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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies were performed measuring parameters of respiratory and circulatory function at rest and during maximum tolerable constant work rate treadmill exercise in 16 clinically well patients who had undergone heart-lung transplantation for end stage pulmonary hypertension. Ten patients were studied before and within eight weeks following transplantation. Long-term function with exercise was further evaluated with follow up studies at one year (n = 10) and two years (n = 6), posttransplantation. Posttransplant gas exchange and ventilation during exercise are essentially normal with neither being limiting to maximal exercise. Exercise capacity is significantly improved posttransplant, primarily as a result of improvement in the circulation over that found pretransplant in uncorrected pulmonary hypertension. Although improved, circulatory limitations of maximal exercise may still persist. Cardiorespiratory function at maximum tolerable exercise is well maintained following heart-lung transplantation for at least two years, providing no complications occur. This suggests that denervation of the heart and lungs, disruption of the bronchial circulation and pulmonary lymphatics, and the graft ischemia encountered at the time of transplantation impose no serious limitations on long-term cardiopulmonary function. The overall functional capacities of the transplanted heart and lungs are more than adequate for meeting the activities of normal life.
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PMID:Cardiopulmonary function at maximum tolerable constant work rate exercise following human heart-lung transplantation. 311 32

Lower torso ischemia and reperfusion has been shown to stimulate the generation of thromboxane (Tx)A2, leading to transient pulmonary hypertension and later to polymorphonuclear leukocyte accumulations in the lungs. This study investigated whether hind limb ischemia leads to increased pulmonary microvascular permeability. Anesthetized sheep (n = 6) previously prepared with a lung lymph fistula underwent 2 hr of tourniquet ischemia of both lower limbs. One minute following tourniquet release mean pulmonary arterial pressure (MPAP) rose from 14 +/- 1 to 36 +/- 4 mm Hg (p less than 0.05) and returned to baseline within 30 min. The pulmonary arterial wedge pressure of 4 +/- 1 mm Hg was unchanged. Plasma TxB2 levels rose from 211 +/- 21 to 304 +/- 52 pg/ml (p less than 0.05) 10 min after tourniquet release and were back to baseline at 30 min. Lymph flow (QL) rose from 4.3 +/- 0.6 ml/30 min to 8.3 +/- 1.8 ml/30 min (p less than 0.05); the lymph/plasma (L/P) protein ratio rose slightly but not significantly. In three sheep, inflation of a left atrial balloon increased left atrial pressure from 3 to 16 mm Hg. MPAP rose from 14 to 24 mm Hg. There was an increase in QL from 3.6 to 17 ml/30 min; the L/P protein ratio declined from 0.63 to 0.41. These results indicate that reperfusion following 2 hr of bilateral hind limb ischemia results in increased pulmonary microvascular permeability.
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PMID:Reperfusion of ischemic lower limbs increases pulmonary microvascular permeability. 336 2

Clinical studies have shown pulmonary and right ventricular hypertension to be important factors increasing the risk to patients during pulmonary angiography. This experiment was undertaken to define the hemodynamic changes induced by the administration of contrast material into the pulmonary arteries of dogs with embolic pulmonary hypertension, and to compare the effects of ionic and nonionic agents. Ten closed-chest dogs under light halothan anesthesia were subjected to pulmonary embolization with sephadex microspheres until severe pulmonary hypertension occurred and the cardiac output decreased to 50%-60% of the pre-embolization baseline. Intra-pulmonary injections of contrast material were performed in eight animals while hemodynamic indices were measured. Sodium methylglucamine diatrizoate induced severe, transient, hypotension associated with a large decrease in systemic vascular resistance and little change in the cardiac output. Hypotension is especially undesirable in the presence of pulmonary hypertension because it worsens the preexisting coronary ischemia and compromised right ventricular function. No elevation in mean pulmonary artery pressure was seen, and pulmonary vascular resistance decreased. Iohexol induced milder effects, perhaps because it exerts a less severe systemic vasodilatory effect and is not a negative inotrope. These findings suggest iohexol may be safer in the high risk patient, however, these data may not be directly applied to unanesthetized humans.
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PMID:The hemodynamic effects of the administration of ionic and nonionic contrast materials into the pulmonary arteries of a canine model of acute pulmonary hypertension. 337 76

Determination of the optimal time for surgical intervention in chronic mitral regurgitation has remained controversial. There are similarly important factors in favor of temporizing with medical treatment alone as there are in support of relatively early surgery (Table 1). Since rheumatic valvulitis may play a subordinate role, in contrast to etiologies such as myxomatous degeneration of the mitral valve, rupture of chordae tendineae, papillary muscle dysfunction due to coronary artery disease and other causes, left ventricular function is generally determined by the adaptations of the myocardium to the volume overload, or to ischemia or infarction from coronary artery disease rather than to a concomitant myocarditis. Based on actuarial survival curves in symptomatic patients with combined mitral regurgitation and stenosis or mitral regurgitation alone, it can be assumed that surgery can result in improved survival, in particular if a reconstructive mitral valve procedure rather than prosthetic valve replacement is performed. Medical treatment is carried out with digitalis to enhance myocardial contractility, diuretics and vasodilators to reduce pre- and afterload with resultant diminished effective mitral orifice area and regurgitant volume, lowering of pulmonary artery and pulmonary venous pressures and an increase in systemic cardiac output. Presently, however, there is no convincing evidence that symptom-status is improved or the natural history favorably affected over a number of years. For assessment of left ventricular myocardial function the end-systolic pressure/volume or the end-systolic stress/volume index appear preferable. Values of the latter less than or equal to 2.2 are associated with increased postoperative mortality and improbable improvement in functional status. Additionally, patients with an ejection fraction less than 40% or end-diastolic volume greater than 140 ml/m2 as well as those with end-diastolic dimension greater than 8 cm or end-systolic dimension greater than 5.5 cm have less favorable postoperative survival or further deterioration in ventricular function. Impaired right ventricular function secondary to the increased afterload imposed by pulmonary hypertension generally can be normalized postoperatively. Depression of right ventricular myocardial contractility is not, however, a common pathophysiologic feature in chronic mitral regurgitation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Timing of surgical intervention in chronic mitral regurgitation. 369 75

Diltiazem, nifedipine, and verapamil inhibit calcium entry into cells via different mechanisms with different pharmacologies. They display different relative effects on different cardiovascular functions, a complex interplay of direct actions and adrenergic reflexes. Peripheral arterial vasorelaxation causes adrenergic reflex activity which opposes their direct negative chronotropic, dromotropic, inotropic, and hypotensive actions. Verapamil's most potent activity is electrophysiologic, and nifedipine's effects are hemodynamic; diltiazem acts like a less-potent combination of verapamil and nifedipine. All three drugs are efficacious in angina. These three drugs may not be interchangeable in all patients, but individualization of therapy is possible. Future indications for calcium channel blocker therapy may include hypertrophic cardiomyopathy, cerebral vasospasm, migraine headaches, pulmonary hypertension, asthma, esophageal spasm, intestinal ischemia, Raynaud's phenomenon, dysmenorrhea, and premature labor.
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PMID:Calcium channel blockers in emergency medicine. 638 Mar 52

The paucity of donor hearts for human transplantation can be remedied by distant heart procurement. In the present study, 12 donor hearts obtained at distant locatins were preserved by infusion with 500 ml of cardioplegic solution at 4 degrees C at 150 mm Hg and immersion in 4 degrees C saline for rapid transmural cooling. They were transported in ice-cold saline. Maximal ischemic times were 110-182 minutes. Septal biopsies before coronary reperfusion showed normal mitochondria (11 and 12), normal nuclei (seven of 12), myofibrillar I-bands (six of 12), and capillary endothelial swelling (12 of 12). Septal biopsies 30 minutes after reperfusion showed mitochondrial swelling (six of 10), nuclear damage (10 of 10), myofibrillar contraction (10 of 10), and endothelial swelling (eight of 10). All grafts functioned satisfactorily. Eight of the 12 patients were alive 6-15 months later; four patients died (one of pulmonary hypertension and three of infection). We concluded that (1) human hearts show significant ultrastructural changes after 3 hours of ischemia, but (2) these worsen after reperfusion, and (3) distant heart procurement is feasible for human transplantation.
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PMID:Distant heart procurement for human transplantation. Ultrastructural studies. 699 23

A reproducible noninvasive monkey model for global brain ischemia with exact insult (no flow x 16 min) to the brain, with survival and with standardized preischemic, ischemic and postischemic variables is described. This model allowed us to demonstrate for the first time: 1) that a substantial part of brain damage early postischemia is reversible and amenable especially to barbiturate treatment; 2) that the postischemic brain shows increased vulnerability for additional insults. Optimal postischemic intensive monitoring and immobilization for 24-48 hours is important for improved outcome; 3) that immediate postischemic reperfusion pressure (MAP 110-150 mm Hg) significantly improves the outcome; 4) that heparinisation during ischemia has no protective effect and 5) that postischemic heparinisation and intravenous hemodilution does not ameliorate the outcome. The protective effect of trimetaphan against neurogenic pulmonary edema can be explained by the prevention of pulmonary hypertension but its protective effect on the development of secondary cerebral edema has to be elucidated.
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PMID:[Pathogenesis and treatment of anoxic encephalopathy. Definition and importance of experimental animal models (author's transl)]. 746 71

We studied the ocular findings of two adult patients with the Eisenmenger's syndrome who had atrial septal defects that were diagnosed before the age of 10 years but not operated on and pulmonary hypertension. Both eyes of these patients showed microaneurysms, multiple small blot hemorrhages, or capillary dilation in the temporal peripheral fundus. Multiple microaneurysms and retinal collaterals were confirmed by fluorescein angiography. One of the patients developed bilateral rubeosis iridis with slow progression. These retinal lesions and the rubeosis iridis are probably related to chronic ocular ischemia caused by chronic systemic hypoxia.
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PMID:Chronic ocular ischemia associated with the Eisenmenger's syndrome. 751 Apr 53

Immediately after hepatic reperfusion in human orthotopic liver transplantation, high amounts of arginase are released from the graft, thereby influencing nitric oxide metabolism. This metabolic alteration may be one component of the ischemia-reperfusion syndrome in OLT with its hemodynamic disturbances (e.g., systemic hypotension, pulmonary hypertension). The aim of this study was to compare hemodynamic and metabolic changes following OLT in the pigs with those obtained under arginase infusions in catheterized, anesthetized pigs. Following liver revascularization in the pigs, plasma arginase concentrations increased from 48 +/- 19 IU/L to 2613 +/- 944 IU/L, resulting in a drop in plasma levels of L-arginine (-87%) and in a drop in nitrite (-82%) and nitrate (-53%) concentrations. Of the measured organ-specific hemodynamic alterations, the mean pulmonary arterial pressure increased from 17 +/- 2 mmHg to 30 +/- 5 mmHg, whereas the flow/pressure index of the portal vein decreased about 60%. A primed continuous infusion of arginase (25,000 IU) increased plasma arginase levels to a maximum of 3,690 +/- 962 IU and evoked a decrease of L-arginine, but did not alter plasma nitrite or nitrate levels. The administration of arginase in healthy pigs did not influence cardiac output, mean arterial pressure, heart rate, or total peripheral resistance, but led to an increase of mean pulmonary arterial pressure from 19 +/- 3 to 48 +/- 5 mmHg and to a reduction of arterial hepatic blood flow from 229 +/- 65 ml/min to 154 +/- 41 ml/min. From this we conclude that high levels of liver arginase cause hemodynamic alterations in the lung and the liver. We hypothesize that the pulmonary hypertension and the reduced hepatic blood flow found during the immediate reperfusion period after OLT are possibly related to the increased arginase release due to the hepatic damage of the graft.
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PMID:Arginase release following liver reperfusion. Evidence of hemodynamic action of arginase infusions. 777 69

Vascular remodeling is a general term describing any change in blood vessel structure caused by hemodynamic changes, such as flow and pressure, injury, or disease. It also encompasses development and vascularity. This review focuses on the implications of remodeling from both structure and function of isolated arteries and on how a remodeled vascular bed responds to vasoactive stimuli. Essential, genetic, experimental, and pulmonary hypertension, endothelial dysfunction in atheroma, vascular surgery, subarachnoid hemorrhage, congestive heart failure, coronary collateralization, ischemia, and pregnancy are among the examples discussed in this review. Research efforts should be directed toward understanding the processes of cell-cell interaction underpinning these changes in structure and function. Much could be gained from better measurement of vascular structure and full stimulus-reactivity relationships under in vivo conditions in a variety of vascular beds and models of animal and human hypertension. Mathematical models of the average vascular structure drawn from experimental data aid clear thinking when discussing the remodeling process.
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PMID:Arteriolar structure and its implications for function in health and disease. 785 Apr 18


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