22.2 versus 31.2 d, p < 0.02). Days on MV were lower when "closed" (prospective 2.3 versus 8.5 d, p < 0.0005; retrospective 3.3 versus 6.4 d, p < 0.05). Pooled data revealed the following: MV predicted ICU LOS; ICU organization and MPM0 predicted days on MV; MV and ICU organization predicted hospital LOS; mortality predictors were open ICU (odds ratio [OR] 1.5, p < 0.04), MPM0 (OR 1.16 for MPM0 increase 0.1, p < 0.002), and MV (OR 2.43, p < 0.0001). We conclude that patient care is more efficient with a closed ICU, and that mortality is not adversely affected.

Adolescent↗
PubMed1997

Effect of beta-carboline-3-carboxoylate-t-butyl ester on ventilatory control.

beta-carboline-3-carboxylate-t-butyl ester (beta CCT) is the most selective antagonist for the alpha 1 beta 2 gamma 2 benzodiazepine (BZ) receptor subtype which blocks anticonvulsant and antipunishment (anxiolytic) but not sedative and myorelaxant effects of diazepam. We sought to determine whether the alpha 1 beta 2 gamma 2 BZ receptor subtype modulates ventilation and whether beta CCT antagonizes respiratory depressant effects of BZ's. Room air (RA) ventilation and the ventilatory response to 6% & 12% CO2 were non-invasively assessed by barometric plethysmography in 30 gm mice, n = 11. Plethysmograph signal amplitude (AMP), respiratory rate (RR) and minute ventilatory effort (MVE = AMP*RR), were measured. Runs were performed pre-drug & after IP injection of saline, vehicle for beta CCT, beta CCT (60mg/kg), midazolam (10mg/kg), and midazolam followed by beta CCT. Compared with pre-drug value, midazolam depressed MVE during RA and CO2 stimulation (% of pre-drug value: RA:57.7 +/- 17.4%, 6% CO2:53.73 +/- 14.3%, 12% CO2:69.1 +/- 26.1%, p < .0001, ANOVA). Subsequent beta CCT partially reversed this depression during RA conditions (72.8 +/- 25.7% of pre-drug value, p < .03 compared with midazolam) and 6% CO2 stimulation (67.1 +/- 10.7% of pre-drug value, p < .006 compared with midazolam) but not with 12% CO2. Thus, the alpha 1 beta 2 gamma 2 BZ receptor subtype modulates ventilation and beta CCT partially antagonizes respiratory depressant effects of BZ's.

Animals↗
PubMed1997

gamma-Aminobutyric acid contributes to modulation of cardiorespiratory control after chronic ventilatory loading.

Diseases imposing chronic ventilatory loads may depress ventilation and cause chronic hypercapnia. This may be a result of mechanical loading imposed on pre-existing decreased respiratory drive or functional alteration of neural circuits involved in ventilatory control. To evaluate these possibilities, chronic resistive airway loading was imposed in rats via a circumferential tracheal band which tripled tracheal resistance (obstructed group). Sham surgery was performed in controls. After 8 weeks, animals were anesthetized (urethane) and tracheostomy performed relieving increased tracheal resistance. The ventral medullary surface (VMS) was exposed and the intermediate area (IA) identified. The integrated diaphragm EMG (EMGDI) was recorded. The obstructed group was hypercapnic while controls were eucapnic (PCO2, 45.1 +/- 7.9 vs. 37.6 +/- 3.4 Torr; P < 0.001). Respiratory rate (RR) remained lower in obstructed than in control animals despite relief of the resistive load by tracheostomy (58.5 +/- 5.1 vs. 75.4 +/- 5.4 bpm; P < 0.05). Application of 1 mM bicuculline soaked pledgets (BIC) to the IA of the VMS significantly increased EMGDI in obstructed but not in control animals (27.5 +/- 5.5 vs. 5.2 +/- 4.4%; P < 0.006). RR was unaffected. Mean arterial pressure increased with BIC in obstructed but not control animals (23.0 +/- 6.5 vs. 4.5 +/- 3.5%; P < 0.02). These data suggest that alteration of cardiorespiratory control occurs during chronic resistive hypercapnic loading and that GABAergic neurons in the VMS participate in this adaptive response.

Airway Obstruction↗
PubMed1997

Effects of periodic obstructive apnoeas on superior and inferior venous return in dogs.

Obstructive apnoeas could cause flow limitation to venous return, resulting in a decrease in cardiac output and a change in the distribution of flow from the upper and lower body. In 14 anaesthetized dogs, we studied the effects of obstructive apnoeas on inferior and superior vena caval flows under baseline conditions and with intra-abdominal pressure increased by approximately equal to 5 torr by binding the abdomen. During obstructive apnoeas in the two groups, respiratory rate decreased by 30% (P < 0.02) and inspiratory airway pressure decreased by approximately equal to 15 torr (P < 0.01). At baseline, the ratio of inferior to superior vena caval flow was 2.4:1 and did not change with abdominal binding or apnoeas. During apnoeas there was no change in cardiac output or in the ratio of inferior to superior vena cava flow either with baseline or abdominal binding conditions. Preservation of total inferior vena caval flow during apnoeas and cardiac output occurred, even though inspiratory flow limitation was found with the abdomen bound. We conclude: (1) there was no change in either cardiac output or the distribution of venous return during apnoeas; (2) there was substantial inspiratory/expiratory variation in venous return during obstructive apnoeas. The large inspiratory-increase in venous return may have implications for the development of pulmonary hypertension during obstructive apnoeas.

Animals↗
PubMed1997

Scorpion venom leads to gastrointestinal ischemia despite increased oxygen delivery in pigs.

OBJECTIVES: Scorpion envenomation may be accompanied by metabolic acidosis even in the absence of hypoxia and cardiovascular derangement. We tested the hypothesis that venom causes ischemia of the gastrointestinal tract rather than failure of delivery of oxygen to the periphery. DESIGN: Repeated measures, prospective study in experimental animals. SETTING: University-affiliated hospital research laboratory. INTERVENTIONS: In ten spontaneously breathing, intubated, sedated pigs, purified dried venom (Leiurus quinquestriatus), 0.05 mg/kg, was administered intravenously. Measurements were obtained before (baseline), and 5, 15, 30, 60, 120, 180, and 240 mins after injection. MEASUREMENTS AND MAIN RESULTS: Variables measured included: mean arterial pressure (MAP), heart rate (HR), mean pulmonary arterial pressure, pulmonary artery occlusion pressure, cardiac output, stroke volume, right ventricular ejection fraction (rapid thermistor), left ventricular dimensions (echocardiography), arterial gas tensions, lactate and catecholamine concentrations, gastric interstitial mucosal pH (tonometry), as well as systemic and pulmonary vascular resistances. Within 5 mins after venom injection, there was a hyperdynamic state accompanied by significantly increased MAP (97 +/- 18 to 136 +/- 47 mm Hg, p < .0003), HR (70 +/- 12 to 121 +/- 24 beats/min, p < .00006), and cardiac output (1.88 +/- 0.35 to 2.95 +/- 0.53 L/min, p < .0003), with no change in stroke volume, or pulmonary artery occlusion pressure. Right ventricular ejection fraction increased from 38.1 +/- 4.3 to 48.6 +/- 9.0% (p < .0009) by 15 mins. No change in left ventricular function was observed. There were significant decreases in systemic vascular resistance and pulmonary vascular resistance following envenomation. Arterial and gastric mucosal pH significantly decreased from 7.40 +/- 0.04 to 7.25 +/- 0.07 (p < .0001) for arterial pH, and 7.33 +/- 0.08 to 7.17 +/- 0.13 (p < .00001) for gastric mucosal pH by 30 mins after envenomation. The decrease in arterial pH was not sufficient to account for the change in gastric mucosal pH, indicating gastric mucosal ischemia. Arterial lactate increased from 2.6 +/- 1.4 to 7.4 +/- 1.9 (p < .05 x 10(-8)). There were significant increases in serum epinephrine and norepinephrine values by 5 mins. All hemodynamic variables and catecholamine concentrations returned to baseline by 4 hrs. However, there was persistent arterial and gastric mucosal acidosis and increased lactate concentrations even at 4 hrs. Oxygen delivery remained normal or supernormal for 4 hrs following envenomation. However, despite this finding, systemic and gastric mucosal pH changes indicate impaired gastrointestinal oxygen delivery. CONCLUSIONS: Despite increased peripheral oxygen delivery, scorpion envenomation was associated with evidence of ischemia of the gastrointestinal tract. This association could be due to shunting of blood from metabolically active areas, possibly associated with massive catecholamine release, or a direct toxic effect of the venom on regional oxygen transport at the cellular level.

Acidosis↗
PubMed1997

Effect of chronic resistive loading on hypoxic ventilatory responsiveness.

Depression of ventilation mediated by endogenous opioids has been observed acutely after resistive airway loading. We evaluated the effects of chronically increased airway resistance on hypoxic ventilatory responsiveness shortly after load imposition and 6 wk later. A circumferential tracheal band was placed in 200-g rats, tripling tracheal resistance. Sham surgery was performed in controls. Ventilation and the ventilatory response to hypoxia were measured by using barometric plethysmography at 2 days and 6 wk postsurgery in unanesthetized rats during exposure to room air and to 12% O2-5% CO2-balance N2. Trials were performed with and without naloxone (1 mg/kg i.p.). Room air arterial blood gases demonstrated hypercapnia with normoxia in obstructed rats at 2 days and 6 wk postsurgery. During hypoxia, a 30-Torr fall in PO2 occurred with no change in PCO2. Hypoxic ventilatory responsiveness was suppressed in obstructed rats at 2 days postloading. Naloxone partially reversed this suppression. However, hypoxic responsiveness at 6 wk was not different from control levels. Naloxone had a small effect on ventilatory pattern at this time with no overall effect on hypoxic responsiveness. This was in contrast to previously demonstrated long-term suppression of CO2 sensitivity in this model, which was partially reversible by naloxone only during the immediate period after load imposition. Endogenous opioids apparently modulate ventilatory control acutely after load imposition. Their effect wanes with time despite persistence of depressed CO2 sensitivity.

Airway Resistance↗
PubMed1997

Comparative hemodynamic effects of periodic obstructive and simulated central apneas in sedated pigs.

It has been speculated that because of increased left ventricular (LV) afterload, decreased intrathoracic pressure (ITP) is responsible for decreased cardiac output (CO) in obstructive sleep apnea. If this were true, then obstructive apnea (OA) should have a greater effect on CO than would central apnea (CA). To assess the importance of decreased ITP during OA, we studied seven preinstrumented sedated pigs with OA and simulated CA that were matched for blood gases and apnea periodicities (with 15- or 30-s apnea duration). Compared with OA, CA with 30-s apnea duration produced comparable decreases in heart rate (from baseline to end apnea: OA, 106.6 +/- 4.8 to 93.4 +/- 4.4 beats/min, P < 0.01; and CA, 111.1 +/- 6.2 to 94.0 +/- 5.2 beats/min, P < 0.01) and comparable increases in LV end-diastolic pressure and LV end-diastolic myocardial segment length but greater increases in mean arterial pressure (97.1 +/- 3.7 to 107.7 +/- 4.3 Torr, P < 0.05; and 97.3 +/- 4.8 to 119.3 +/- 7.4 Torr, P < 0.01) and systemic vascular resistance (2,577 +/- 224 to 3,346 +/- 400 dyn . s . cm-5, P < 0.01; and 2,738 +/- 294 to 5,111 +/- 1,181 dyn . s . cm-5, P < 0.01) and greater decreases in CO (3.18 +/- 0.31 to 2.74 +/- 0.26 l/min, P < 0. 05; and 3.07 +/- 0.38 to 2.30 +/- 0.36 l/min, P < 0.01) and stroke volume (32.2 +/- 2.9 to 25.9 +/- 2.4 ml, P < 0.05; and 31.5 +/- 1.9 to 19.8 +/- 3.1 ml, P < 0.01). Only CA increased LV end-systolic myocardial segment length. Similar findings were observed with 15-s apnea duration. We conclude that CA produced greater depression of CO and greater changes of afterload-related LV dysfunction than did OA. Therefore, decreased ITP was not the dominant factor determining LV function with apneas.

Animals↗
PubMed1996

A comparison between the acute effects of nitric oxide synthase inhibition and fluid resuscitation on myocardial function and metabolism in entotoxemic dogs.

PURPOSE: Nitric oxide (NO) synthase inhibitors increase mean arterial pressure (MAP) and systemic vascular resistance (SVR) in animal models of sepsis and in humans with septic shock. However, NO synthase inhibitors may cause coronary vessel constriction leading to myocardial ischemia and increased mortality in endotoxemic animals. This study was designed to test the acute effect of NG-nitro-L-arginine (L-NAME) on left ventricular (LV) function and coronary blood flow in a dog model of endotoxemia. METHODS: In open chest, anesthetized dogs endotoxemia was induced intravenously (IV) by Escherichia coli lipopolysaccharide at 2 mg/kg for 60 minutes. This resulted in hypotension, acidosis, and decreased SVR while cardiac index (CI) was maintained. When MAP was < or = 60 mm Hg, animals were resuscitated with either dextran (group I), or L-NAME 30 mg/kg IV bolus (group II). Group III received L-NAME only. A fourth group of dogs was given endotoxin and not resuscitated. Animals were followed up for 30 minutes after intervention. Animals in the fourth group were followed up until the MAP was approximately 30 mm Hg. Heart rate, CI, MAP, LV end systolic and diastolic pressures, dP/dt at a pressure of 40 mm Hg, left anterior descending artery coronary blood flow, regional LV contraction (sonomicrometer crystals), coronary pressures, gas tension, and lactates were continuously recorded. A catheter placed in the coronary sinus allowed measurement of coronary sinus pressure, as well as coronary sinus lactate and gas tensions. Stroke volume index, stroke work index, systemic vascular resistance index (SVRI), coronary vascular resistance, percent myocardial shortening, myocardial oxygen consumption (Mvo2) and net myocardial lactate production were calculated. RESULTS: In Group I, fluid administration increased MAP, stroke work index, coronary blood flow, percent myocardial shortening, and Mvo2. In Group II, L-NAME increased MAP to the same extent as fluid administration without evidence of coronary ischemia or myocardial dysfunction. L-NAME did not alter Mvo2 in either endotoxemic or nonendotoxemic animals. In group III, L-NAME alone resulted in a significant increase in MAP and SVRI, but its effects on coronary blood flow and LV function were not significant. We did not observe net lactate production in any of the groups. Coronary blood flow increased out of proportion to Mvo2 in group I animals. CONCLUSIONS: We conclude that although L-NAME at 30 mg/kg causes vasoconstriction, its effects on coronary blood flow and LV function were not significant.

Animals↗
PubMed1996

Effects of continuous positive airway pressure on cardiac output and plasma norepinephrine in sedated pigs.

Continuous positive airway pressure (CPAP) increases cardiac output (CO) in congestive heart failure (CHF). In six sedated pigs that were normovolemic (NV) and hypervolemic (HV), and seven previously instrumented pigs with pacing-induced CHF, we tested the hypothesis that this is associated with decreased total body sympathetic nerve activity (SNA). Hemodynamic variables and plasma norepinephrine level measurements were measured at baseline, CPAP 5 and 10 cm H2O, and recovery. Arterial O2 saturation was maintained at greater than or equal to 90% and PCO2 did not change. For NV baseline plasma norepinephrine level (PNE) was 97 +/- 61 pg/mL, CO 2.4 +/- .5 L/min, and pulmonary wedge pressure (Pw) 10.1 +/- 2.4 mmHg and did not change with CPAP. HV and CHF were associated with increased baseline Pw (18-21 mmHg). Baseline CO was increased with HV and unchanged with CHF. Baseline PNE was increased 4 to 5-fold with both HV and CHF. CO increased at CPAP 5 compared with baseline with both HV and CHF. However, PNE decreased with CPAP in HV, and increased with CPAP in CHF. Increased CO was always associated with decreased systemic vascular resistance. We conclude the following: (1) increased CO with CPAP can be associated with either increasing or decreasing SNA; (2) CPAP can produce increases in CO when the heart is distended whether baseline LV function is relatively normal (HV) or depressed (CHF); and (3) there are probably a number of different mechanism increasing CO with CPAP and these may vary from condition to condition.

Animals↗
PubMed1996

The effects of high dose NG-nitro-L-arginine-methyl ester on myocardial blood flow and left ventricular function in dogs.

PURPOSE: Nitric oxide (NO) synthase inhibition has been reported to cause elevation in mean arterial pressure (MAP) and a decrease in cardiac index (CI), the cause of which is not completely understood. It has been shown that increased concentrations of NO synthase inhibitors cause a further drop in cardiac output without a corresponding increase in arterial pressure, prompting the conclusion that NO inhibition results in direct myocardial depression. However, myocardial ischemia was not completely ruled out as a cause for myocardial dysfunction in these studies. The purpose of this study was to examine the effects of 30 mg/kg of the NO synthase inhibitor NG-nitro-L-arginine-methyl ester (L-NAME) to those of 300 mg/kg and assess the effects on coronary ischemia and myocardial function. MATERIALS AND METHODS: Eight anesthetized dogs underwent median sternotomy and pericardiectomy. L-NAME 30 mg/kg was administered and the effects were recorded at 5, 15, and 30 minutes. Thereafter, 300 mg/kg was administered and the effects were observed for 5, 15, and 30 minutes. We measured MAP, heart rate (HR), CI, left ventricle (LV) and systolic and diastolic pressures, the first derivative of LV pressure (dP/dt), left anterior descending artery blood flow, regional LV contraction, gas tensions, and lactates. A coronary sinus catheter allowed for measurements of coronary sinus pressure, lactate, and gas tensions. Stroke volume, percent myocardial shortening (dL/dt) myocardial oxygen consumption, and net lactate myocardial production were calculated. RESULTS: Whereas 30 mg/kg had minimal effects on coronary blood flow and LV function, 300 mg/kg resulted in profound hypotension, drop in CI, and acidocsis. CONCLUSIONS: L-NAME at 30 mg/kg caused a rise in MAP and systemic vascular resistance; however, it had no effect on ventricular function. High dose NO synthase inhibition causes myocardial depression not related to increased afterload, coronary vasoconstriction, or myocardial ischemia.

Animals↗
PubMed1996

Myocardial mechanics and energetics during continuous positive airway pressure in sedated pigs.

OBJECTIVE: To test the hypothesis that increased cardiac output with continuous positive airway pressure (CPAP) leads to increased myocardial metabolic cost. DESIGN: Prospective, repeated-measures, laboratory studies. SETTING: University-affiliated hospital animal research laboratory. SUBJECTS: Eight sedated pigs that had been previously instrumented for collection of hemodynamic data. INTERVENTIONS: Application of CPAP at 0, 5, 10, and 15 cm H2O and recovery under conditions of normal blood volume (normovolemia) and after administration of hetastarch 35 mL/kg (hypervolemia). MEASUREMENTS AND MAIN RESULTS: We measured mean arterial pressure, cardiac output, systemic vascular resistance index, the first derivative of the left ventricular pressure at a left ventricular pressure of 50 mm Hg, rate-pressure product, left ventricular tension-time index, stroke work index, myocardial pressure-myocardial segment length area, coronary artery blood flow and coronary vascular resistance, and myocardial oxygen consumption (four pigs). With normovolemia, cardiac output decreased with CPAP (4.9 +/- 1.2 L/min at CPAP of 0 cm H2O to 4.5 +/- 1.3 L/min at CPAP of 15 cm H2O, p < .005) and systemic vascular resistance index increased (2509 +/- 702 to 3095 +/- 1080 dyne.sec/cm5.m2, p < .01). With hypervolemia, cardiac output increased at low-level CPAP (5.7 +/- 1.4 L/min at CPAP of 0 cm H2O to 6.4 +/- 1.6 L/min at CPAP of 5 cm H2O, p < .05) and systemic vascular resistance index decreased (2412 +/- 552 to 2033 +/- 436 dyne.sec/cm5.m2, p < .01). There were no associated significant changes in myocardial oxygen consumption, or its major correlates when cardiac output increased with CPAP (hypervolemic conditions). CONCLUSIONS: In normal pigs, there is no change in myocardial oxygen demand with CPAP, whatever the change in cardiac output. Thus, increased cardiac output with CPAP carries little extra metabolic cost. Increased cardiac output with low-level CPAP in hypervolemia is associated with systemic vasodilation.

Alfaxalone Alfadolone Mixture↗
PubMed1996

Effects of continuous positive airway pressure on cardiac output in experimental heart failure.

Continuous positive airway pressure (CPAP) is used to treat congestive heart failure (CHF). Mechanisms for improved cardiac output (CO) include increased left ventricular (LV) surface pressure, changes in sympathoadrenal tone, nonadrenergic vasodilation, or shifting blood volume from intra- to extrathoracic compartments. At CPAP = 0 and CPAP = 5 cm H2O we measured CO, LV surface pressure, plasma norepinephrine (PNE), and systemic vascular resistance (SVR) in normal and hypervolemic pigs and pigs with CHF (rapid ventricular pacing). In normovolemia CPAP led to no change in CO. With both hypervolemia and CHF. CPAP led to increased CO (10-20%). With CPAP, LV surface pressure increased slightly in normovolemia, but did not increase, or even decreased, in hypervolemia. With CPAP, PNE did not change in normovolemia, increased in hypervolemia, and decreased in CHF, SVR always decreased when cardiac output increased with CPAP. We conclude that changes in cardiac surface pressure and overall sympathoadrenal tone cannot explain changes in CO with CPAP. Non-adrenergic mediated vasodilation could lead to unloading the LV. Alternatively, volume shift from intra- to extrathoracic compartments could lead to greater decreases in systolic than diastolic volume, thus increasing stroke volume. CPAP increases CO in the presence of cardiac distension whether or not myocardial function is impaired.

Animals↗
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↗