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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Venous hypertension in the extremities has been associated with new bone formation and with degenerative joint disease. The relationship between increased intraosseous pressure and bone remodeling was investigated in the vertebrae of the tail of the Wistar rat. In 5 of 15 animals, prolonged venous hypertension resulted in osteoblastic activity with new bone formation. The vertebral changes observed are likened to those seen in some spinal degenerative diseases.
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PMID:Chronic venous hypertension in the tail of the Wistar rat. 47 97

In cats, brain tissue pressure (BTP) was measured by the wick-catheter method. The BTP was positive, but lower than cerebrospinal fluid pressure. Elevation on central venous pressure led only to a transient proportional increase of BTP. When the calvaria and dura of one hemisphere were removed, the rise of BTP was even less. Water content of the brain was normal in either case, even after prolonged venous hypertension. Venous hypertension led in all cases to a marked increase of the brain volume which was caused by vessel dilatation. In brain edema, produced by rinsing the brain surface with ouabain and concentrated saline, BTP was increased permanently by venous hypertension. The water content of the brain was much greater than normal. From these results it was concluded that congestive edema does not occur in the brain unless the tissue is damaged. However, venous hypertension does cause brain swelling.
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PMID:Effect of central venous pressure on brain tissue pressure and brain volume. 93 5

The effects of portal hypertension on gut function may be mediated by venous congestion and altered circulating levels of enteric hormones and neuropeptides. We designed this study to determine the effects of chronic intestinal venous hypertension (VHT), in isolation, on gut motility and absorption. In 10 dogs, a 20- to 25-cm loop of jejunum was isolated from the fecal stream, but myoneural continuity was maintained with the proximal bowel by a seromuscular bridge. In 5 dogs, VHT was created in the loop by a fixed stenosis of its venous drainage; a sham procedure was performed in a further 5 animals. Serosal monopolar electrodes were placed in all animals. Absorptive function and myoelectrical activity were studied over a 4-week period. Venous hypertension was achieved and sustained in the VHT animals; loop vein pressures for VHT vs control in cm H2O (means +/- SEM) are: initial--29.8 +/- 1.8 vs 7.5 +/- 0.4 (P less than 0.01), and at 4 weeks--17.6 +/- 6.88 vs 7.3 +/- 0.2 (P less than 0.01). Absorption of Na+, Cl-, glucose, and water was impaired in VHT loops. Normal patterns of fasting and postprandial myoelectrical activity were preserved in the VHT animals. We conclude that chronic VHT, in the absence of portosystemic shunting, results in impaired absorption of water, glucose, and electrolytes without any change in intestinal motility.
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PMID:The effect of mesenteric venous hypertension on gut motility and absorption. 236 16

Venous hypertension of lesser circulation was used as a criterion for differential diagnosis of diffuse lesion of the myocardium and exudative pericarditis. In 57 patients (31 with diffuse myocardial lesion and 26 with exudative pericarditis) the results of assessment of common x-ray symptoms were compared with signs of venous hypertension in this disease. The presence or absence of venous hypertension in the recognition of exudate into the pericardial cavity was emphasized.
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PMID:[The x-ray diagnosis of exudative pericarditis]. 259 2

Intracerebral pulse waves were recorded in cat and monkey while intracranial pressure (ICP) manipulations were performed. The intracerebral pulse waves appeared comparable to cerebrospinal fluid (CSF) pulsations. The wave forms were divided into multiple smaller waves, designated P1 to P4. The P1 component was primarily of arterial origin and was accentuated by increasing ICP unrelated to increased venous pressure, most commonly from a mass lesion. Bilateral carotid occlusion resulted in decreased amplitude of P1. Venous hypertension from jugular venous or sagittal sinus occlusion, on the other hand, accentuated waves P2 and P3 more than P1. This is consistent with a Starling resistor model of the cerebral venous system in which mass lesions may compress low-pressure veins and accentuate the arterial pressure-dependent P1 wave, whereas venous hypertension causes increased prominence of the later P2 and P3 waves.
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PMID:Supratentorial pressures. Part II: Intracerebral pulse waves. 289 Oct 69

A short-term canine model of lower extremity venous hypertension was created to study the hemodynamics of crossfemoral venous bypass grafts (CFB). Specifically, the hemodynamic effects of bypass conduit diameter and adjunctive arteriovenous fistulas (AVFs) were investigated. Unilateral hind limb venous hypertension was produced by iliofemoral venous ligation in six groups of five greyhounds each. Group I had venous ligation alone. CFBs were constructed in the remaining five groups: group II, 3 mm bypass conduit alone; group III, 3 mm bypass plus sequential AVF; group IV, 3 mm bypass plus caudad AVF; group V, 3 mm bypass plus cephalad AVF; group VI, 6 mm bypass conduit alone. Venous hypertension was significantly reduced by CFB (group II, p less than 0.025; group VI, p less than 0.001); increasing the diameter of the bypass conduit from 3 to 6 mm produced significantly greater graft flow (p less than 0.05), while completely relieving venous hypertension. Addition of adjunctive AVFs significantly augmented graft flow (p less than 0.001) but tended to aggravate ipsilateral venous hypertension (group III, p less than 0.01; group IV increase, NSS; group V, p less than 0.001). During the 4 hours of pressure monitoring, venous hypertension diminished significantly (p less than 0.05) with the sequential AVF but not with the other AVF. We conclude that (1) AVFs may be required for adequate graft flow if a small-diameter (3 mm) bypass conduit is used to relieve venous hypertension; (2) adjunctive AVFs aggravate venous hypertension; (3) sequential AVFs seem to be the most hemodynamically efficacious; (4) AVFs may not be necessary if a large, isodiametric (6 mm) conduit is used.
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PMID:Hemodynamics of revascularization for iliofemoral venous occlusion: a short-term canine model. 318 15

The etiology of venous ulceration is far more complex than Homans' theory of stagnation and hypo-oxygenation. Indeed, studies have shown that flow in lipodermatosclerotic limbs is actually faster than normal. We suggest, therefore, that the terms "stasis dermatitis" and "stasis ulcer" be dropped from medical parlance. The term "lipodermatosclerosis with ulceration" as used by the British, or simply "venous ulcer," would seem more appropriate. Venous hypertension, produced by incompetence of deep and communicating vein valves and thrombosis of segments of the deep system, is closely correlated with the development of venous ulcers. Precisely how this venous hypertension translates into ulceration is unclear. Burnand et al showed that fibrin cuffs are deposited around the capillaries in lipodermatosclerotic limbs. These cuffs may serve as barriers to the diffusion of oxygen, leading to local ischemia and epidermal necrosis. Others suggest that trapped leukocytes in the microcirculation alter capillary permeability by releasing various inflammatory mediators that hasten the flow of fibrinogen across the capillary membrane and promote the formation of fibrin cuffs. Proof of this hypothesis is still lacking, but may eventually come from using radioactive WBC tagging procedures. A synthesis of these two theories may in fact explain the etiology of venous ulceration.
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PMID:Etiology of venous ulceration. 821 32

The best treatment for deep-seated dural arteriovenous malformations (AVMs) remains controversial. Therapeutic options include transarterial and transvenous embolization, surgical excision of the dural nidus, ligation of draining veins, and stereotactically guided radiation treatment. The authors report on their experience with the application and technique of skull base surgical approaches for deep-seated dural AVMs. Their series includes six patients who were surgically treated for five tentorial dural AVMs and one inferior petrosal sinus dural AVM between 1991 and 1995. Three patients presented with progressive brainstem dysfunction, one had progressive myelopathy, and two suffered subarachnoid hemorrhage. Venous hypertension caused progressive neurological deterioration in four patients and ruptured venous aneurysms caused hemorrhage in two patients. Four of the five tentorial dural AVMs received bilateral arterial supply from the internal carotid arteries and external carotid arteries (ECAs). The dural AVM of the inferior petrosal sinus was fed from both vertebral arteries and ECAs. In this series, all dural AVMs drained into deep cerebral veins. Intra- and postoperative angiographic studies were used to document complete obliteration in each case. After surgery, three patients developed transient, delayed (24-72 hours) neurological worsening. One month postsurgery, all six patients showed improvement from their preoperative neurological function. Surgical resection of these deep-seated dural AVMs was accomplished by eliminating the arterial supply rather than ligating the draining veins to avoid aggravating the underlying venous hypertension. This study demonstrates an important role for skull base surgical approaches in the management of patients with deep-seated dural AVMs that have hemorrhaged, are not obliterated by embolization, and for which stereotactically guided radiation therapy is an unsuitable option.
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PMID:Surgical management of deep-seated dural arteriovenous malformations. 925 82

Chronic leg ulceration is a common cause of morbidity in Jamaican patients with homozygous sickle cell (SS) disease. Ulcers heal more rapidly on bed rest and deteriorate on prolonged standing, suggesting a role of venous hypertension in their persistence. This hypothesis has been tested by Doppler detection of venous competence in SS patients and in matched controls with a normal haemoglobin (AA) genotype in the Jamaican Cohort Study. Venous incompetence was significantly more frequent in SS disease [137/183 (75%)] than in non-pregnant AA controls [53/137 (39%)]. Past or present ulceration occurred in 78 (43%) SS patients, with a highly significant association between leg ulceration and venous incompetence in the same leg (P < 0.001). Prominence and/or varicosities of the veins and spontaneous leg ulcers were more common among patients with multiple sites of incompetence. The association of venous incompetence with chronic leg ulceration identifies a further pathological mechanism contributing to the morbidity of SS disease. The cause of venous incompetence is unknown but the sluggish circulation associated with dependency, turbidity and impaired linear flow at venous valves, hypoxia-induced sickling, the rheological effects of high white cell counts, and activation of components of the coagulation system may all contribute. Venous hypertension in SS patients with leg ulceration suggests that firm elastic supportive dressings might promote healing of chronic leg ulcers.
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PMID:Chronic leg ulceration in homozygous sickle cell disease: the role of venous incompetence. 1240 2

The histological changes that occur in brain tissue have rarely been documented in patients with dural arteriovenous fistulas (AVFs). In this study the authors report on two patients with dural AVFs in the transverse-sigmoid sinus who presented with subarachnoid hemorrhage or progressive dementia. Histological studies of the cerebellar cortices showed a selective loss of Purkinje cells, indicating an ischemic insult caused by venous hypertension. Admission N-isopropyl-p-123I-iodoamphetamine single-photon emission computerized tomography scans demonstrated a decrease in cerebral blood flow, including flow through the cerebellum. Venous hypertension caused by transverse-sigmoid sinus dural AVFs provokes an ischemic condition severe enough to cause selective neuronal damage in the cerebellum.
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PMID:Selective loss of Purkinje cells in transverse and sigmoid dural arteriovenous fistulas. Report of two cases. 1265 Apr 37


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