Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute lung injury as a remote sequela of severe lower torso ischemia-reperfusion has been demonstrated experimentally, in a process involving leukosequestration and generation of the arachidonate derivatives thromboxane and leukotriene B4. However, contemporary clinical reports have been limited to development of transient, subclinical "reperfusion pulmonary edema" several hours after declamping in patients undergoing elective abdominal aortic aneurysm repair. This report refocuses attention on the clinical syndrome of severe, acute deterioration in pulmonary function occurring several hours after restoration of perfusion to an ischemic lower torso in two patients. The lung injury is characterized by progressive hypoxemia, pulmonary hypertension, decreased lung compliance, and non-hydrostatic pulmonary edema, consistent with adult respiratory distress syndrome (ARDS). This report reinforces the concept that humoral mediators generated at reflow may induce end-organ injury at a site remote from the focus of ischemia-reperfusion, and that the lung is a target organ.
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PMID:Pulmonary failure following lower torso ischemia: clinical evidence for a remote effect of reperfusion injury. 789 94

Indomethacin, a prostaglandin synthetase inhibitor, is an effective tocolytic agent that may have adverse fetal side effects such as constriction of the ductus arteriosus, pulmonary hypertension, and reduced urine production. We describe an unusual neonatal complication following 6 days of tocolysis with indomethacin. A 22-year-old gravida 5, para 3104 was admitted at 25 weeks of gestation in labor. Attempts to stop labor using magnesium sulfate and terbutaline failed. The contractions stopped following the administration of indomethacin, which was continued for 6 days. On day 7, due to contractions and vaginal bleeding, she underwent a classic cesarean section. The female newborn, weighting 1044 g, did well for 2 days, when she developed pneumoperitoneum. On laparotomy, an isolated midileal perforation was found, with otherwise normal-appearing bowel. Isolated intestinal perforation has been described in premature neonates who were treated with indomethacin for patent ductus arteriosus. This complication is caused by splanchnic ischemia secondary to the loss of the vasodilatory effect of prostaglandins. This case indicates that this rare but serious complication may also follow intrauterine exposure to indomethacin.
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PMID:Isolated small bowel perforation following intrauterine treatment with indomethacin. 794 25

In the complex setting of cardiac surgery and cardiopulmonary bypass, several potent mediators are released that by interacting may cause clinical syndromes like coronary ischemia, systemic hypertension, pulmonary hypertension, and renal failure. One of the mediators is serotonin, released from aggregating platelets, and causing vasoconstriction by activating S2-serotonergic receptors, particularly in patients with an impaired endothelial function, as in atherosclerosis. The most important available specific S2-serotonergic receptor antagonist is ketanserin. If administered during or after cardiac surgery, ketanserin lowers systemic and pulmonary blood pressure, and improves peripheral and pulmonary perfusion without causing reflex tachycardia or an increase in pulmonary shunt fraction.
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PMID:The role of serotonin blockers in cardiac anesthesia. 794 6

Abnormal smooth muscle cell (SMC) proliferation is observed in several pathological situations such as atherosclerosis, pulmonary hypertension, and venous pathologies, resulting in a thickening of the vessel wall. If endothelial cells have been assumed to play a role in the triggering of this proliferation, no direct evidence is available. As ischemia is often linked to these situations, we exposed human umbilical vein endothelial cells (HUVEC) to hypoxia. The HUVEC-conditioned medium was then added to SMC and the proliferation of these cells was measured. We observed a pro-proliferative activity for SMC of the hypoxic HUVEC-conditioned medium but not of the normoxic HUVEC one. This pro-proliferative activity could not be inhibited if HUVEC were treated with cycloheximide but was blocked if the synthesis of prostaglandins by HUVEC was inhibited during hypoxia. PGD2, and especially PGF2 alpha at the concentration found in the hypoxic HUVEC-conditioned medium, were demonstrated to have a mitogenic effect on SMC. PGE2 also showed a pro-proliferative activity but at higher concentrations. In addition, the kinetics of increase in SMC proliferation induced by a mixture of the four prostaglandins at the corresponding concentrations was the same as the one observed with hypoxic HUVEC-conditioned medium. However, when tested on fibroblasts which do not respond to PGF2 alpha, hypoxic HUVEC-conditioned medium also had a pro-proliferative activity. In addition, anti-bFGF antibodies but not anti-PDGF blocked the mitogenic activity of this conditioned medium for SMC. Finally, the mitogenic effects of PGF2 alpha and of bFGF on SMC are additive. These results indicate that bFGF is probably also involved. These results indicate that these prostaglandins act in synergy with bFGF and are the molecules responsible for the pro-proliferative activity observed in hypoxic HUVEC-conditioned medium. We propose that these findings can explain the excessive growth of SMC in blood vessels following chronic ischemic situations.
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PMID:Hypoxia stimulates human endothelial cells to release smooth muscle cell mitogens: role of prostaglandins and bFGF. 802 Jun 5

In 31 patients who had undergone cardiac orthotopic transplantation, valvular regurgitation was studied by echocardiographic and pulsed Doppler over 2 years. The first week after cardiac transplantation, transplant recipients had an increase in the severity of tricuspid, mitral (group II), and aortic regurgitation, as well as a greater number of simultaneously regurgitating valves when compared with those in a group of 60 normal subjects of similar age to heart donors: transplant recipients, trivalvular regurgitation 48% (95% confidence interval [CI] 30 to 66) vs control group, 5% (CI 1 to 13; p < 0.001). Moderate-severe tricuspid regurgitation (TR) was the most frequent occurrence (55%, CI 36 to 73) followed by pulmonary (PR) (42%, CI 25 to 61), moderate mitral (MR) (32%, CI 15 to 51), and mild aortic (AR) (23%, CI 10 to 43) regurgitation. These regurgitations were asymptomatic at rest except for TR. TR was associated with right-sided heart failure in 76% of patients in the early postoperative period and controlled with diuretic drugs. This regurgitation correlated with persistence of post-transplant pulmonary hypertension (r = 0.6) and was not related to pulmonary hypertension before cardiac transplant. There was also no relation found between donor ischemia time or episodes of cardiac rejection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Quantitative assessment of valvular function after cardiac transplantation by pulsed Doppler echocardiography. 820 38

Early cardiac graft failure has been reported to occur in 4-25% of patients undergoing orthotopic heart transplantation. To further elucidate the characteristics and prognosis of patients with graft failure, we retrospectively identified 10 patients from a series of 212 consecutive recipients with catastrophic graft dysfunction in the absence of acute cellular rejection, right ventricular failure secondary to pulmonary hypertension and technical factors. We present a case report and the experience from one transplant center, a review of the literature and possible strategies for the management of early graft failure. Mean onset of graft failure was 6.5 days (range intraoperative to 23 days). Multivariable analysis revealed a longer total ischemic time in patients with early graft dysfunction (200 +/- 14 vs. 166 +/- 4 min). No episodes of hyperacute rejection were observed. Pathologic changes noted on biopsy or autopsy included ischemia in 9 and vascular rejection in 1. The mortality at 60 days was 50%. Early use of aggressive mechanical and pharmacological support is described and appears to be important for graft salvage.
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PMID:Early cardiac allograft failure after orthotopic heart transplantation. 827 37

The value of pulsed-wave transmitral Doppler for the diagnosis of moderate acute rejection was examined in a total of 347 Doppler recordings obtained in 32 consecutive cardiac allograft recipients. Serial Doppler examinations (median, 11 per patient; range, 1 to 23) were performed simultaneously with endomyocardial biopsies from the first week after heart transplantation to a follow-up of 186 days (median; range, 10 to 395 days after transplantation). Pulsed-wave transmitral Doppler did not allow noninvasive diagnosis of moderate acute rejection in individual patients. Peak filling rate normalized for mitral stroke volume, early diastolic velocity, and mean diastolic velocity were significantly increased, whereas diastolic filling period was decreased during moderate acute rejection compared to other biopsy classes. The wide overlap of measurements in individual recipients with or without rejection may be due, however, to a variety of hemodynamic factors after transplantation affecting diastolic function, which are superimposed on the restrictive left ventricular filling pattern caused by persistent mild acute rejection and left ventricular hypertrophy. These hemodynamic factors include pulmonary hypertension, perioperative ischemia, reperfusion injury, and changes in both blood pressure and loading conditions caused by hypertension and its treatment. Differences between studies with regard to the detection of moderate acute rejection by transmitral Doppler may be caused by chance, because most studies were relatively small. Differences in methods, patient selection, duration of follow-up, prevalence of hypertension and left ventricular hypertrophy, and differences in antihypertensive drug regimens may also play a role. Furthermore differences in the incidence of mild acute rejection, its treatment, and the type of maintenance immunosuppressive regimen used may have influenced the outcome of these studies considerably.
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PMID:Pulsed-wave transmitral Doppler do not diagnose moderate acute rejection after heart transplantation. 832 11

Right ventricular ischemia occurs in experimental models of pulmonary hypertension. We analyzed right ventricular size and function and 201Tl uptake to determine if there was a relationship between 201Tl uptake and systolic function in 19 patients with pulmonary artery hypertension who were being evaluated for heart-lung transplantation. All patients had dipyridamole stress 201Tl scintigraphy, radionuclide angiography and echocardiography. In nine patients (Group 1), right ventricular ejection fraction was < 30% (mean 22% +/- 8%). In 10 patients (Group 2) it was > 30% (mean 45% +/- 11%). In Group 1, right ventricular 201Tl uptake in the lateral wall after dipyridamole was increased compared to Group 2 (40% +/- 7% versus 28% +/- 15% counts/pixel, p < 0.05) while left ventricular free wall uptake was similar. The ratio of right to left ventricular 201Tl uptake was increased in Group 1 versus Group 2 (0.81% +/- 0.30% versus 0.49% +/- 0.18%, p < 0.05). At 4 hr, right ventricular free wall 201Tl clearance was comparable, 51% +/- 13% versus 51% +/- 18% in Groups 1 and 2, respectively. No patient had perfusion abnormalities. Right ventricular ejection fraction was inversely related to dipyridamole stress right ventricular 201Tl uptake, r = -0.49, p < 0.03, s.e.e. = 13.6. Right ventricular 201Tl uptake was directly related to right ventricular wall thickness (r = 0.56, p = 0.18, s.e.e. = 10.4). Therefore, patients with more severe right ventricular systolic dysfunction have greater 201Tl uptake after dipyridamole stress, suggesting increased myocardial mass and possibly blood flow in response to hypertrophy. Patients with the most marked hypertrophy have impairment of right ventricular systolic function, independent of ischemia.
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PMID:Right ventricular thallium-201 kinetics in pulmonary hypertension: relation to right ventricular size and function. 841 Feb 84

Right ventricular ejection may be modified by alterations in pulmonary vascular properties during acute pulmonary hypertension. Pulmonary artery impedance and reflection properties were analyzed during coronary angioplasty in nine patients with single-vessel disease involving the left anterior descending artery by use of high-fidelity catheter recordings of pulmonary pressure and flow made before angioplasty balloon inflation and at peak ischemia. Acute pulmonary hypertension in this resting model resulted in a significant decrease in pulmonary vascular resistance (142 +/- 54 to 92 +/- 64 dyn.s.cm-5, P < 0.05), increase in low-frequency impedance (67 +/- 36 to 101 +/- 43 dyn.s.cm-5, P < 0.05), and no change in high-frequency (characteristic) impedance (38 +/- 14 to 41 +/- 13 dyn.s.cm-5). Pulmonary wave reflection amplitudes were increased, and the amount of hydraulic power expended per unit of net forward flow significantly increased (3.1 +/- 0.7 to 4.3 +/- 0.7 mW.ml-1.s-1, P < 0.001). These findings indicate that, during acute pulmonary hypertension in humans, 1) recruitment of additional resistance vessels can occur, 2) pulsatile pulmonary artery properties are significantly altered, and 3) right ventricular power output requirements are increased. Because episodic pulmonary hypertension occurs frequently in coronary artery disease, these changes may help explain eventual right ventricular hypertrophy or failure.
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PMID:Pulmonary impedance and right ventricular-vascular coupling during coronary angioplasty. 844 88

Exposure of isolated perfused rabbit lungs (IPL) to ischemia-reperfusion causes a transient increase in pulmonary arterial (PA) pressure at the onset of reperfusion. Because thromboxane A2 (TxA2) is a potent vasoconstrictor, we hypothesized that it may contribute to the ischemia-reperfusion-induced pressor response. To evaluate this hypothesis, we exposed IPL perfused with a cell-free solution to 40 min of warm ischemia followed by reperfusion and measured perfusate immunoreactive thromboxane B2 (iTxB2) and 6-ketoprostaglandin F1 alpha (i6-keto-PGF1 alpha). We observed that ischemia-reperfusion IPL compared with controls had an increase in PA pressure (40.2 +/- 4.8 vs. 9.3 +/- 0.3 mmHg, P < 0.05), lung edema (29.3 +/- 6.3 vs. -0.2 +/- 0.2 g, P < 0.05), iTxB2 perfusate levels (155 +/- 22 vs. < 50 pg/ml, P < 0.05), and i6-keto-PGF1 alpha (436 +/- 33 vs. 61 +/- 16 pg/ml, P < 0.05). In ischemia-reperfusion IPL, infusion of SQ 29548 (10(-6) M), a specific TxA2/prostaglandin H2 receptor antagonist, attenuated the PA pressor response and the degree of edema. We conclude that pulmonary hypertension associated with ischemia-reperfusion results in part from pulmonary release of TxA2. Furthermore, TxA2 directly through membrane effects or indirectly through hydrostatic mechanisms increases the severity of ischemia-reperfusion-induced lung edema.
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PMID:Thromboxane contributes to pulmonary hypertension in ischemia-reperfusion lung injury. 844 95


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