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

This review provides a summary and assessment of research involving renal prostaglandins. Arachidonic acid released from phospholipids is converted by prostaglandin cyclo-oxygenase in the kidney to PGF2, PGF2alpha, PGD2, and, possibly, to PGI2 and thromboxane A2. Production of PGE2 and PGF2alpha is predominately but not exclusively in the medulla, whereas degradative enzymes are present in both cortex and medulla. Prostaglandins enter the tubular lumen by facilitated transport and are partially reabsorbed from the urine in the distal nephron. Urine prostaglandins probably reflect renal synthesis. PGE2 and endoperoxides stimulate and PGF2alpha and indomethacin inhibit renal renin synthesis. In response to ischemia, vasoconstriction, or angiotensin II the kidney increases prostaglandin synthesis to modulate renal vascular resistance. In conscious animals or man no role has been established for prostaglandins in the maintenance of basal renal blood flow or renal sodium excretion. PGE influences renal water excretion by inhibiting the action vasopressin. Despite conflicting data there is evidence that renal prostaglandins are involved either primarily or secondarily in many types of hypertension. Inhibitors of prostaglandin cyclooxygenase have been used with success in Bartter's syndrome. Conflicting results in many areas of investigation may be resolved by the use of more accurate and reliable assays, careful handling of samples, and the use of urine to further investigate renal prostaglandin synthesis.
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PMID:Prostaglandins and the kidney. 33 46

In 30 human subjects, experimental pain was produced by either ischemia or cold-water immersion. In a double-blind procedure, intravenous doses of up to 10 milligrams of naloxone hydrochloride in saline were indistinguishable from similarly administered saline alone. There were no effects on subjective pain ratings, finger plethysmograph recordings, or responses to mood-state questionnaires. These laboratory procedures do not activate any functionally significant pain-attenuating or mood-altering effect of endorphins.
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PMID:Endorphins: naloxone fails to alter experimental pain or mood in humans. 34 50

Current evidence is inconclusive regarding the possibility that positive end-expiratory pressure (PEEP) redistributes flow and may be directly responsible for systemic organ dysfunction. This study tests the hypothesis that PEEP may induce abnormalities in the distribution of cardiac output (CO). Eight anesthetized dogs were studied during (1) 0 cm H2O PEEP (Z1), (2) 15 cm H2O PEEP (P), (3) Z2, and (4) bleeding (B) to reduce the CO to the same level as P. At each of the four periods, a different 15 mu radiolabelled microsphere was injected into the left atrium. Another four dogs were used to varify that each type of microsphere had the same flow distribution. CO fell from 3.1 liters/min to 1.9 during P (P smaller than 0.01) and to 2.0 during B (P smaller than 0.01). Mean arterial pressure (MAP) declined from 102 to 83 mm Hg (P smaller than 0.01) and 86 mm Hg (P smaller than 0.01(, respectively. Left atrial pressure (LAP) rose from 5.0 to 7.9 mm Hg during P (P smaller than 0.01) and fell during B to 2.7 mm Hg. c0 and its distribution were the same during Z1 and Z2. P caused selective reductions in hepatic (52%), adrenal (25%), and bronchial (24%) blood flows (P smaller than 0.01). In contrast, total flow to these organs during B was the same as during Z. Total renal flow was unchanged by P or B, but the cortical:medullary flow ratio increased during P from 24 to 49 (P smaller than 0.01) and was unchanged by B. P induced a decrease in fundal nucosal flow as compared with Z (P smaller than 0.01). Total coronary flow fell from 100 to 64 ml/min during both P and B (P smaller than 0.01). P led to a selective fall in subendocardial flow (67 ml/min X 100 gm) as compared with B (82.5 ML/MIN X 100 gm, P smaller than 0.01) as well as in the subendocardial:subepicardial flow ratio (1.069 vs. 1.112 ml/min X 100 gm, P smaller than 0.05). It is likely that the higher left ventricular filling pressure (LAP) during P as compared with during B compressed the endocardium and induced relative ischemia. Similarly the high airway pressure during P may have impeded bronchial mucosal flow. The causes and consequences of the other P-induced variations in flow are speculative.
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PMID:Abnormalities in organ blood flow and its distribution during positive end-expiratory pressure. 37 48

Altering the position (elevated or dependent) had no immediate effect on the blood supply of delayed or transplanted delayed tubed flaps. However, after 72 hours the mean survival length in the dependent tubes was less than that in the elevated tubes. (This difference was only significant in the delayed untransplanted flaps, and not so in the delayed transplanted flaps). All of the dependent tubes had a significant increase in water content (compared to the elevated tubes). This increase was greater in the transplanted delayed tubed flaps. The tissue pCO2 levels were significantly increased after 24 hours in the dependent transplanted tubes, reflecting poor circulation and ischemia in them. The rate of clearance of subcutaneously injected technetium-99m was significantly increased in the dependent transplanted tubes after 72 hours, while in the elevated tubes the clearance rate was similar to that in normal skin. The morphological appearance of the vessels in these flaps complemented the results of the functional study.
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PMID:The effects of gravity on delayed and transplanted delayed tubed flaps. 37 36

The tissue H2O of rabbit heart and rat liver was partially exchanged in situ with D2O. In rat liver, the loss of ATP, resulting from normothermic ischemia, was decreased after perfusion with D2O. The maximal protective effect was found when the proportion of D2O in the water of the liver tissue was 0.20. In both organs the protective effect of D2O could be correlated with a marked decrease in severe ischemic damage of cellular organelles, in particular mitochondria. D2O also increased the protective action of Mg-ions in the heart.
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PMID:[Organ preservation by heavy water (D2O). Morphological and biochemical studies on heart and liver (author's transl)]. 43 27

The efficacy of surface cooling and intraluminal antiseptic solutions for short term preservation of intestinal segments in preparation for free tissue transfer were investigated. Five segments of the small intestine and five segments of the colon were allocated to each group as follows: group 1, ischemia at 37 degrees C.; group 2, ischemia at 6 to 12 degrees C., and group 3, ischemia at 6 to 12 degrees C. plus povidone-iodine intraluminally. Histologic grading of segments allowed assessment of the efficacy of short term protection against ischemic changes. Surface cooling effectively prevented histologic evidence of ischemia. No additional benefit was observed using povidone-iodine intraluminally. Significant changes in tissue water content and evidence of bacterial invasion were not observed.
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PMID:Effects of cooling and intraluminally administered antiseptics on surgically induced ischemia of the intestine in dogs. 47 99

Potassium (34 mEq/L) cardioplegia was induced with cold blood (CBK) in three groups of six dogs undergoing 60 minutes of myocardial ischemia at a systemic temperature of 27 degrees +/- 2 degrees and a myocardial temperature of 7 degrees +/- 2 degrees C (crushed ice). Group 1 (CBK) animals were reperfused initially with 400 ml cold blood over 8 to 10 minutes at increasing pressures of up to 75 mm Hg. Group II (CBK-K) dogs were reperfused in the same manner as Group I with the addition of potassium chloride, 30 mEq/L. In Group III (CBKG-KG) glutathione, 30 mg/100 ml, was added to both the pre- and postischemic perfusions with CBK. After 30 minutes of reperfusion control studies were repeated. Heart rate, peak systolic pressure, rate of rise of left ventricular pressure, maximum velocity of contractile element, pressure-volume curves, coronary flow distribution, muscle stiffness, and heart water were not significantly different from control values. Total coronary flow and myocardial uptake of oxygen, lactate, and pyruvate did not serve to separate the three groups; the same was true for right ventricular creatine phosphate, adenosine triphosphate, and adenosine diphosphate during ischemia and recovery. Ultrastructural myofibrillar lesions were noted in all groups. thus, postischemic cardioplegia and use of a physiological reducing agent do not enhance CBK cardioplegia with topical and systemic hypothermia.
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PMID:Cold-blood potassium cardioplegia: evaluation of glutathione and postischemic cardioplegia. 50 72

The left cerebral hemisphere of Mongolian gerbils was used to elucidate the mechanisms of brain edema which develop during cerebral ischemia and after restoration of cerebral blood flow following temporary ischemia. Water content was measured by the tissue-drying method. Sodium and potssium ion concentration was measured by flame photometry. Passage of 131I-albumin (RISA) from blood to the cerebral parenchyma was measured on a gamma scintillation counter. Our findings indicate that pure cytotoxic edema develops during ischemia and during a short period after restoration of cerebral blood flow. Vasogenic edema, which is accelerated by the leakage of plasma constitutents from blood due to blood-brain barrier damage, developed after restoration of the cerebral blood flow. After less than 1 hr of ischemia, restoration of the cerebral blood flow drastically reduced the degree of brain edema. However, restoration of the cerebral blood flow greatly worsened the brain edema following more than 3 hr of ischemia.
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PMID:Brain edema during ischemia and after restoration of blood flow. Measurement of water, sodium, potassium content and plasma protein permeability. 50 96

Cold blood with potassium, 34 mEq/L, was compared with cold blood and with a cardioplegic solution. Three groups of 6 dogs had 2 hours of aortic cross-clamp while on total bypass at 28 degrees C with the left ventricle vented. An initial 5-minute coronary perfusion was followed by 2 minutes of perfusion every 15 minutes for the cardioplegic solution (8 degrees C) and every 30 minutes for 3 minutes with cold blood or cold blood with potassium (8 degrees C). Hearts receiving cold blood or cold blood with potassium had topical cardiac hypothermia with crushed ice. Peak systolic pressure, rate of rise of left ventricular pressure, maximum velocity of the contractile element, pressure volume curves, coronary flow, coronary flow distribution, and myocardial uptake of oxygen, lactate, and pyruvate were measured prior to ischemia and 30 minutes after restoration of coronary flow. Myocardial creatine phosphate (CP), adenosine triphosphate (ATP), and adenosine diphosphate (ADP) were determined at the end of ischemia and after recovery. Changes in coronary flow, coronary flow distribution, and myocardial uptake of oxygen and pyruvate were not significant. Peak systolic pressure and lactate uptake declined significantly for hearts perfused with cold blood but not those with cold blood with potassium. ATP and ADP were lowest in hearts perfused with cardioplegic solution, and CP and ATP did not return to control in any group. Heart water increased with the use of cold blood and cardioplegic solution. Myocardial protection with cold blood with potassium and topical hypothermia has some advantages over cold blood and cardioplegic solution.
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PMID:Cold blood as the vehicle for potassium cardioplegia. 51 80

The effect of dehydration on intrarenal blood flow was investigated in 11 dogs, using polarographic determination of H2-gas desaturation for measuring local blood flow in inner cortex (ICF) and outer cortex (OCF). Dehydration was induced by 48 h water deprivation +2-300 mg ethacrynic acid (EA) per os the day before the experiment. Compared to a control group (n=9) ICF was markedly reduced to 2.40 +/- 0.47 ml/min X g (control 3.23 +/- 0.64) whereas OCF 3.29 +/- 0.80 ml/min X g was nearly unchanged (control 3.59 +/- 0.85). The ratio OCF/ICF was increased to 1.37 (1.11). Further dehydration by hypertonic peritoneal dialysis for 3 h increased Hct to 60 +/- 4 and further reduced OCF and ICF, without significant change of the OCF/ICF-ratio. At Hct above 55 sudden and intermittent changes in local cortical blood flow were recorded randomly at individual electrode sites, showing ischemic periods lasting for 1 to 60 min. Such flow changes were observed in 13 of 14 expts. and were not accompanied by changes in RBF. It is concluded that moderate dehydration causes a greater reduction of ICF than of OCF. Severe dehydration gives in addition rise to patchy, intermittent ischemia in both cortical layers.
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PMID:Effect of dehydration on renal blood flow in dog. 59 1


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