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)

Histologic evidence of intrarenal vasomotor changes were observed in the rat in the course of acute renal failure caused by the injection of HgCl2. Male Wistar rats injected s.c. with 2.5 or 4.7 mg HgCl2 per kg b. wt. developed fibrinoid damage in the media segments of preglomerular renal vessels, mostly in the arcuate and interlobular arteries. The lesions were patchy and irregularly scattered throughout the kidneys. 24 h post-injection the lesions were very rare and of only mild degree, whereas they were fully developed and regularly seen 48 h post-injection. A high percentage of similar changes was found in certain extrarenal vascular areas especially in the mesentery and pancreas. The damaged vascular segments were usually dilated. The results of various thichrome stains and histochemical reactions suggested edema of vascular smooth muscle cells and imbibition of the media by blood plasma substances, sometimes reaching the degree of fibrinoid necrosis. These findings were confirmed by electron microscopy. The imbibition of the smooth muscle cells by blood plasma material was clearly evidenced by the demonstration of intracellular fibrin precipitations. In connection with the degeneration of smooth muscle cells, accumulations of crystal-like fibrin formations could often be shown. Subendothelial fibrin formations were not observed. 96 h after the 2.5 mg injection the changes were already regressing, but edema of the vascular wall and signs of disturbed vasotonia persisted for several days. The maximum of the vascular changes usually coincided with the maximum of azotemia and the formation of debris cylinders in the renal tubules. However, no clear relationship was recognizable in individual cases between vascular damage, extent of tubular necrosis and renal function. The pathogenesis of the vascular changes is obscure, but neurogenic factors, increased release of catecholamines and/or vasoactive agents of renal origin in connection with other factors might play a decisive role. Arterial hypertension was absent. It is assumed that the structural damage of the vascular media is mainly brought about by prolonged or recurring vasospasms, or by alternating spasm and vasodilatation with local ischemia and increased tension of the vascular wall in the dilated segments. The altered function and structure of the vascular wall might, to a certain extent, contribute to renal insufficiency.
 ...
PMID:Intra- and extrarenal vascular changes in the acute renal failure of the rat caused by mercury chloride. 13 13

71 patients undergo myocardial revascularisation for Prinzmetal's angina; among them, 50 p. cent are operated upon in emergency according to three ways of anaesthesia: neuroleptanalgesia, analgesic anaesthesia, combined anaesthesia. The authors lay stress on the importance of per- and post-operative complications: electrocardiographic ischemia in 22 p. cent of the cases, severe ventricular excitability perturbations were observed in 21 p. cent, myocardial necrosis in 14 p. cent, cardiovascular collapse in 21 p. cent and hypertensions in 22 p cent. These complications are often associated. In the discussion, the authors underline anesthetic induction as a cause of Prinzmetal's angina in 50 p. cent of the cases. They put the accent on the severity of peroperative crisis followed in 50 p. cent of the cases by serious ventricular excitability perturbations. In 25 p. cent of the cases myocardial necrosis is a complication of the spasm of a coronary artery. In this field, posterior necrosis are more frequent and correspond to the spasm of the right coronary artery. All the patients of this series, except one, develop necrosis in the spastic area (by-passed or not). Per-operative hypertension has no incidence on the occurrence of post-operative complications. Lastly, continuous per-operative infusions of nitroglycerine has been performed in several patients in order to reduce morbidity of this type of surgery.
 ...
PMID:[Prinzmetal's angina during myocardial revascularisation. Cardiovascular complications in 71 patients (author's transl)]. 31 82

The physiological mechanisms of known importance in the control of cerebral blood flow (CBF) and smooth muscle contraction and relaxation are reviewed. The pathophysiology of vasospasm following subarachnoid hemorrhage (SAH) is correlated with an alteration of these mechanisms. It is emphasized that smooth muscle relaxation is an energy-dependent process and that vasodilators require a functional smooth muscle membrane that may be severely impaired in ischemia or subarachnoid hemorrhage. The temporal profile of ischemia from spasm is correlated with the pathophysiology of altered metabolism of smooth muscle. The relevance of this complication to the timing of aneurysm surgery in 337 cases operated by one surgeon is considered along with various drug regimens suggested for its management.
 ...
PMID:Physiological considerations important for the management of vasospasm. 32 8

The etiology of sudden-death ischemic heart disease (SDIHD) remains an enigma. Data will be presented which suggest that SDIHD may be due to hypomagnesemia in and around the coronary arterial and arteriolar vessels. We have found that blood vessels (especially arteries and arterioles) deficient with respect to Mg can undergo constriction and spasm; the greater the reduction in Mg2+, the greater the magnitude of the spontaneous contractile responses. The higher the Ca2+:Mg2+ ratio, the greater are the magnitudes of these contractile responses. A severe deficit in surface membrane Mg2+, in particular, results in intense vasospasm. Using direct in situ high resolution microscopy (3000 x), we have found that a lowering of Mg2+ around perfused arterioles (15--20 microns i.d.) will also result in spontaneous vasoconstriction and, in addition, increased arteriolar resistance, tissue ischemia and reduced venous outflow. We have also found that the constrictor actions of certain circulating vasoconstrictor hormones (i.e., angiotensin, serotonin, acetylcholine) are enhanced when [Mg2+] is lowered below the levels normally found in plasma. Other direct studies, from our laboratory, indicate that [Mg2+]o regulates calcium exchange and content of vascular smooth muscle. In summary, the concept to be presented suggests that a deficiency in dietary Mg2+ is a key factor in the high incidence of mortality noted in SDIHD in nations of the Western world. The hypomagnesemia produces progressive vasoconstriction, vasospasm and ischemia, which, given time, will lead to SDIHD.
 ...
PMID:Sudden-death ischemic heart disease and dietary magnesium intake: is the target site coronary vascular smooth muscle? 39 Mar 30

A 24-year-old woman developed bilateral blindness after recovery from coma secondary to acute intermittent porphyria. Gradual return of vision in the right eye with a permanent unilateral visual field defect and optic atrophy followed. We believe the pathophysiologic mechanism was spasm of the vessels supplying the optic disk leading to ischemia and infarction of the optic nerve.
 ...
PMID:Optic atrophy in acute intermittent porphyria. 43 76

From a larger series of autopsies with subarachnoid hemorrhage (SAH), 20 cases were selected for the known complication of cerebral vasospasm. Evidence for vasospasm was radiological and pathological in 17 cases and pathological alone in three. A systematic histological examination of the large arteries in places known formerly to have been in spasm showed that, in the 12 early cases (death before 3 weeks), there were relevant changes in all the layers of the arterial wall, the most significant being evidence of necrosis in the tunica media. In the eight late cases (death after 3 weeks), in addition to the sequelae of the earlier acute changes, there was marked concentric intimal thickening by subendothelial fibrosis, again located in the segments of arteries formerly in spasm. Changes were also found in the small arteries, capillaries, and veins, both in the early and late cases but these changes, although striking, were thought to be caused by the ischemia due to the vasospasm; similar changes were also seen in the control cases with ischemia from arterial occlusion.
 ...
PMID:Cerebral artery spasm. A histological study at necropsy of the blood vessels in cases of subarachnoid hemorrhage. 63 76

Experience with 105 lower limb arterial injuries in 103 patients in a general hospital is described. The pathology is discussed: it is noted that spasm per se could not be incriminated as a cause of ischemia. Management of the injuries and associated fractures is outlined. A plea is made for use of external fixation in compound injuries. An aggressive approach to the degloved limb, open three-compartment fasiotomy for severe vascular injury with signs of ischemia, and delayed primary closure for wounds with septic complications are recommended. Associated soft-tissue injury requires arterial reconstruction even in the presence of muscle rigor and anesthesia.
 ...
PMID:Arterial trauma involving the lower limb. 66 Jun 85

A group of 20 necropsies of subarachnoid hemorrhage (SAH) were selected because of the known complication of cerebral vasospasm. Evidence for vasospasm was radiological and pathological in 17 cases and pathological alone in 3 cases. A histological examination of the large arteries in areas known formerly to be in spasm showed that in the 13 early cases (death before 3 weeks) there were relevant changes in all layers of the arterial wall, the most significant being a degeneration of the media and elastica. In the 7 late cases (death after 3 weeks), in addition to the sequelae of the acute changes, there was marked concentric intimal thickening; and the localization was again in the particular segments of arteries formerly in spasm. Changes found in the small arteries, capillaries, and veins in the early and the late cases were thought to be caused by the ischemia due to the vasospasm. These changes were also seen in control material.
 ...
PMID:Cerebral artery spasm: histological changes in necropsies of cases of subarachnoid hemorrhage. 67 16

The Po2 was measured in the tissue of the ileal wall of dogs before, during, and up to one hour after reversible occlusion of segmental arteries. The occlusion was then released and the reoxygenation of the bowel wall was observed. Sodium nitroprusside (50 mg in 100 ml of solution) applied topically to the ischemic segment enhanced reoxygenation as compared to control animals. Nitroprusside absorbed into the portal system did not cause hypotension, as is usual with systemic administration, because nitroprusside is inactivated by passage through the liver. Topically applied sodium nitroprusside alleviates intestinal ischemia by direct local vasodilatation and relaxation of smooth muscle spasm in the ischemic bowel wall. The intraperitoneal use of sodium nitroprusside should be clinically evaluated in situations where visceral perfusion is impaired.
 ...
PMID:Enhancement of tissue Po2 of strangulated bowel by topical application of sodium nitroprusside. 68 8

107 patients presenting Raynaud's phenomenon attacks were studied. It has been demonstrated by means of arteriographies that in pallid phase of Raynaud's phenomenon attacks not only the digital but also the radial ulnar and interosseous arteries are in spasm. In the cyanotic phase of Raynaud's phenomenon the natural arteriovenous anastomoses are widely open bringing about peripheral skin ischemia. On the assumption that the opening of arteriovenous anastomoses in Raynaud's phenomenon attacks is due to injury of that part of the peripheral nerve which lies in contact with the cervical vertebral column all 107 studied patients were submitted to detailed cervical vertebral column X-ray examinations. In 103 patients i.e. in 96.3% characteristic degenerative changes of cervical vertebrae were recognised. In 100 controls who never had neither Raynaud's phenomenon attacks nor cervico-brachial neuritis the same type of degenerative changes were found in 10% only. The authors presume that the Raynaud's phenomenon attacks are due to peripheral mixed nerve or their roots injury. The blue phase of Raynaud's phenomenon attacks is due to opening of arteriovenous anastomoses.
 ...
PMID:The origin of Raynaud's phenomenon. 73 33


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