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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pulmonary arterial hypertension, defined as a mean pulmonary artery pressure exceeding 20 mmHg has been observed both in experimental animal and human sepsis, even before development of the adult respiratory distress syndrome. In this article we review several mechanisms that have been invoked for the pulmonary arterial hypertension associated with sepsis (and the adult respiratory distress syndrome): obstruction of the pulmonary microcirculation with microthrombi composed of platelets and leukocytes, and active pulmonary vasoconstriction induced by the autonomous nervous system, hypoxia or vasoactive humoral factors ("mediators"). Some of these mediators, in particular serotonin and arachidonic acid metabolites have been the subject of substantial research and therapeutic manipulation. Since pulmonary arterial hypertension imposes an increased afterload to the right ventricle and because right ventricular dysfunction appears to be a major determinant of the outcome of sepsis, the study of the mechanisms involved in pulmonary arterial hypertension may lead to improved management of sepsis and septic shock.
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PMID:Pulmonary arterial hypertension in sepsis and the adult respiratory distress syndrome. 131 81

EDRF is a potent, endogenous vasodilator that is produced and released from endothelial cells and subsequently causes the relaxation of VSM through the activation of soluble guanylate cyclase and an increase in VSM cyclic GMP. Structurally, EDRF is likely to be NO or a related nitrogen oxide-containing compound. It is synthesized in endothelial and other cell types from L-arginine by a calcium-calmodulin and NADPH-dependent enzyme. Its action is very similar to the nitrovasodilators that act directly on VSM. EDRF is present in all vascular beds, large and small vessels, and in a wide range of species. Its role in human vascular physiology and pathophysiology is just beginning to be understood. EDRF is a potent endogenous vasodilator and inhibitor of platelet aggregation and adhesion. Its activity is impaired in hypertension and atherosclerosis, and its absence due to endothelial damage may play a role in cerebral and coronary vasospasm. It is a mediator of flow-dependent vasodilation, and its inhibition by hypoxia may contribute to the hypoxic pulmonary vasoconstrictor response. Endothelial cell damage and impairment of EDRF production may also contribute to acute and chronic pulmonary hypertension. A further understanding of the chemical nature and synthetic pathways of EDRF should lead to the production of analogs and antagonists, which may play an important role in future treatments for atherosclerosis, myocardial infarction, angina, hypertension, and other vascular diseases. The recent realization that EDRF serves as the second messenger for guanylate cyclase activation and cyclic GMP production in a variety of cell types outside of the cardiovascular system, including renal and respiratory epithelium, cerebellar neurons, macrophages, and adrenocytes, suggests even broader implications. The importance of EDRF to the anesthesiologist may go beyond an understanding of its role in cardiovascular physiological and pathophysiological states. Initial studies have shown that the endothelium may play a role in mediating the vascular actions of anesthetics, and that anesthetics can inhibit the production, release, or action of EDRF. How are these interactions mediated? Are there significant differences between anesthetics with regard to their effects on EDRF? Is there a clinically significant effect of anesthetics on basal activity of EDRF, or only in response to exogenous stimulation? Conversely, it is important to determine if alterations in endothelial cell function by various disease states such as hypertension, atherosclerosis, adult respiratory distress syndrome, cerebral vasospasm, and others cause changes in the vascular actions of anesthetics. The potential interactions of anesthetics with EDRF production and action in cell types other than the endothelium have not yet been explored.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Endothelium-derived relaxing factor: basic review and clinical implications. 186 89

Alterations in right ventricular (RV) performance are critical to the cardiac dysfunction witnessed in adult respiratory distress syndrome (ARDS), septic shock (SS), and as a consequence of positive end-expiratory pressure (PEEP) administration during mechanical ventilation. The authors review evidence for right heart dysfunction in these circumstances. In ARDS, an increase in RV afterload with the onset of pulmonary artery hypertension is the predominant factor promoting RV dysfunction. In SS, most investigators agree that a primary decrease in myocardial contractility is the major factor limiting RV performance. The application of PEEP during mechanical ventilation can potentiate alterations in RV preload, afterload, and/or contractility, all of which promote RV dysfunction and compromise left ventricular filling. As RV dysfunction may seriously affect global myocardial performance in all of these settings, the clinician must identify that RV function is impaired, discern the contributing mechanism, and select an appropriate therapeutic regimen targeted at addressing this predominant mechanism. Assessment and management strategies are described.
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PMID:Noncardiogenic mechanisms of right heart dysfunction. 194 Oct 46

Several approaches to non-respiratory management of adult respiratory distress syndrome (ARDS) are discussed. (1) Diagnosis and therapy of the underlying disease is a primary goal in order to avoid the ongoing process of lung injury. (2) Specific pharmacologic therapy for primary lung injury is not available even after 25 years of immunologic research, because no specific mediator has yet been identified as a primary pathogenic factor in ARDS, which is a heterogenous clinical syndrome. (3) Supportive therapy (i.e. improving right ventricular dysfunction and treating pulmonary arterial hypertension) should be emphasized. (4) The most important approach is to optimize prophylactic management to avoid nosocomial infection by eliminating unnecessary invasive techniques, changing the patients' positioning and conserving organ function. So far the latter approach seems to be the only way to improve survival in respiratory failure.
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PMID:[Non-respiratory therapy of adult respiratory distress syndrome]. 194 50

Severe pulmonary edema occurred in a patient during the third trimester of two consecutive pregnancies, 17 months apart. Noncardiac origin of the pulmonary edema was demonstrated by normal pulmonary capillary wedge pressures, normal roentgenographic cardiac dimensions with absence of effusions, normal echocardiographic ejection fraction, and elevated thermodilution cardiac outputs; moderate reduction in serum albumin levels may have contributed. In the setting of pregnancy-induced hypertension, the development of ARDS on each occasion suggests a pathophysiologic link.
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PMID:Recurrent noncardiac pulmonary edema accompanying pregnancy-induced hypertension. 195 25

Hemodynamic and respiratory parameters were continuously monitored in 45 septic shock patients, 15 of whom developed adult respiratory distress syndrome (ARDS). Low oxygenation index (OI = PaO2/FIO2), pulmonary artery hypertension (high mean pulmonary artery pressure, MPAP) and elevated pulmonary vascular resistance (PVR) were observed in all ARDS, as well as in non-ARDS septic patients, as a baseline. These same pulmonary factors were compared between those who survived and those who died during the first few days (early fatalities) in both the ARDS group (5 patients) and the non-ARDS group (8 patients). The results showed that the early fatalities in the ARDS group had a significantly lower (p less than 0.001) OI than the survivors, as well as a lower MPAP (p less than 0.01). In the non-ARDS group, the MPAP of the early fatalities was significantly lower (p less than 0.01) than that of survivors, but their OI was not significantly lower. PVR, when compared between groups (ARDS versus non-ARDS) or between subgroups within each group, was elevated concurrently with the elevation of MPAP. It is concluded that patients with septic shock and ARDS who show a severely depressed OI and a modestly elevated MPAP and PVR during the first few days can be predicted to have a poor outcome.
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PMID:Low oxygenation index and pulmonary artery hypertension in predicting early death from adult respiratory distress syndrome (ARDS). 197 59

Since 1978, decompressive craniotomy was performed according to a standardized protocol. Exclusion criteria were age greater than or equal to 40 years, deleterious primary brain damage, operable space occupying lesions, larger infarctions in CT scan or irreversible brain stem incarceration/ischaemic damage as shown by bulbar syndrome, loss in BAEP or oscillating flow in TCD. Indication was given by progressive intracranial hypertension not controllable by conservative methods, if ICP decompensation was correlated with clinical (GCS, extension spasms, mydriasis) and electrophysiological (EEG, SEP, CCT) deteriorations. 18 patients were decompressed by unilateral. 19 by bilateral craniotomy with large fronto-parieto-temporal bone flap and a dura enlargement by use of temporal muscle/fascia. 37 patients at an age of 18 +/- 7 (4-34) years were operated 5 h-10 d after trauma. Recovery was surprisingly good: only 5 died, 2 due to an ARDS; 3 remained vegetative, all others achieved full social rehabilitation or remained moderately disabled. The best predictor of a favourable outcome was an initial posttraumatic GCS greater than or equal to 7. These in younger patients with delayed posttraumatic decompensation before irreversible ischaemic damage occurs.
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PMID:Traumatic brain swelling and operative decompression: a prospective investigation. 208 28

A good model of adult respiratory distress syndrome is lung injury induced by phorbol myristate acetate (PMA). In the present study we examined the effect of mepacrine, an inhibitor of phospholipase A2, on lung injury induced by PMA in isolated blood-perfused rat lungs. In the isolated lung, saline (1 ml) or mepacrine (75 microM) alone in the perfusion system did not discernibly change the pulmonary arterial pressure (PAP) and lung weight (LW). After administration of PMA (0.16 micrograms/ml), severe hypertension and lung edema developed (delta PAP = 40.1 +/- 6.0 mmHg, p less than 0.001; delta LW = 5.5 +/- 0.7 g, p less than 0.001). Whereas, the addition of mepacrine (75 microM) prevented PMA-induced lung edema and pulmonary hypertension (delta PAP = 4.7 +/- 2.2 mmHg, delta LW = 0.2 +/- 0.2 g). To further elucidate the protective mechanism of mepacrine on lung injury, a vasodilator (nitroprusside) was given to decrease PAP levels to +6 mmHg from baseline values in the PMA group, as well as in the mepacrine-pretreated PMA (MPMA) group. During a subsequent venous pressure challenge, severe lung injury developed in the PMA group (delta LW = 9.5 +/- 2.1 g, p less than 0.001). However, with the same venous pressure challenge in the MPMA the lung weight was markedly less than that of the PMA group (delta LW = 1.0 +/- 0.2 g). Histologic findings examined by light microscopy presented intraalveolar hemorrhage and fluid accumulation, disruption of vascular basements and alveolar septa, and aggregation of inflammatory cells within the parenchyma in the lungs of the PMA group. In the MPMA group there was no evidence of intraalveolar hemorrhage and alveolar fluid accumulation, however, the occasional presence of granulocytes in the parenchyma and slight interstitial edema were still observed. In addition, depressed the chemiluminescence release from PMA activated granulocytes which were in a dose-dependent manner in vitro. These observations suggest that mepacrine inhibits PMA-induced lung injury chiefly by protection of vascular permeability. The mechanism of the protection may be due to the inhibition of oxygen radicals released from activated neutrophils and the reduction of neutrophil chemotaxis.
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PMID:The protective effect of mepacrine on acute lung edema induced by phorbol myristate acetate in rats. 209

Nine patients who had developed pulmonary artery hypertension during the adult respiratory distress syndrome (ARDS) were treated with an infusion of prostacyclin (PGI2) (12.5-35.0 ng.kg-1.min-1). Whether PGI2 might decrease the pulmonary capillary pressure (PCP) obtained by analysis of the pulmonary artery occlusion pressure decay curve and improve systemic oxygen delivery was examined. Gas exchange alterations induced by PGI2 were analyzed by using the multiple inert gas elimination technique. PGI2 reduced the pulmonary artery pressure from 35.6 to 28.8 mmHg (P less than 0.001) and the PCP from 22.9 to 19.7 mmHg (P less than 0.01) without changing the contribution of the pulmonary venous resistance to the total pulmonary vascular resistance. The cardiac index increased from 4.2 to 5.7 1.min-1.m-2 (P less than 0.001) due to both increased stroke volume and heart rate. Despite a marked deterioration of ventilation-perfusion (VA/Q) matching with increased true intrapulmonary shunt flow from 28.6% to 38.6% (P less than 0.01) of the cardiac output, the PaO2 was unchanged due to increased mixed venous oxygen content indicated by an augmented mixed venous PO2 (from 37.0 to 41.9 mmHg, P less than 0.01). This caused a 35% (P less than 0.001) increase of the systemic oxygen delivery rate. Thus, short-term infusions of PGI2 reduced PAP and PCP without deleterious effects on arterial oxygenation in patients with ARDS. Hence, PGI2 may be useful to lower pulmonary vascular pressures in patients with ARDS.
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PMID:Prostacyclin for the treatment of pulmonary hypertension in the adult respiratory distress syndrome: effects on pulmonary capillary pressure and ventilation-perfusion distributions. 211 82

Eight patients who developed pulmonary artery hypertension during the adult respiratory distress syndrome (ARDS) were treated with an infusion of prostacyclin (PGI2, 12.5-35.0 ng.kg-1.min-1) for 45 min. We examined whether reducing the right ventricular (RV) outflow pressures by PGI2 infusion would increase the right ventricular ejection fraction (RVEF) measured by thermodilution. PGI2 reduced the pulmonary artery pressure (PAP) from 35.6 to 29.1 mmHg (p less than 0.01). The cardiac index (CI) increased from 4.2 to 5.81.min-1.m-2 (p less than 0.01) partly due to an increased stroke volume. The decreased PAP together with the increased CI resulted in a fall of the calculated pulmonary vascular resistance index (PVRI, from 5.1 to 2.5 mmHg.min.m2.1-1, p less than 0.01). In the patients with subnormal baseline RVEF the increased stroke volume was associated with an increased RVEF (from 47.6% to 51.8%, p less than 0.05) suggesting improved RV function. This result was underscored by a significant relationship between the changes in PVRI and RVEF (r = 0.789, delta % RVEF = 2.11.delta PVRI-1.45). Despite an increased venous admixture from 27.8% to 36.9% (p less than 0.05) the arterial PO2 remained constant resulting in an increased oxygen delivery from 657 to 894 ml.min-1.m-2 (p less than 0.01). We conclude that short term infusions of PGI2 increased CI concomitant to improved RV function parameters when baseline RVEF was depressed. Since improved oxygen availability should be a major goal in the management of patients with ARDS PGI2 may be useful to lower pulmonary artery pressure in ARDS.
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PMID:Prostacyclin and right ventricular function in patients with pulmonary hypertension associated with ARDS. 211 42


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