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Biomedical subjects

B T Thompson

Publications and source records attributed to B T Thompson.

At least 37 records · Page 2Linked to original sources
PubMed1994

Inhibition of hypoxic pulmonary hypertension by heparins of differing in vitro antiproliferative potency.

Heparin inhibits smooth-muscle cell (SMC) growth in vitro and inhibits the development of hypoxic pulmonary hypertension and vascular remodeling in vivo. We wondered whether preparations of heparin with different antiproliferative potency in vitro would differ in their ability to inhibit the development of hypoxic pulmonary hypertension in vivo. Two such heparins, a weakly antiproliferative lot of Elkins-Sinn (E-S) (% inhibition of SMC growth at 10 micrograms/ml = 13 +/- 9% [mean +/- SEM, n = 24]) and a more active lot from Upjohn (UJ) (% inhibition = 71 +/- 12% [n = 12, p < 0.05 versus E-S]), were infused subcutaneously (300 U.S.P. units/day; E-S 300 versus UJ 300) via an osmotic pump into guinea pigs exposed to hypoxia (10% O2) for 10 d, after which pulmonary artery pressure (PAP; mm Hg) and cardiac index (CI; ml/min/kg) were measured in room air. Hypoxic controls (HC) received saline. PAP increased from 11 +/- 1 mm Hg in normoxic controls (NC) (n = 5) to 24 +/- 1 mm Hg in HC (n = 8, p < 0.05). The PAP was lower in the E-S 300 (21 +/- 1; n = 7, p < 0.05 versus HC and NC) and even lower in the UJ 300-treated group (18 +/- 0.5; n = 7, p < 0.05 versus HC and NC). Total pulmonary vascular resistance (TPR; mm Hg/ml/min/kg) increased significantly from 0.038 +/- 0.002 in NC to 0.076 +/- 0.003 (p < 0.05) in HC. There was no difference in TPR between the HC and the E-S 300-treated group.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1994

Indexing guidelines: applications in use of pulmonary artery catheters and pressure ulcer prevention.

In a busy clinical environment, access to knowledge must be rapid and specific to the clinical query at hand. This requires indices which support easy navigation within a knowledge source. We have developed a computer-based tool for trouble-shooting pulmonary artery waveforms using a graphical index. Preliminary results of domain knowledge tests for a group of clinicians exposed to the system (N = 33) show a mean improvement on a 30-point test of 5.33 (p < 0.001) compared to a control group (N = 19) improvement of 0.47 (p = 0.61). Survey of the experimental group (N = 25) showed 84% (p = 0.001) found the system easy to use. We discuss lessons learned in indexing this domain area to computer-based indexing of guidelines for pressure ulcer prevention.

Abstracting and Indexing↗
PubMed1993

Chronic hypoxic pulmonary hypertension in the guinea pig: effect of three levels of hypoxia.

Chronic hypoxia [inspiratory PO2 (PIO2) = 76 Torr for 10 days] produces pulmonary hypertension and vascular remodeling in the guinea pig. Increasing the duration of hypoxia from 10 to 21 days does not increase further pulmonary arterial pressure or medial thickening. To see if increasing severity of hypoxia affects the magnitude of pulmonary hypertension and remodeling, we exposed three groups of male Hartley guinea pigs to three levels of normobaric hypoxia for 10 days: PIO2 = 90 (n = 6), 78 (n = 6), and 65 Torr (n = 5). Pulmonary arterial pressure increased from 14 +/- 1 (+/- SE, n = 7) in room air to 23 +/- 3 mmHg when PIO2 = 90 Torr (P < 0.05). Pulmonary arterial pressure was slightly higher when PIO2 = 78 or 65 Torr (25 +/- 1 and 26 +/- 1 mmHg, respectively) but did not reach statistical significance vs. PIO2 = 90 Torr. Total pulmonary vascular resistance increased from 0.049 +/- 0.004 in room air to between 0.084 +/- 0.006 and 0.101 +/- 0.003 mmHg.min.kg.ml-1 (P < 0.05) in the three hypoxic groups; again there was no difference in total pulmonary vascular resistance among hypoxic groups. Medial thickness of alveolar duct and terminal bronchiole arteries increased with hypoxia, but there was no significant difference among the hypoxic groups. The percentage of intra-acinar vessels with thick walls (a measure of muscular extension) increased when PIO2 = 78 Torr and nearly doubled when PIO2 = 65 Torr in comparison to control.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Effect of aerosol heparin on the development of hypoxic pulmonary hypertension in the guinea pig.

Chronic hypoxia produces pulmonary artery hypertension through vasoconstriction and structural remodeling of the pulmonary vascular bed. The present study was designed to test the effect of heparin administered via aerosol on the development of hypoxic pulmonary hypertension. Anesthetized, intubated, and mechanically ventilated guinea pigs received an aerosol of either 2 ml normal saline (hypoxic control, HC) or 4,500 units of heparin diluted in 2 ml normal saline via an ultrasonic nebulizer (hypoxic heparin, HH). After 24 h of recovery, the animals were placed in a hypoxic chamber (10% O2) for 10 days. Animals kept in room air served as normoxic controls (NC). Hypoxia increased mean pulmonary artery pressure from 11 +/- 1 (SEM) mm Hg in NC to 24 +/- 1 mm Hg in HC (p < 0.05). Pulmonary artery pressure was significantly lower in HH-treated animals (20 +/- 1 mm Hg, p < 0.05 versus HC) as was the total pulmonary vascular resistance (0.15 +/- 0.01 in HH versus 0.20 +/- 0.01 mm Hg/ml/min in HC, p < 0.05). There was no difference in cardiac output (146 +/- 12 in HH versus 126 +/- 7 ml/min in HC), hematocrit (57 +/- 2 in HH versus 56 +/- 2% in HC), partial thromboplastin time (30 +/- 2 in HH versus 32 +/- 3 s in HC), prothrombin time (46 +/- 1 in HH versus 48 +/- 4 s in HC) or room air arterial blood gas values after 10 days of hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Aerosols↗
PubMed1993

Providing clinicians with problem-based access to knowledge: troubleshooting pulmonary artery catheter waveforms.

This paper describes a microcomputer system for providing computer-based access to expert knowledge in the area of troubleshooting pulmonary artery (PA) catheter waveforms. The system is used by both nurses and physicians in an 18-bed medical intensive care unit. Its dominant features are 1) problem-focused access to knowledge, and 2) heavy use of graphics and images to explicate knowledge. The system is used by both nurses and physicians in an 18-bed medical intensive care unit. An evaluation protocol is in place to examine the impact of the system on clinicians' knowledge, their decision-making skills, their satisfaction with the system, and costs of orientation related to PA waveform troubleshooting.

Catheterization, Swan-Ganz↗
PubMed1992

A prospective investigation of pulmonary embolism in women and men.

OBJECTIVE: The aim of this study was to compare, in women and men suspected of pulmonary embolism, the frequency, risk factors, diagnosis, and presentation of pulmonary embolism as well as the accuracy of the ventilation/perfusion scan (V/Q scan) as a diagnostic tool. DESIGN: Data were collected during a prospective study (the Prospective Investigation of Pulmonary Embolism Diagnosis) to establish the accuracy of the V/Q scan compared with pulmonary angiograms. SETTING: Six tertiary medical centers in Massachusetts, Michigan, Connecticut, Pennsylvania, and North Carolina. PARTICIPANTS: Patients suspected of pulmonary embolism for whom a request was made for a V/Q scan or pulmonary angiogram (496 women and 406 men). RESULTS: Women 50 years old and under had a decreased frequency of pulmonary embolism compared with men of that age (16% vs 32%), but there was no difference in patients over 50 years old (Breslow-Day test, P less than .01). Risk factors for pulmonary embolism, the usefulness of the V/Q scan, and 1-year mortality were not different for women and men. Estrogen use in women was not associated with an increased frequency of pulmonary embolism, except in women using oral contraceptives who had undergone surgery within 3 months; four of five (80%) had emboli compared with four of 28 (14%) age-matched surgical patients not using estrogens (P less than .01). CONCLUSION: Women 50 years old and under (even young women using oral contraceptives) who were suspected of having pulmonary emboli and were enrolled in the Prospective Investigation of Pulmonary Embolism Diagnosis study had a smaller frequency of pulmonary embolism than men of that age, The risk factors for pulmonary embolism were the same for women and men, except that women using oral contraceptives had an increased risk of pulmonary embolism following surgery. Although the V/Q scan was a useful tool in the preliminary evaluation for pulmonary embolism in these women, a pulmonary angiogram was often needed for accurate diagnosis.

Adolescent↗
PubMed1992

The clinical course of pulmonary embolism.

BACKGROUND: Pulmonary embolism is a potentially fatal disorder. Information about the outcome of clinically recognized pulmonary embolism is sparse, particularly given that new treatments for more seriously ill patients are now available. METHODS: We prospectively followed 399 patients with pulmonary embolism diagnosed by lung scanning and pulmonary angiography, who were enrolled in a multicenter diagnostic trial. We reviewed all hospitalizations, all new investigations of pulmonary embolism, and all deaths among the patients within one year of diagnosis. RESULTS: Of the 399 patients, 375 (94 percent) received treatment for pulmonary embolism, usually conventional anticoagulation. Only 10 patients (2.5 percent) died of pulmonary embolism; 9 of them had clinically suspected recurrent pulmonary embolism. Clinically apparent pulmonary embolism recurred in 33 patients (8.3 percent), of whom 45 percent died during follow-up. Ninety-five patients with pulmonary embolism (23.8 percent) died within one year. The conditions associated with these deaths were cancer (relative risk, 3.8; 95 percent confidence interval, 2.3 to 6.4), left-sided congestive heart failure (relative risk, 2.7; 95 percent confidence interval, 1.5 to 4.6), and chronic lung disease (relative risk, 2.2; 95 percent confidence interval, 1.2 to 4.0). The most frequent causes of death in patients with pulmonary embolism were cancer (in 34.7 percent), infection (22.1 percent), and cardiac disease (16.8 percent). CONCLUSIONS: When properly diagnosed and treated, clinically apparent pulmonary embolism was an uncommon cause of death, and it recurred in only a small minority of patients. Most deaths were due to underlying diseases. Patients with pulmonary embolism who had cancer, congestive heart failure, or chronic lung disease had a higher risk of dying within one year than did other patients with pulmonary embolism.

Adult↗
PubMed1992

Partial reversal of hypoxic pulmonary hypertension by heparin.

Chronic hypoxia produces pulmonary hypertension and an increase in medial thickness of pulmonary arteries that reach maximal values after 10 days of hypoxia. We previously showed that heparin given during the first 10 days of hypoxia reduced the development of both pulmonary hypertension and vascular remodeling in the guinea pig. To determine if heparin could reverse established hypoxic pulmonary hypertension and vascular remodeling, we administered heparin by continuous subcutaneous infusion (20 U/kg/h) for the last 7 days of a 21-day exposure to hypoxia (10% O2, balance N2) and compared these animals with normal saline-infused hypoxic control and room air-exposed animals. Hypoxia increased pulmonary artery pressure from 11 +/- 1 mm Hg (mean +/- SEM) in room air animals to 20 +/- 2 mm Hg (p less than 0.05) in saline-treated hypoxic control animals. Heparin reduced pulmonary artery pressure to 16 +/- 1 mm Hg (p less than 0.05 versus hypoxic control and room air control animals). Total pulmonary resistance (TPR) increased with hypoxia from 0.043 +/- 0.003 mm Hg x min x kg-1 x ml-1 in room air to 0.090 +/- 0.004 in hypoxia (p less than 0.05), and in the rise in TPR was also partially reversed by heparin to 0.068 +/- 0.0003 (p less than 0.05). The percentage of medial thickness of alveolar duct arteries increased from 5.8 +/- 0.6% in room air to 9.5 +/- 0.1% (p less than 0.05) after 3 wk of hypoxia, and heparin therapy partially reversed the increase in medial thickness to 7.2 +/- 0.7% (p less than 0.05 versus both hypoxia control and room air).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

The diagnosis of acute pulmonary embolism in patients with chronic obstructive pulmonary disease.

The clinical features and noninvasive tests, including ventilation perfusion (V/Q) lung scans, were assessed in 108 patients with chronic obstructive pulmonary disease (COPD) suspected of having pulmonary embolism (PE). Twenty-one (19 percent) of 108 patients had PE. In the majority of patients, it was impossible to distinguish between patients with and without PE by clinical assessment alone. However, when a high clinical index of suspicion was present, PE was confirmed by angiography in three of three patients, but the V/Q scan was of intermediate probability. No roentgenographic abnormalities distinguished between PE and no PE. There was no difference between the alveolar-arterial oxygen gradients in either group, nor was there evidence of a reduction in the PaCO2 in patients with PE who had prior hypercapnia. Among the 108 patients with COPD, high, intermediate, low, and normal/near normal probability scans were present in 5 percent, 60 percent, 30 percent, and 5 percent, respectively. The frequency of PE in these V/Q scan categories was five (100 percent) of five, 14 (22 percent) of 65, two (6 percent) of 33, and zero (0 percent) of five, respectively. In conclusion, in the majority of patients, the V/Q scan diagnosis is usually intermediate and such patients require further investigational studies, including angiography. However, among the few patients who demonstrated a high probability lung scan, there was a high positive predictive value for PE effectively avoiding the need for further studies. In those patients with low probability or near normal/normal V/Q scans, the negative predictive value was not lower than the general hospital population.

Acute Disease↗
PubMed1991

Polycythemia and vascular remodeling in chronic hypoxic pulmonary hypertension in guinea pigs.

Chronic hypoxia increases pulmonary arterial pressure (PAP) as a result of vasoconstriction, polycythemia, and vascular remodeling with medial thickening. To determine whether preventing the polycythemia with repeated bleeding would diminish the pulmonary hypertension and remodeling, we compared hemodynamic and histological profiles in hypoxic bled (HB, n = 6) and hypoxic polycythemic guinea pigs (H, n = 6). After 10 days in hypoxia (10% O2), PAP was increased from 10 +/- 1 (SE) mmHg in room air controls (RA, n = 5) to 20 +/- 1 mmHg in H (P less than 0.05) but was lower in HB (15 +/- 1 mmHg, P less than 0.05 vs. H). Cardiac output and pulmonary artery vasoreactivity did not differ among groups. Total pulmonary vascular resistance increased from 0.072 +/- 0.011 mmHg.ml-1.min in RA to 0.131 mmHg.ml-1.min in H but was significantly lower in HB (0.109 +/- 0.006 mmHg.ml-1.min). Hematocrit increased with hypoxia (57 +/- 3% in H vs. 42 +/- 1% in RA, P less than 0.05), and bleeding prevented the increase (46 +/- 4% in HB, P less than 0.05 vs. H only). The proportion of thick-walled peripheral pulmonary vessels (53.2 +/- 2.9% in HB and 50.6 +/- 4.8% in H vs. 31.6 +/- 2.6% in RA, P less than 0.05) and the percent medial thickness of pulmonary arteries adjacent to alveolar ducts (7.2 +/- 0.6% in HB and 7.0 +/- 0.4% in H vs. 5.2 +/- 0.4% in RA, P less than 0.05) increased to a similar degree in both hypoxic groups. A similar tendency was present in larger bronchiolar vessels.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Contribution of Na+/H+ exchange to pH regulation in pulmonary artery smooth muscle cells.

In blood vessels in the systemic circulation, the plasmalemmal Na+/H+ exchanger has been implicated in a variety of cellular functions, including the regulation of intracellular pH (pHi) and cell volume, and the response to smooth muscle mitogens. The role of this transport system in pulmonary vascular smooth muscle has not been explored. The present study examined the characteristics of Na+/H+ exchange in cultured guinea pig pulmonary artery smooth muscle cells. These cells were subjected to an acid load, and the recovery from acid loading was monitored using the fluorescent pH-sensitive dye 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein (BCECF). In the absence of HCO3-, pHi recovery from acid loading was dependent on external Na+ and was inhibited by the Na+/H+ exchange inhibitor dimethylamiloride (DMA) (recovery rate was reduced from 54.4 +/- 5.5 to 12.8 +/- 2.0 mmol H+/liter.min). This exchanger was also active in the presence of HCO3-; DMA reduced resting pHi and slowed the rate of recovery from acid loading in HCO3- buffers. However, in the presence of HCO3-, other transport systems, presumably HCO3-/Cl- exchange, also contribute to the regulation of pHi. In HCO3- buffers, the rate of recovery from acid load averaged 40.8 +/- 1.8 mmol H+/liter.min. Addition of 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), an inhibitor of HCO3-/Cl- exchange, slowed this recovery to 25.5 +/- 1.6 mmol H+/liter.min. A combination of DIDS and DMA further slowed the recovery to 19.7 +/- 1.5 mmol H+/liter.min. These findings indicate that the Na+/H+ exchanger plays a significant role in the regulation of pHi in pulmonary artery smooth muscle cells, even in HCO(3-)-containing buffers.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1991

Clinical, laboratory, roentgenographic, and electrocardiographic findings in patients with acute pulmonary embolism and no pre-existing cardiac or pulmonary disease.

The history, physical examination, chest radiograph, electrocardiogram and blood gases were evaluated in patients with suspected acute pulmonary embolism (PE) and no history or evidence of pre-existing cardiac or pulmonary disease. The investigation focused upon patients with no previous cardiac or pulmonary disease in order to evaluate the clinical characteristics that were due only to PE. Acute PE was present in 117 patients and PE was excluded in 248 patients. Among the patients with PE, dyspnea or tachypnea (greater than or equal to 20/min) was present in 105 of 117 (90 percent). Dyspnea, hemoptysis, or pleuritic pain was present in 107 of 117 (91 percent). The partial pressure of oxygen in arterial blood on room air was less than 80 mm Hg in 65 of 88 (74 percent). The alveolar-arterial oxygen gradient was greater than 20 mm Hg in 76 of 88 (86 percent). The chest radiograph was abnormal in 98 of 117 (84 percent). Atelectasis and/or pulmonary parenchymal abnormalities were most common, 79 of 117 (68 percent). Nonspecific ST segment or T wave change was the most common electrocardiographic abnormality, in 44 of 89 (49 percent). Dyspnea, tachypnea, or signs of deep venous thrombosis was present in 107 of 117 (91 percent). Dyspnea or tachypnea or pleuritic pain was present in 113 of 117 (97 percent). Dyspnea or tachypnea or pleuritic pain was present in 113 of 117 (97 percent). Dyspnea or tachypnea or pleuritic pain or atelectasis or a parenchymal abnormality on the chest radiograph was present in 115 of 117 (98 percent). In conclusion, among the patients with pulmonary embolism that were identified, only a small percentage did not have these important manifestations or combinations of manifestations. Clinical evaluation, though nonspecific, is of considerable value in the selection of patients in whom there is a need for further diagnostic studies.

Acute Disease↗
PubMed1991

Esmolol and ventilatory function in cardiac patients with COPD.

To assess the effects of acute cardioselective beta blockade on ventilatory function in patients with COPD and active cardiac disorders, 50 patients were studied during intravenous infusion of esmolol. All patients had an obstructive ventilatory component on baseline pulmonary function testing, and 58 percent had a significant bronchodilator response to inhaled albuterol. Esmolol infusion (8 to 24 mg/min) produced large decreases in heart rate (84 +/- 2 to 69 +/- 2 beats/min, p less than 0.01) and SBP (124 +/- 3 to 106 +/- 3 mm Hg, p less than 0.01). Despite this marked hemodynamic response, there was no significant group effect of beta blockade on pulmonary function. No patient experienced dyspnea or wheezing with acute esmolol infusion; however, three patients (6 percent) developed asymptomatic decreases of FEV1. It is concluded that acute beta blockade with esmolol can be achieved in patients with COPD and cardiac disorders with little risk of bronchospasm.

Adrenergic beta-Antagonists↗
PubMed1989

Wheezing on maximal forced exhalation in the diagnosis of atypical asthma. Lack of sensitivity and specificity.

STUDY OBJECTIVE: To determine whether wheezing on maximal forced exhalation is a predictor of asthma in persons with normal or nearly normal baseline spirometry. DESIGN: Prospective study of patients referred for methacholine challenge testing. SETTING: Pulmonary function laboratory at a hospital. PATIENTS: Forty-four patients referred for methacholine challenge testing because of the clinical suspicion of cough variant or otherwise difficult to diagnose asthma, with normal or nearly normal baseline spirometry and without wheezing on routine lung auscultation during quiet breathing. INTERVENTIONS: We listened for wheezing on maximal forced exhalation. Wheezing was defined as a continuous sound with a musical quality. Methacholine challenge testing was done. The concentration of methacholine required to produce a 20% fall in baseline FEV1 (PC20) of less than 8 mg/mL was considered a positive test for asthma. MEASUREMENTS AND MAIN RESULTS: Wheezing was present on maximal forced exhalation in 8 of 14 patients with a positive methacholine challenge test (sensitivity = 57%) and absent in 11 of 30 patients with a negative test (specificity = 37%). Furthermore, wheezing on maximal forced exhalation was present in 13 of 27 patients with a PC20 greater than 16 mg/mL and absent in 2 of 7 with a PC20 less than 4 mg/mL. CONCLUSIONS: Wheezing on maximal forced exhalation is neither sensitive nor specific for airway hyperreactivity.

Adult↗
PubMed1989

Impact of C-reactive protein (CRP) on surfactant function.

Plasma levels of the acute-phase reactant, C-reactive protein (CRP), increase up to one thousand-fold as a result of trauma or inflammation. CRP binds to phosphorylcholine (PC) in a calcium-ion dependent manner. The structural homology between PC and the major phospholipid component of surfactant, dipalmitoyl phosphatidylcholine (DPPC), led to the present study in which we examined if CRP levels might be increased in patients with adult respiratory distress syndrome (ARDS), and subsequently interfere with surfactant function. Our results showed that CRP levels in the bronchoalveolar fluid (BALF) was increased in patients with ARDS (97.8 +/- 84.2 micrograms/mg total protein vs. 4.04 +/- 2.2 micrograms/mg total protein in normals). Our results show that CRP binds to liposomes containing DPPC and phosphatidylglycerol (PG). As a result of this interaction, CRP inhibits the surface activity of a PG-DPPC mixture when tested with a Wilhelmy surfactometer or with the Enhorning pulsating bubble apparatus. Furthermore, the surface activity of a clinically used surfactant replacement, Surfactant TA (2 mg/ml), was also severely impaired by CRP in a dose-dependent manner (doses used ranging from 24.5 to 1,175 micrograms/ml). In contrast, human serum albumin (HSA) at 500 and 900 micrograms/ml had no inhibitory effect on Surfactant TA surface activity. These results suggest that CRP, although not an initiating insult in ARDS, may contribute to the subsequent abnormalities of surfactant function and thus the pathogenesis of the pulmonary dysfunction seen in ARDS.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1989

Acute and chronic hypoxic pulmonary hypertension in guinea pigs.

To determine whether the strength of acute hypoxic vasoconstriction predicts the magnitude of chronic hypoxic pulmonary hypertension, we performed serial studies on guinea pigs. Unanesthetized, chronically catheterized guinea pigs increased mean pulmonary arterial pressure (PAP) from 11 +/- 0.5 to 13 +/- 0.7 Torr in acute hypoxia (10% O2 for 65 min). The response was maximal at 5 min, remained stable for 1 h, and was reversible on return to room air. Cardiac index did not change with acute hypoxia or recovery. Guinea pigs exposed to chronic hypoxia increased PAP, measured in room air 1 h after removal from the hypoxic chamber, to 18 +/- 1 Torr by 5 days with little further increase in PAP to 20 +/- 1 Torr after 21 days. Cardiac index fell from 273 +/- 12 to 206 +/- 7 ml.kg-1.min-1 (P less than 0.05) after 21 days of hypoxia. Medial thickness of pulmonary arteries adjacent to terminal bronchioles and alveolar ducts increased significantly by 10 days. The magnitude of the pulmonary vasoconstriction to acute hypoxia persisted and was unabated during the development and apparent stabilization of chronic hypoxic pulmonary hypertension, suggesting that if vasoconstriction is the stimulus for remodeling, then the importance of the stimulus lessens with duration of hypoxia. In individual animals followed serially, we found no correlation between the magnitude of the acute vasoconstrictor response before chronic hypoxia and the severity of chronic pulmonary hypertension that subsequently developed either because the initial response was small and variable or because vasoconstriction may not be the sole stimulus for vascular remodeling in the guinea pig.

Acute Disease↗