SEARCH · PubMed Health

Results for “Cerebral Small Vessel Diseases”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

18 recordsLinked to original sources

PubMed2026

Glymphatic dysfunction mediates inflammation-driven vascular burden and cognitive decline in cerebral small vessel disease.

BACKGROUND: Cerebral small vessel disease (CSVD) is increasingly recognized as a disorder involving microvascular dysfunction, impaired perivascular clearance, and inflammatory processes. However, how systemic inflammatory burden, neurovascular coupling (NVC), glymphatic MRI markers, vascular lesion burden, and cognition are interrelated remains unclear. MATERIALS AND METHODS: In this prospective study, 155 patients with CSVD and 70 healthy controls (HCs) underwent multimodal MRI. NVC was quantified using the cerebral blood flow/fractional amplitude of low-frequency fluctuations ratio. Glymphatic function was assessed via the diffusion tensor image analysis along the perivascular space (ALPS) index, choroid plexus volume (CPV), and perivascular space (PVS) fractions. Structural equation modeling (SEM) was employed to evaluate the direct and indirect effects of inflammatory markers on vascular burden and cognitive performance. RESULTS: Patients with CSVD exhibited significantly diminished NVC (specifically in the right median cingulate and left frontal gyri) and impaired glymphatic function (lower ALPS-index; higher CPV and PVS fractions) compared to HCs. SEM revealed that inflammatory biomarkers exerted both a direct effect on vascular burden and a substantial indirect effect (accounting for 66.3% of the total effect) mediated through two pathways: a single-mediation path via glymphatic function (42.8%) and a serial-mediation path via NVC and glymphatic function (23.5%). Increased vascular burden was significantly associated with poorer cognitive performance. CONCLUSION: Inflammation drives CSVD progression and cognitive decline primarily through the disruption of NVC and glymphatic clearance mechanisms. These findings highlight glymphatic dysfunction as a critical mediator of inflammation-related structural brain damage.

Humans↗

PubMed2026

Association Between cnm-Positive Streptococci and Cerebral Small Vessel Disease: Insights From Oral Health and Microbiome Status.

INTRODUCTION AND AIMS: Cerebral small vessel disease (CSVD) is associated with various severe neurological outcomes; while oral cnm-positive streptococci are suggested to be involved in cerebrovascular lesions, the specific associative features between these bacteria and CSVD have not yet been systematically investigated. This study aims to investigate the prevalence of cnm-positive streptococci in patients with CSVD and explore the correlation between infection and CSVD severity. By integrating oral health indices and microbiome sequencing, we evaluate the oral hygiene status and microbial dysbiosis characteristics of cnm-positive streptococci carriers. Furthermore, cnm-positive streptococci derived from CSVD patients will be isolated, identified, and subjected to whole-genome sequencing to provide a foundation for future research. METHODS: To explore cnm-positive streptococci prevalence and its association with CSVD, we conducted a case-control study comparing their oral detection rates between healthy controls and CSVD patients. We also performed 16S rRNA gene high-throughput sequencing of oral plaque microbiota and assessed oral health, including the simplified oral hygiene index (OHI-S), the decayed, missing, and filled teeth (DMFT) index, oral hygiene practices, gingival status, and saliva scores. RESULTS: cnm-positive streptococci were more prevalent in CSVD patients, correlating with higher OHI-S and microbial dysbiosis. Multivariable regression models (adjusted for demographic/vascular risk factors) linked cnm positivity to periventricular hyperintensities (PVH), deep white matter hyperintensities (DWMH), Fazekas score, and total CSVD burden (not cerebral microbleeds (CMBs)/lacunes). CONCLUSION: Oral cnm-positive streptococci are independently associated with CSVD phenotypes, particularly those characterized by white matter injury. These findings presents a potential oral-cerebrovascular interaction and imply that managing specific virulent oral strains may be a noteworthy consideration in future clinical research.

Humans↗

PubMed2026

A comparative evaluation of multiple enlarged perivascular space segmentation tools.

BACKGROUND: Enlarged perivascular spaces (ePVS) are a marker of cerebral small vessel disease, potentially reflecting reduced waste clearance. Because manual quantification is unfeasible in large datasets, we developed and evaluated an automated tool. METHODS: Detection Of Regions of Enlarged perivascular Spaces (DORES), a 3D nnU-Net-based deep learning algorithm was developed for ePVS segmentation using T1-weighted and fluid-attenuated inversion recovery magnetic resonance imaging (MRI). DORES was developed in two stages: an initial model trained on 35 manually segmented scans and a final model on 1460 pseudo-labeled sessions from the Vanderbilt Memory and Aging Project (VMAP). A subset of VMAP participants with 3 T brain MRI underwent whole-brain manual ePVS tracing (n = 35, 73 ± 9 years, 51% male) and visual rating (n = 388, 71 ± 8 years, 54% male) by a neuroradiologist. DORES was evaluated and compared against three other segmentation tools using Dice and F1 scores, absolute volume and element differences, correlation, and agreement. External validation used an Alzheimer's Disease Neuroimaging Initiative 3 subset with manual tracings (ADNI3, n = 18, 73 ± 9 years, 67% female). RESULTS: DORES achieved Dice scores of 0.61 ± 0.16 (white matter) and 0.72 ± 0.08 (basal ganglia) in VMAP, with strong correlations and agreement for ePVS count and volume. Performances modestly declined in ADNI3 across algorithms. Scanner-stratified analyses showed stronger correlations for Philips versus Siemens images in the basal ganglia, indicating scanner-dependent differences in measurement consistency. CONCLUSIONS: DORES provides a multimodal nnU-Net-based pipeline for ePVS segmentation in older adults. The model demonstrates robust within-cohort performance and reasonable external validity, though scanner-related effects limit application across sites.

Humans↗

PubMed2026

Downregulation of Trpv4 and Klf2 in brain microvessels is associated with the progression of neurovascular dysfunction and cognitive impairment in a model of heart failure with preserved ejection fraction.

Vascular cognitive impairment (VCI) shares major risk factors with heart failure with preserved ejection fraction (HFpEF), including obesity, diabetes and hypertension. Yet VCI research often relies on single-stimulus models, whereas patients experience combined risk factors. We therefore assessed cerebrovascular and cognitive phenotypes in an HFpEF model and investigated underlying mechanisms. Male Lean and Obese ZSF1 rats underwent longitudinal assessments of blood pressure, glucose, cardiac function and behavioural performance. Cerebral blood flow and neurovascular coupling were assessed by laser speckle contrast imaging. White matter integrity, blood-brain barrier (BBB) permeability and vascular density were analyzed by (immuno)histochemistry. Cortical microvessels were isolated for transcriptomic profiling, and selected targets were validated using multiplex in-situ hybridization. Obese rats exhibited neurovascular uncoupling and impaired short- and long-term memory and spatial learning, accompanied by brain atrophy and reduced myelin. BBB permeability increased at 22-23 weeks and vascular density at 34-35 weeks in Obese versus Lean rats. Transcriptomic analysis of brain microvessels revealed altered processes related to angiogenesis, vasoreactivity, immune mechanisms and vascular remodelling, with consistent downregulation of Trpv4 and Klf2. Obese ZSF1 rats develop progressive neurovascular dysfunction associated with HFpEF onset and reduced Trpv4 and Klf2 expression in cerebral microvessels, two key vasoprotective genes.

Diastolic dysfunction↗

PubMed1976

Role of hypertension in atherosclerosis and cardiovascular disease.

Clinical, experimental and pathologic studies strongly indicate that hypertension is a major factor in coronary heart disease, sudden death, stroke congestive heart failure and renal insufficiency. The deleterious effect of the elevated blood pressure on the cardiovascular system appears to be due mainly to the mechanical stress placed on the heart and blood vessels. Humoral factors and vasoactive hormones such as angiotensin, catecholamines and prostaglandins may play a role in the pathogenesis of hypertensive cardiovascular disease but this role has not yet been defined and is probably secondary. Hypertension and the resulting increase in tangential tension on the myocardial and arterial walls, leads to the development of hypertensive heart disease and congestive heart failure as well as hypertensive vascular disease that affects not only the kidneys but also the heart and brain. Hypertensive vascular disease involves both large and small arteries as well as arterioles and is characterized by fibromuscular thickening of the intima and media with luminal narrowing of the small arteries and arterioles. The physical stress of hypertension on the arterial wall also results in the aggravation and acceleration of atherosclerosis, particularly of the coronary and cerebral vessels. Moreover, hypertension appears to increase the susceptibility of the small and large arteries to atherosclerosis. Thus the patient with hypertension is a candidate for both hypertensive and atherosclerotic vascular disease of the coronary and cerebral vessels leading to occlusive disease of both the large and small arteries and resulting in myocardial infarction and stroke. Other major complications of hypertensive vascular disease include rupture and thrombotic occlusion of blood vessels, especially in the brain. Disease of the arterial media, which begins in childhood with the deposition of calcium in the vessels, may be an important cause of arterial hypertension. This form of hypertension may manifest itself in adults as arteriosclerotic hypertension and lead to cardiovascular complications very similar to those of essential hypertension. The relation of arteriosclerotic hypertension to nutritional factors, including dietary salt intake, deserves study.

Angiotensin II↗

PubMed2026

Potential contributors to variable penetrance of NOTCH3 p.Arg1231Cys Variant.

Missense mutations in NOTCH3, especially cysteine-altering pathogenic variants, are the cause of cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy. The NOTCH3 p.Arg1231Cys variant, located in EGFr domain 31, is classified as low-risk under the three-tiered EGFr domain risk stratification system. We report two cases of p.Arg1231Cys heterozygosity presenting with early-onset dementia, strokes, and extensive leukoencephalopathy. These cases highlight the potential contributing factors to increasing penetrance of p.Arg1231Cys variant, and the need for functional evaluation to improve the clinical utility of genetic testing in hereditary small vessel disease.

Humans↗

PubMed1975

[Clinical value of magnification cerebral angiography (author's transl)].

Magnification carotid and vertebral angiography was performed via femoral catheter with magnification factor of 2.5 to 3.0, utilizing 0.1 X 0.1 ultra fine focal spot, manufactured by Shimadzu Seisakusho, Ltd. The standard angiograms were compared with magnification angiograms in a group of 67 patients with brain tumors and vascular disorders. The magnification angiography was more valuable than conventional angiography in 12 of 17 vascular tumors, while it was rarely valuable for diagnosis of vascular tumors. Aneurysms, occlusive diseases, collateral vessels, and capillary blush were also visualized to better advantage on magnification angiograms. Magnification cerebral angiography is a useful tool for elucidating small vascular branches, but further refinement in the design of focal spots and angiographic techinques is required for further improvement of magnification cerebral angiography.

Adenocarcinoma↗

PubMed1976

[Angio-tomographic aspects of cerebral aneurysms and angiomas (author's transl)].

Angio-tomography is a selective radiological method which can be used to complement serial angiographs in order to demonstrate better detail. This results from the fact that selective levels can be demonstrated without super-imposition of bone or other vessels. Angio-tomography combines the advantages of tomography, subtraction and selective procedures. The method has been used for all types of intracranial disease; aneurysms and angiomas are the most common conditions for which angio-tomography has been employed. The present paper is based on a total of 60 cerebral aneurysms and angiomas in various situations; angiotomography was indicated for these amongst a larger material of intracranial vascular malformations in which the diagnosis was possible without its use. The indications consist of: 1) Demonstration of very small aneurysms and their differentiation from vessel loops, 2) Demonstration of the origin of an aneurysm which is situated at the confluence of several major vessels, 3) Point of origin of a so-called hugeaneurysms which cannot otherwise be shown by oblique views, 4) Demonstration of so-called micro-angiomas and of the afferent and efferent vessels in central arterio-venous malformations. Unusual aneurysms of the internal carotid artery, of the anterior choroidal and vertebral arteries are described. Some new concepts in the localisation of aneurysms of the anterior communicating artery are discussed. Many of the examinations were carried out with an angio-tomographic apparatus made in the department.

Basilar Artery↗

PubMed1979

Cerebral vascular changes in systemic lupus erythematosus.

Cerebral vascular lesions of 26 cases in systemic lupus erythematosus during a period from 1963 to 1978 were examined histologically and the following conclusions were made: 1. The prominent vascular changes of the brain were thrombosis, fibrinoid degeneration, endothelial swelling and proliferation, arteriolosclerosis, and perivascular infiltration of inflammatory cells. 2. From clinico-pathological viewpoints, thrombosis seemed to play an important role in the development of neurological signs. In five cases, characteristic granular or homogeneous thrombi were observed in the small blood vessels including venule. Infarct without proved vascular obstruction but probably due to thrombosis was seen in four cases. The true character of the granular thrombi was not determined, either electronmicroscopically or immunohistochemically. These suggested the presence of a tendency for in situ formation of thrombus. 3. Fibrinoid degeneration seen in four cases mainly affected arterile of less than 50 micrometer in diameter in the cerebral cortex, basal ganglia, and brain stem. This change of arteriole did not play a significant role in neurological signs. 4. Endothelial swelling and proliferation of the small blood vessels were prominent in the cases with thrombosis and fibrinoid degeneration. 5. Perivascular infiltration of the inflammatory cells was observed in about one-half of the cases but its significance was not clear.

Adolescent↗

PubMed1977

Strokes: A complication of mitral-leaflet prolapse?

During a prospective trial of platelet-inhibiting drugs in patients with transient ischaemic attacks (T.I.A.s), 14 patients had serious neurological dysfunction and normal cerebral angiograms. The patients (mean age 37 years) had neurological episodes over a period of 1-4 years consisting of acute non-progressive strokes with residual symptoms. In 3 patients, the two cerebral hemispheres were involved on different occasions. Cerebral angiograms showed no significant atheromatous disease in the intracranial or extracranial vessels. 3 patients had mid-systolic clicks, 5 had systolic murmurs, and 2 patients had both a click and a murmur. Holter electrocardiographic monitoring revealed atrial, junctional, or ventricular extrasystoles (5 patients), paroxysmal atrial fibrillation (3), and paroxysmal ventricular tachycardia (1). Left ventricular angiography confirmed mitral-leaflet prolapse in all the patients. The focal nature of the T.I.A.s suggests an embolic event, the embolus arising from the abnormal mitral valve. In a patient not included in this series, a small antemortem left atrial thrombus was found at necropsy.

Adolescent↗

PubMed1975

The chemical composition of idiopathic nonarteriosclerotic cerebral calcifications.

Calculi from a case of cerebral idiopathic nonarteriosclerotic calcification (Fahr's disease) were examined. The stone consists of hydroxyapatite and possesses a typical structure: the calcification process seems to be initiated by the formation of small round bodies that are cemented to each other to form the final stone. Calcified vessels are also present, but seem to be a secondary effect. From a comparison with other calcifications, it is concluded that no pathologic significance should be attached to the relatively high levels of trace metals such as zinc, iron, copper, magnesium, lead, and others, with the possible exception of manganese. The organic matrix of the stone contains large quantities of protein. On hydrolysis of this fraction, an important unidentified ninhydrin-positive peak was found. No mucopolysaccharides were found.

Activation Analysis↗

PubMedDate not supplied

Rheoencephalographic and other studies of betahistine in humans. IV. Prolonged administration with improvement in arteriosclerotic dementia.

The effects of prolonged betahistine administration were studied in institutionalized geriatric patients with particularly severe and long-standing arteriosclerotic dementia. Thirty received betahistine hydrochloride (SERC) or placebo orally in fixed dosage for six months on a double-blind basis and were followed by ward behavioral and psychometric ratings. Six others received active medication and were additionally followed by intracranial rheoencephalography (IREG). Thirty patients successfully completed the two studies. No adverse effects ascribable to the drug were encountered. The results show that betahistine caused definite, strong, and highly significant cerebral and scalp arterial vasodilation and circulatory improvement and that these caused equally definite, strong, and highly significant global improvement in the patients' dementias. Bethahistine, thus, acts in humans as a potent and efficacious cerebral and peripheral microcirculatory and arterial vasodilator which can significantly improve cerebrovascular insufficiency and any associated dementia, no matter how severe either may be and despite the possible presence of large-vessel disease. These improvements sometimes were detected within two weeks or less, developed rapidly to maxima by about 90 days, and were sustained quite well there-after by continued therapy, They may, however, be drug dependent as they regressed in two patients following withdrawal. Various mechanisms whereby a microcirculatory vasodilator can cause arterial vasodilation are considered. The evidence apparently favors that prolonged microcirculatory vasodilatation can cause secondary passive arterial responses. The possibility that the IREG contains external carotid contamination is again examined. Significant discrepancies between the scalp and IREG effects of bethahistine indicate, however, that the response of any such component was negligible within experimental error and that the component, itself, must have comprised but a small percentage of the IREG. Since the circulatory responses detected by the IREG thus arose essentially completely from the effects of betahistine on the cerebral circulation alone, this appears to be the first direct demonstration that cerebral circulatory improvement can cause improvement in mental function in patients with even severe, longstanding, and apparently clinically irreversible arteriosclerotic dementia and that such improvements can be effected pharmacologically.

Aged↗

PubMed2026

VINE-seq and MultiVINE-seq for single-nucleus and multiome profiling of the brain vasculature.

The human cerebrovasculature is a critical yet historically understudied component of neurological health. Dysfunction of the diverse endothelial, mural, and perivascular cells that comprise cerebral vessels is central to diseases ranging from stroke to Alzheimer's disease. However, characterizing these cell populations at a molecular level has proven exceptionally challenging. Encased within a robust basement membrane, vascular cells resist standard dissociation methods, leading to their systematic depletion and underrepresentation in existing single-nucleus genomic atlases. This has created a major blind spot in neuroscience. To overcome this barrier, we developed vessel isolation and nucleus extraction for sequencing (VINE-seq) and its advanced iteration, MultiVINE-seq. The protocol provides a robust, reproducible workflow for the enrichment and high-resolution profiling of vascular, perivascular, and immune cells from fresh or frozen human and mouse brain tissue. First, intact vessels (predominantly capillaries and small arterioles/venules, 100 µm in diameter) are isolated from homogenized brain tissue via dextran-based density-gradient centrifugation, separating the vascular pellet from myelin and the parenchymal fraction. Second, the collected vessels are rigorously washed over a cell strainer to remove trapped contaminants. A critical innovation lies in the third stage: the optimized extraction of nuclei from purified vessels using enzymatic digestion. After extraction, the protocol uses fluorescence-activated cell sorting (FACS) to ensure collection of high-purity nuclei suitable for widely used droplet-based sequencing platforms (e.g., 10x Genomics single cell 3' or multiome). This protocol requires 4-5 h to complete and can be carried out by researchers with single-cell and flow cytometry training.

Journal Article↗

PubMedDate not supplied

Controlled trial of aspirin in cerebral ischemia. Part II: surgical group.

Patients (125) who had carotid transient ischemic attacks (TIAs) and one or more accessible carotid lesions visualized angiographically had reconstructive operations of the carotid artery and were then randomly assigned to aspirin or placebo treatment. The were followed to determine the incidence of subsecquent TIAs, death, cerebral infarction, or retinal infarction. Life table analysis (for 24 months follow up) that eliminated deaths which were not stroke-related revealed a significant difference in favor of aspirin. Because of the small number of patients and the short period of follow up, these results should be interpreted only as consistent with those reported in the initial publication but not conclusive of an aspirin effect in preventing cerebral infarction.

Adult↗

PubMed1976

[Combination of the syndrome of Sturge-Weber and the syndrome of Klippel-Trénaunay (author's transl)].

Up until now 39 cases of combined Klippel-Trénaunay syndrome and Sturge-Weber syndrome have been described. Here follows the report of a girl, now 4 years of age, displaying a full combination of these syndromes. Only a small part of the body surface is not covered with naevi teleangiectatici laterales. The patient has clear hypertrophy of the left cheek and of the left lower extremity, less noticeable on the left upper extremity. For therapeutic reasons the left side of the head and the left lower extremity were thoroughly angiographically examined--this revealed typical abnormalities. The vessel-alteration of the lower extremity are not extremely far developed and arteriovenous fistulas on a large scale are also absent. This allows us to dismiss the F.P. Weber syndrome on the one hand, while it explains the absence of complications of the Klippel-Trénaunay syndrome, as described in literature, on the other. The significance of the alterations of lymph nodes in this disease, which we are the first to describe, is at present not fully clear. The cerebral attacks have until now showed only a temporary response to medication.

Angiography↗

PubMed1979

Hyperacute experimental allergic encephalomyelitis in rhesus monkeys as a model of acute necrotizing hemorrhagic encephalomyelitis.

A comparative study of clinical and morphological findings in three fatal cases of acute necrotizing hemorrhagic encephalomyelitis (ANHE) and hyperacute experimental allergic encephalomyelitis (HEAE) in rhesus monkeys is reported. In all cases ANHE was characterized clinically by definite prodromal respiratory infection. The course was rapidly progressive with fatal termination. The salient histopathological changes were necrosis of blood vessels with plasma exudation and fibrin impregnation, hemorrhages and inflammatory reaction in the damaged cerebral tissue. Perivascular lymphoid histiocytic infiltration with glial proliferation was also noted in all cases. Numerous compound granular cells were found in one case. HEAE was detected in five rhesus monkeys immunized with homological spinal cord emulsion with complete Freund adjuvant. The illness was acute or subacute and the course was rapidly progressive with a fatal end. There was multiple necrosis of small blood vessels with plasma exudation, fibrin impregnation and massive neutrophila infiltration of the damaged brain tissue in all rhesus monkeys with HEAE. There was also widespread glial proliferation and numerous compound granular cells alongside with necrosis of blood vessels in the brain. These findings suggest that HEAE in rhesus monkeys can be viewed as an adequate model of ANHE.

Adolescent↗

PubMed1976

Computerized tomography (CT) in acute head trauma.

The retrospective evaluation of 100 cases of head trauma that were subjected to computerized tomography (CT) leads to the following conclusions: (1) Computerized tomography and plain skull survey, should be the first neuroradiological procedures to perform. (2) Angiography may be carried out after computerized tomography when necessary, but as proved by this series, it will be needed in a relatively small number of cases. These include patients with technically limited CT scans or those in whom the possibility of an associated vascular lesion of the cervical or intracranial vessel is clinically suspected. (3) It is essential to obtain CT scans of the best possible quality. Sedation will be required in many instances, but this is considered worth doing because a normal CT scan, without significant technical limitations, will exclude the presence of lesions requiring prompt surgical intervention. Those patients who require surgery will need general anesthesia under any circumstances. (4) There is generally a direct relationship between the severity of clinical presentation and the CT demonstration of the abnormality responsible for the clinical status. Seventy percent of the patients clinically diagnosed as contusion had positive CT scans, and for all practical purposes, 100 percent of patients having trauma more severe than our Group III (contusion) had abnormal CT scans. Likewise, the number and intensity of tissue abnormalities on CT scans increase proportionately with the severity of the clinical signs and symptons. (5) It is foreseen that, with the advent of faster computerized tomographic scanners, the usefulness of this method will increase further, owing to a reduction in the total examination time and the lessened requirement for sedation.

Acute Disease↗

PubMed1976

Increased sensitivity of in vivo platelet aggregation in rabbits after alloxan or streptozotocin.

In 14 rabbits previously injected intravenously with alloxan (dose 75-150 mg/kg) with subsequent hyperglycaemia, intra-arteriolar aggregation of platelets at the sites of small standardized electrical injuries to cerebral cortical vessels showed an increased sensitivity (P is less than 0.001) to application of adenosine diphosphate (ADP) in animals anaesthetized with either urethane or Pentothal. Intravenous injection of streptozotocin (10 rabbits, dose 30-200 mg/kg) was not followed so regularly by hyperglycaemia but even so many of these animals also showed increased sensitivity to ADP. After neither alloxan nor streptozotocin did the increased sensitivity correlate with the dose of agent used, the time between its injection and ADP testing, or changes in the rabbit's body weight. Again, ADP sensitivity did not correlate with the degree of hyperglycaemia, hyperketonaemia or hyperlactacidaemia. There was no rapid change in ADP sensitivity after i.v. injection of glucose to produce hyperglycaemia in normal rabbits, nor after parenteral or topical administration of insulin. Use of a removable skull capsule allowed serial observations on individual animals and these, together with observations on rabbits injected first with alloxan and later with daily insulin, showed reversibility of the increased ADP sensitivity by regular insulin injection for at least 5 days; this effect did not depend upon return of blood glucose levels to normal. In cross-perfusion experiments the increased ADP sensitivity was found to be dependent upon a blood factor for such sensitivity was shown by the head of a normal rabbit perfused with blood from a diabetic trunk. The results did not exclude a contribution of a mural factor to the results in intact animals after alloxan. The results are in keeping with in vitro observations of increased sensitivity to ADP of platelet aggregation in diabetic patients and demonstrate that such an effect holds within living blood vessels, as well as providing a model for further experiment.

Adenosine Diphosphate↗