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

The study of 148 cases of sudden cardiac death revealed in 25 (17%) of them morphological signs of cardiogenic shock characterized by severe microcirculatory disorders: uneven blood-filling of the vessels of the microcirculatory bed and increasing number of nonfunctioning capillaries in the myocardium and hypothalamus; signs of juxtamedullar shunting in the kidneys and the development of sludge phenomenon in different parts of their microcirculatory bed combined with high activity of renin in the plasma. The signs of cardiogenic shock in the group of observations of sudden cardiac death were noted predominantly in the presence of myocardial infarction, large foci of ischemia in the heart or multiple scattered foci of cardiomyocyte damage. Cardiogenic shock was found to occur in sharp reduction of the density of adrenergic nerve structures in the myocardium.
 ...
PMID:[Cardiogenic shock and sudden cardiac death]. 667 Sep 44

In a 71-year-old female with severe hypertension, bilateral renal artery stenosis and renal adenocarcinoma, a renal vein renin study revealed suppressed renin secretion from the kidney with carcinoma and contralateral ischemia. The hypertension was not cured by surgical removal of the kidney with carcinoma. Hypertension is frequently noted in patients with renal adenocarcinoma (28% of 603 patients reported in the literature). This type of hypertension is frequently improved after removal of the tumor (83% of 36 surgically treated patients). In certain patients the pathogenesis of hypertension associated with renal adenocarcinoma may be related to renin secretion from the tumor or to renin activation due to regional ischemia caused by vascular compression. In other patients the renin-angiotensin system does not appear to play a pathogenic role in the development of hypertension associated with renal adenocarcinoma.
 ...
PMID:[Arterial hypertension: adenocarcinoma of the kidney or bilateral renal artery stenosis$]. 672 21

In order to investigate effects of hydration state, different techniques of collecting blood samples, and of acute, stepwise hemorrhage, we studied plasma vasopressin (AVP) concentration, and plasma renin activity (PRA) in 80 female Wistar rats. Plasma AVP was decreased following hydration with 10 ml of water (1.0 +/- 0.3 pg/ml, mean +/- S.E.M.) as compared to controls (6.1 +/- 2.0 pg/ml), while withdrawal of water for 48 hours stimulated AVP release (29 +/- 8 pg/ml). AVP values in jugular venous blood during light ether anesthesia (9.6 +/- 4 pg/ml) were slightly higher than in trunk blood following decapitation (2.7 +/- 0.7 pg/ml). There was no effect of sham gastric lavage on AVP. PRA was slightly increased in trunk blood and in jugular venous blood following ether anesthesia, and 5-fold increased following 48 h of water withdrawal. In aortic blood obtained during ether anesthesia, AVP-levels were 12- to 560-fold those in control trunk blood. Rapid hemorrhage, 2.0 ml stepwise, resulted in corresponding increases of AVP blood concentration, presumably due to hypothalamohypophyseal ischemia. PRA values showed a similar, albeit less pronounced increase. These results show the importance of controlling conditions of blood sample collection for AVP and PRA analysis, and demonstrate massive release of AVP in response to acute hemorrhage. The amount of AVP released is well about the threshold for pressor activity, and may be of importance in vasoconstrictive adaptation to acute hypovolemic hypotension.
 ...
PMID:Plasma vasopressin concentration and renin in the rat: effect of hydration and hemorrhage. 675 86

Aortic ligation between the origins of the renal arteries in the rat produces a left renal ischemia, renin-dependent hypertension, and a transitory hindlimb paralysis of less than 2 h. Removal of the left ischemic kidney at the time of aortic ligation curtails the rise of blood pressure, plasma renin activity is normal, and paralysis is still present 24 h after surgery. Administration of an angiotensin-converting enzyme inhibitor or saralasin also prevents recuperation from paralysis after aortic ligation. Independent manipulation of the mean arterial pressure or plasma renin activity by pretreatment with reserpine or deoxycorticosterone before surgery shows that the presence or absence of paralysis is dependent on the plasma renin activity and not on the high blood pressure. Blood flow measurements show that paralysis is due to a persistent impairment of blood supply to the hindlimb muscle and not to ischemia of the spinal cord. Infusion of angiotensin II to aortic-ligated, left-renoprival animals tends to restore blood flow to muscle. It is concluded that after renal ischemia the renin-angiotensin system, independent of its hypertensive effect, restores blood flow by stimulating the development of collateral circulation.
 ...
PMID:Renin-angiotensin and development of collateral circulation after renal ischemia. 675 70

90 min of renal artery occlusion in previously unilaterally nephrectomized rats produce acute renal failure (ARF) (plasma creatinine at 48 h after ischemia: 636 +/- 44 vs. 133 +/- 9 mumol/l in controls). Between 1 and 48 h after releasing the occlusion, two populations of superficial nephrons could be observed, one with dilated tubules and elevated proximal tubular pressures (PTP: 39 +/- 1 vs. 12 +/- 1 mm Hg in controls) and the other with collapsed tubules and decreased PTP (9 +/- 1 mm Hg). Proximal tubular passage time (PPT) could not be determined with the Lissamine green technique. Seven methods of pretreatment were tested, 5 of which provided partial functional protection (DOCA/NaCl/NaCl, furosemide infusion, inosine bolus, mannitol bolus and the combination of the last two). Neither renal renin levels nor urinary NaCl excretion were consistently correlated with protection. Functionally protected rats consistently showed no PTP increase and normal PPT in the tubules at the kidney surface. However, plasma creatinine at 48 h differed markedly within the 5 protected groups, ranging from 168 +/- 18 to 398 +/- 35 mumol/l. Extensive medullary congestion was seen at 1-6 h after ischemia only in those rats with obstructed, high pressure nephrons at the kidney surface. To conclude: (1) Functional protection from ischemic ARF, both with and without an accompanying increase in solute excretion, was achieved by the abolition of tubular obstruction. (2) Despite similar degrees of restoration of superficial nephron function, the persisting impairment of whole kidney function differed markedly between the protected groups. (3) Impairment of deeper nephron function must therefore play a major role, perhaps through persisting obstruction in the long loops of Henle. (4) High pressure nephrons may compromise medullary venous outflow in the outer zone of the outer medulla.
 ...
PMID:Superficial nephron obstruction and medullary congestion after ischemic injury: effect of protective treatments. 675 72

Uteroplacental ischemia is associated with uterine renin release in pregnant nephrectomized rabbits. In the present study, uterine and renal renin release after uteroplacental ischemia were investigated in 10 Australian white rabbits at 24 to 28 days' gestation. Pentobarbital was administered, and both uterine arteries were ligated close to their origins. Blood samples were taken for plasma renin activity (PRA) determinations from the femoral artery, uterine vein, and right renal vein before ligation and at 30 and 60 minutes after ligation. Mean arterial blood pressure (MAP) was monitored throughout. In five additional pregnant rabbits renal blood flow (RBF) was measured with an electromagnetic flowmeter. The preligation uterine vein-artery PRA difference was not significant (1.9 +/- 1.1 ng/ml/hr). Postligation uterine vein-artery PRA was 11.4 +/- 3.2 at 30 minutes and 6.6 +/- 1.9 ng/ml/hr at 90 minutes (p less than 0.02). Preligation renal vein-artery PRA was 32.3 +/- 10.5 ng/ml/hr (p less than 0.02) and did not change significantly after ligation. MAP remained stable and RBF was unchanged after uterine artery ligation. These observations confirm the finding that the kidney is the primary source of renin in the normal pregnant rabbit and demonstrate that following acute uteroplacental ischemia there is significant uterine renin release even when the kidneys are intact.
 ...
PMID:Uterine and renal renin release after ligation of the uterine arteries in the pregnant rabbit. 698 78

The objective of the present work was to study the changes in the brain and renal renin-angiotensin system (RAS) during their simultaneous stimulation by ischemia. Experiments were carried out on the following groups of male normotensive Wistar rats: intact, with brain ischemia, with renal ischemia, with combined brain and renal ischemia. The three ischemic groups of animals had some arterial pressure elevation without reaching hypertensive values. In animals with combined brain and renal ischemia brain renin concentration (BRC) was raised, while plasma renin activity (PRA) was reduced relative to the intact controls, i.e. as in animals with brain ischemia alone. Renal renin concentration (RRC) in the ischemic kidney was at the level of the one in intact animals and in animals with brain ischemia. In the intact contralateral kidney of rats with combined ischemia RRC was reduced relative to the intact kidney of animals with renal ischemia and statistically insignificantly reduced relative to the RRC in intact controls and in animals with brain ischemia. The results of this study showed that inverse ratio between renal and brain RAS exists also in the single clamped--birenal model of hypertension. Interaction between the two RAS is manifested when they both are simultaneously stimulated, with prevalence of the effect of brain RAS, which affects renin secretion in the kidney.
 ...
PMID:[Brain and kidney renin-angiotensin system in rats with simultaneously induced cerebral and renal ischemia]. 699 Dec 47

Many potential cadaveric kidney donors have been exposed to shock or hypotension before or during organ donation. Renin-mediated vasoconstriction has been implied in the pathogenesis of acute renal failure. High renin levels have been associated with poor graft survival under hypothermic pulsatile perfusion. An attempt was made to block renin effect with Saralasin (1-Sar-8-ala-angiotensin II), a competitive blocker. Eight conditioned mongrel dogs had their renal arteries exposed, and Saralasin, 100 microgram, was injected intra-arterially. Warm ischemia was then induced for 30 min. Thereafter, the kidney was removed and placed under hypothermic pulsatile perfusion for 24 hours, during which time Saralasin was given continuously at a rate of 1 microgram/min. The kidneys were reimplanted in the same animal on the contralateral iliac fossa, Saralasin, 100 microgram, was given intraarterially after implantation, and a contralateral nephrectomy was performed. Four control animals were given saline solution instead of Saralasin. No significant differences were noted in perfusion characteristics and postoperative creatinine values between treated and control groups. This apparent lack of protective effect of angiotensin II competitive blocker suggests that in the pathophysiology of acute renal failure other factors could be involved besides renin release.
 ...
PMID:Failure of saralasin in preventing renal failure in ischemic transplanted kidneys. 700 66

The present study was carried out on male rats, using three models of experimental hypertension: cerebroischemic, single clamp bilateral and combined, induced by ischemia of the brain and one of the kidneys. The authors determined DA, NA, A in the hypothalamus and medulla oblongata as well as A, NA in plasma in view of the connection between CA (catecholamine) and cerebral and renal renin-angiotensin system (RAS). In rats with cerebral hypertension there was activation of noradrenergic neurons in the hypothalamus and medulla oblongata. There were no changes in the content of A. In rats with renal hypertension the activation of noradrenergic neurons in the hypothalamus was due to exhaustion of NA stores with normal amount of DA, but still the adrenergic neurons were activated. In rats with combined hypertension there was lowering of NA and DA in the hypothalamus, but A was not altered, e.g. the changes, observed singly and in cerebral and renal hypertension were combined. In the three forms of hypertension there were similar changes in medulla oblongata (reduced DA, increased NA and unaltered) and in plasma (A without significant changes). The changes in the level of CA in cerebral and combined hypertension could be explained by a change in the sinocarotid reflex, but in the renal-with the increased level of plasma angiotensin. The authors suggest that the connection between cerebral CA and cerebral RAS is not a direct one and RAS is not directly involved in the inverse interrelationships between cerebral and renal RAS.
 ...
PMID:[Central and peripheral catecholamines in combined cerebral and renal hypertension]. 701 87

Obesity is characterized by a number of cardiovascular alterations, and whether these alterations involve arterial compliance is unknown. In 12 young, obese, normotensive subjects (age, 23.9 +/- 1.3 years; mean +/- SEM) and 12 age- and sex-matched lean control subjects we measured blood pressure, radial artery diameter, and radial artery compliance continuously over the systodiastolic pressure range with a Finapres device and recently developed echo-tracking device. Measurements were obtained at baseline and after prolonged ischemia, that is, when diameter and compliance are increased. Blood pressure values were normal in both groups (obese subjects: 109.2 +/- 4.9/68.2 +/- 2.7 mm Hg; lean control subjects: 108.2 +/- 4.1/60.7 +/- 3.8 mm Hg), but in addition to a marked increase in body mass index (38.5 +/- 0.8 versus 23.1 +/- 0.9 kg/m2, P < .01), obese subjects showed a slight and nonsignificant increase in heart rate (71.1 +/- 3.2 versus 66.7 +/- 3.3 beats per minute, P = NS), increases in left ventricular wall thickness and left ventricular mass index (121.5 +/- 4.8 versus 103.4 +/- 3.3 kg/m2, P < .01), no changes in plasma renin activity and plasma norepinephrine (compared with normal values), and a marked reduction in total body glucose uptake (glucose clamp technique). Obese subjects showed radial artery diameter and compliance values that were greater than those seen in control subjects throughout the systodiastolic pressure range. The differences were 13% (P < .05) and 96% (P < .01), respectively, and both diameter and compliance remained higher in obese than lean subjects after forearm ischemia. In obese and lean subjects baseline radial artery diameter values correlated highly with body weight, body surface area, and body mass index.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Radial artery compliance in young, obese, normotensive subjects. 749 Jan 59


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>