Calcium-activated potassium channels contribute to human coronary microvascular dysfunction after cardioplegic arrest.

BACKGROUND: Cardioplegic arrest (CP) followed by reperfusion after cardiopulmonary bypass induces coronary microvascular dysfunction. We investigated the role of calcium-activated potassium (K(Ca)) channels in this dysfunction in the human coronary microvasculature. METHODS AND RESULTS: Human atrial tissue was harvested before CP from a nonischemic segment and after CP from an atrial segment exposed to hyperkalemic cold blood CP (mean CP time, 58 minutes) followed by 10-minute reperfusion. In vitro relaxation responses of precontracted arterioles (80 to 180 mum in diameter) in a pressurized no-flow state were examined in the presence of K(Ca) channel activators/blockers and several other vasodilators. We also examined expression and localization of K(Ca) channel gene products in the coronary microvasculature using reverse transcriptase-polymerase chain reaction, immunoblot, and immunofluorescence photomicroscopy. Post-CP reperfusion relaxation responses to the activator of intermediate and small conductance K(Ca) channels (IK(Ca)/SK(Ca)), NS309 (10(-5) M), and to the endothelium-dependent vasodilators, substance P (10(-8) M) and adenosine 5diphosphate (10(-5) M), were significantly reduced compared with pre-CP responses (P<0.05, n=8/group). In contrast, relaxation responses to the activator of large conductance K(Ca) channels (BK(Ca)), NS1619 (10(-5) M), and to the endothelium-independent vasodilator, sodium nitroprusside (10(-4) M), were unchanged pre- and post-CP reperfusion (n=8/group). Endothelial denudation significantly diminished NS309-induced vasodilatation and abolished substance P- or adenosine 5 diphosphate-induced relaxation (P<0.05), but had no effect on relaxation induced by either NS1619 or sodium nitroprusside. The total polypeptide levels of BK(Ca), IK(Ca), and SK(Ca) and the expression of IK(Ca) mRNA were not altered post-CP reperfusion. CONCLUSIONS: Cardioplegic arrest followed by reperfusion after cardiopulmonary bypass causes microvascular dysfunction associated with and likely in part due to impaired function of SK(Ca) and IK(Ca) channels in the coronary microcirculation. These results suggest novel mechanisms of endothelial and smooth muscle microvascular dysfunction after cardiac surgery.

The cardiac microvasculature in hypertension, cardiac hypertrophy and diastolic heart failure.

Recent studies revealed an exceedingly high mortality with diastolic heart failure that was previously regarded as relatively benign compared to systolic heart failure. Prominent risk factors for diastolic heart failure are increasing age, hypertension and diabetes. These risk factors are associated with coronary microvascular rarefaction and resultant decreased coronary flow reserve, thereby rendering the myocardium vulnerable to ischemia. We discuss the importance of angiogenic gene programming in preserving the coronary microvasculature, preserving cardiac function and altering disease course. Further, we discuss the possible utility of therapies that activate hypoxia inducible factor-1 in preventing rarefaction of the coronary microvasculature and maintaining cardiac diastolic function.

Altered vascular responses to circulating angiotensin II in familial combined hyperlipidemia.

OBJECTIVES: Patients with familial combined hyperlipidemia (FCHL) are at increased risk of hypertension and cardiovascular disease. We examined if patients with FCHL have altered microvascular and macrovascular responses to angiotensin II, a principal mediator of the renin-angiotensin-aldosterone system. METHODS: Sixteen patients with FCHL and 16 healthy controls were investigated before, during and after a 3 h intravenous infusion of angiotensin II (10 ng/kg/min). Forearm skin microcirculation was studied by laser Doppler fluxmetry during rest and local heating to 44 degrees C (microvascular hyperemia). RESULTS: Baseline systolic blood pressures were 129 +/- 13 and 123 +/- 12 mmHg in FCHL patients and controls (P = 0.11), respectively. Angiotensin II elicited a greater systolic blood pressure response in the FCHL group (+32 +/- 13 mmHg) than in the control group (+20 +/- 11 mmHg; P < 0.001). At 3 h angiotensin II infusion, microvascular hyperemia increased in the controls (P < 0.001), whereas microvascular hyperemia was unchanged in the FCHL patients (P < 0.01, between groups). CONCLUSION: In healthy individuals, a 3 h intravenous infusion of angiotensin II enhances heat-induced microvascular hyperemia. In FCHL, this microvascular hyperemia is impaired and the systolic blood pressure response is increased. A reduced microvascular dilatation capacity in FCHL may contribute to the observed blood pressure elevation and promote development of micro- and macrovascular complications.

The microcirculation in health and critical disease.

The microcirculation is a complex system, which regulates the balance between oxygen demand and supply of parenchymal cells. In addition, the peripheral microcirculation has an important role in regulating the hemodynamics of the human body because it warrants arterial blood pressure as well as venous return to the heart. Novel techniques have made it possible that the microcirculation can be observed directly at the bedside in patients. Currently, research using these new techniques is focusing at the central role of the microcirculation in critical diseases. Experimental studies have demonstrated differences in microvascular alterations between models of septic and hypovolemic shock. In human studies, the microcirculation has most extensively been investigated in septic syndromes and has revealed highly heterogeneous alterations with clear evidence of arteriolar-venular shunting. Until now, the microcirculation in acute heart failure syndromes such as cardiogenic shock has scarcely been investigated. This review concerns the physiologic properties of the microcirculation as well as its role in pathophysiologic states such as sepsis, hypovolemic shock, and acute heart failure.

Mecanismo de Lesión Tisular en Criocirugía / Mechanisms of Tissue Injury in Cryosurgery

La criocirugía, modalidad efectiva de tratamiento médico, es una técnica quirúrgica que emplea la congelación a temperaturas criogénicas para destruir tejidos biológicos no deseados. El objetivo de la criocirugía es congelar un determinado volumen tisular (para maximizar la destrucción celular) en una región predefinida y provocar necrosis sin daño significativo del tejido sano periférico. Las bases de la criocirugía son: "una rápida congelación, una lenta y completa descongelación, y repetición de los ciclos de congelación-descongelación". Para explicar el daño en una criolesión se han propuesto muchos mecanismos de injuria inducidos por la congelación. Los mecanismos son: (a) lesión celular directa, (b) lesión vascular, (c) apoptosis y (d) lesión inmunológica. La lesión que resulta de la criocirugía es compleja; por lo tanto, para controlar el resultado de este procedimiento es necesario comprender los mecanismos de daño en criocirugía.

Cryosurgery, an effective medical treatment modality, is a surgical technique that employs freezing at cryogenic temperatures to destroy undesirable biological tissue. The goal of cryosurgery is to freeze a specified volume of tissue (to maximize cell destruction) within a predefined target region, resulting in necrosis without significant damage to the surrounding healthy tissues. Factors that facilitate this are: rapid freezing, slow and complete thawing, and repetition of the freeze-thaw cycle. To explain the injury within a cryolesion, many freezing induced injury mechanisms have been proposed. These mechanisms are 1) direct cell injury, 2) vascular injury, 3) cellular apoptosis, and 4) immunologic injury. The injury that results from cryosurgery is complex; therefore, to control the outcome of cryosurgery it is necessary to understand the mechanisms of damage in cryosurgery.

Absence of glutathione peroxidase-1 exacerbates cerebral ischemia-reperfusion injury by reducing post-ischemic microvascular perfusion.

Mice deficient in the anti-oxidant enzyme glutathione peroxidase-1 (Gpx1) have a greater susceptibility to cerebral injury following a localized ischemic event. Much of the response to ischemia-reperfusion is caused by aberrant responses within the microvasculature, including inflammation, diminished endothelial barrier function (increased vascular permeability), endothelial activation, and reduced microvascular perfusion. However, the role of Gpx1 in regulating these responses has not been investigated. Wild-type and Gpx1-/- mice underwent focal cerebral ischemia via mid-cerebral artery occlusion followed by measurement of cerebral perfusion via laser Doppler and intravital microscopy. Post-ischemic brains in wild-type mice displayed significant deficit in microvascular perfusion. However, in Gpx1-/- mice, the deficit in cerebral blood flow was significantly greater than that in wild-type mice, and this was associated with significant increase in infarct size and increased vascular permeability. Ischemia-reperfusion also resulted in expression of matrix metalloproteinase-9 (MMP-9) in endothelial cells. The absence of Gpx1 was associated with marked increase in pro-MMP-9 expression as well as potentiated MMP-9 activity. Pre-treatment of Gpx1-/- mice with the anti-oxidant ebselen restored microvascular perfusion, limited the induction and activation of MMP-9, and attenuated the increases in infarct size and vascular permeability. These findings demonstrate that the anti-oxidant function of Gpx1 plays a critical role in protecting the cerebral microvasculature against ischemia-reperfusion injury by preserving microvascular perfusion and inhibiting MMP-9 expression.

Spontaneous electromyographic activity during microvascular decompression in trigeminal neuralgia.

Intraoperative monitoring of spontaneous facial nerve electromyographic activity during surgery for microvascular decompression in trigeminal neuralgia was evaluated. Fifteen patients with trigeminal neuralgia underwent surgery for microvascular decompression. During the entire operation, free-running facial nerve electromyographic signals were recorded. The data were analyzed with respect to waveform patterns known from vestibular schwannoma-surgery. Special regard was given to the occurrence of A-trains that are associated with postoperative paresis in patients operated on vestibular schwannoma. The spectrum of the observed activities matched patterns known from surgery of vestibular schwannoma; even A-trains, a pattern known to be an indicator of postoperative deterioration of facial nerve function (Romstöck et al., J Neurosurg 2000;93:586-593), were seen in 3 of the 15 patients with trigeminal neuralgia. The quantity of A-trains observed was much less than it is known from patients operated on tumors of the cerebellopontine angle. None of the trigeminal neuralgia-patients experienced postoperative deterioration of facial nerve function. The present study shows that A-trains do not only occur during tumor surgery, but also during procedures with indirect manipulation of the facial nerve. They do not necessarily lead to postoperative paresis as long as certain thresholds concerning amount and length of these A-trains are not exceeded.

Diabetes, cognitive function, and the blood-brain barrier.

From a complications standpoint, diabetes mellitus is a disease of the vasculature. Diabetics face a considerably higher risk of developing cardiovascular and cerebrovascular diseases. Both large and small blood vessels are susceptible to alterations from diabetes. Endothelial cell dysfunction associated with small vessel (known as microangiopathy) is a primary factor in the development and progression of diabetes-related disabilities, including blindness, kidney failure, and peripheral neuropathy. Recent clinical evidence show that people with diabetes have increased incidences of vascular dementia, ventricular hypertrophy, lacunar infarcts, hemorrhage, and may be a predisposing factor for Alzheimer's disease. However, the effects of diabetes mellitus on the cerebral microvascular are still largely unknown. This communication will review the relationship between diabetes mellitus and changes in cognition with a particular focus on how alterations in blood-brain barrier structure and function may play a long term role in worsened cognitive abilities.

Treatment with melagatran alone or in combination with thrombolytic therapy reduced ischemic brain injury.

Melagatran is a potent direct thrombin inhibitor and it is an effective agent in the prevention of stroke in patients with atrial fibrillation (AF); however, there are no data about its actions in the treatment of acute ischemic stroke. In the present study, we evaluated the neuroprotective actions of melagatran using an embolic model of stroke in rats. We first examined protective effects at increasing doses of melagatran. Then, we examined the effects of melagatran administered at different time points following middle cerebral artery (MCA) occlusion. We also evaluated the effects of combination therapy with melagatran and tissue plasminogen activator (tPA) in this model. Finally, we examined if melagatran can improve compromised microcirculation in the ischemic injured brain. The medication alone or in combination with tPA was well tolerated. Melagatran reduced ischemic brain injury in a dose-response manner, and also in a time dependent manner. Combination treatment of melagatran and tPA was superior to either treatment alone. There was no significant increase in symptomatic or asymptomatic hemorrhages in the treated animals. Melagatran treatment also reduced perfusion deficits in the ischemic injured brain. The present study is the first report on the usefulness of melagatran in embolic ischemic stroke. Our research shows that melagatran is an effective agent in the treatment of ischemic brain injury. The protective effects of this medication are likely due to its actions in enhancing thrombus dissolution and preventing formation of microthrombosis in the ischemic injured brain. Finally, the combination with melagatran and tPA appears safe and superior to each treatment offered alone.

Substance P-mediated expression of the pro-angiogenic factor CCN1 modulates the course of colitis.

Substance P (SP) regulates important intestinal functions, such as mucosal permeability, motility, chloride secretion, and inflammation via the neurokinin-1 receptor (NK-1R). Previous reports showed that vascularization and expression of angiogenic factors are evident in the colonic mucosa of rats with colitis and patients with inflammatory bowel disease. Here we determined whether SP is associated with angiogenesis. Human NCM460 colonocytes stably transfected with the human NK-1R (NCM460-NK-1R cells) and mice with dextran sodium sulfate-induced colitis were used. We found that expression of the angiogenic factor CCN1 was increased in the colons of patients with Crohn's disease and ulcerative colitis. Mucosal extracts from inflammatory bowel disease patients induced human intestinal microvascular endothelial cell migration that was inhibited by blockade of CCN1 and its receptor integrin alphavbeta3. Both the degree of angiogenesis and CCN1 expression were elevated in the colons of mice with dextran sodium sulfate-induced colitis, which was reduced by treatment with the NK-1R antagonist CJ-12255. SP also increased CCN1 expression in NCM460-NK-1R colonocytes. SP exposure to human intestinal microvascular endothelial cells co-cultured with NCM460-NK-1R cells induced angiogenic activity that was inhibited by CCN1 silencing. In addition, intracolonic overexpression of CCN1 induced angiogenesis in mouse colon. Thus, SP mediates angiogenesis via CCN1 during colitis.

Pathophysiological role of platelets and platelet system in acute pancreatitis.

The most successful approach for restoring normal long-term glucose homeostasis in type I diabetes mellitus is whole-organ pancreas transplantation. Graft pancreatitis is observed in up to 20% of patients and may lead to loss of the transplanted organ. Several pathophysiological events have been implicated in this form of pancreatitis. The most important cause of early graft pancreatitis is ischemia/reperfusion (I/R)-related disturbance of microvascular perfusion with subsequent hypoxic tissue damage. Recently, considerable evidence accumulated that, among a variety of other pathophysiological events, the activation of platelets can contribute to I/R injury in the course of acute pancreatitis experimentally and clinically. This review summarizes the events affecting platelet function and, therefore, pancreatic microcirculation leading to acute pancreatitis. Therapeutic approaches and own results are presented.

Measurement of blood flow in the rotator cuff using laser Doppler flowmetry.

The aim of this study was to define the microcirculation of the normal rotator cuff during arthroscopic surgery and investigate whether it is altered in diseased cuff tissue. Blood flow was measured intra-operatively by laser Doppler flowmetry. We investigated six different zones of each rotator cuff during the arthroscopic examination of 56 consecutive patients undergoing investigation for impingement, cuff tears or instability; there were 336 measurements overall. The mean laser Doppler flowmetry flux was significantly higher at the edges of the tear in torn cuffs (43.1, 95% confidence interval (CI) 37.8 to 48.4) compared with normal cuffs (32.8, 95% CI 27.4 to 38.1; p = 0.0089). It was significantly lower across all anatomical locations in cuffs with impingement (25.4, 95% CI 22.4 to 28.5) compared with normal cuffs (p = 0.0196), and significantly lower in cuffs with impingement compared with torn cuffs (p < 0.0001). Laser Doppler flowmetry analysis of the rotator cuff blood supply indicated a significant difference between the vascularity of the normal and the pathological rotator cuff. We were unable to demonstrate a functional hypoperfusion area or so-called 'critical zone' in the normal cuff. The measured flux decreases with advancing impingement, but there is a substantial increase at the edges of rotator cuff tears. This might reflect an attempt at repair.

[Current conception of stress and adaptation subject to new data of tissue hypoxia genesis].

State-of-the-art conception of stress is represented as an interrelation between stress, tissue hypoxia and adaptation. Under the influence of stressors the cell metabolism changes with producing of chemical substances capable pathologically to get bound with cell receptors. These substances change in cells optimal energy transformation (biochemical stage) and disturb cell functions (pharmacological stage). Biochemical and pharmacological stages of stress in uncellulates and in human cells are homotypic. The clinical stage of stress is typical only for humans and animals. Dysfunction of plane muscles (PM) myocytes leads to local microcirculation disturbances, transitory hypoxia and partial disorder in affected organ function. Local microcirculation disturbances are accompanied by serotonin release from damaged platelets, which leads to complete functional recovery of PM myocytes, microcirculation and affected organ function, or to formation of local "mute" focuses of tissue necrosis--the adaptation is effective. Insufficient serotonin release from damaged platelets leads to extension of hypoxia focus, lesion, tissue necrosis. The stress loses its nonspecificity and turns into infarction of myocard, brain etc., with specific clinical course--the adaptation is not effective.

[Changes in microcirculation of the urinary bladder in patients with stage II prostatic adenoma depending on the treatment method].

To determine microcirculation in the wall of the urinary bladder in prostatic adenoma, we used a laser analyzer of capillary circulation LAKK-01. Two groups participated in the trial: 105 males with stage II prostatic adenoma (the study group) and 25 volunteers (the control group). We estimated normal parameters of microcirculation in the wall of the bladder. In stage II prostatic adenoma the above microcirculation decreased to a subcritical perfusion level. Significantly earlier and complete recovery of microcirculation was observed in patients who had taken cardura (Pfizer) in a dose 2 mg/day for 3 months after transurethral resection of prostatic gland. Thus, 2 mg/day cardura (Pfizer) in patients with prostatic adenoma of stage II after TUR of the prostate promotes early and effective recovery of microcirculation.

[Defects in spermatogenesis and their correction in patients with chronic abacterial prostatitis].

A total of 28 males aged 20-46 years with chronic abacterial prostatitis (CAP) were divided into two groups. Group 1 patients received standard therapy (prostatotropic, vitamin, antioxidant); group 2 received the same standard treatment plus peloid therapy including silver-containing clay "Bekhtemirskaya". Eleven males with documented fertility (sperm donors) comprised a control group. The participants of the trial were examined for ejaculate indices, activity of the antioxidant system, ion composition of ejaculate, prostatic microcirculation before the treatment, on treatment day 14 and 90. The examination revealed the following disorders in CAP patients: low activity of anti-oxidant enzymes, abnormal static microcirculation, low content of normal spermatozoa in ejaculate. Complex rehabilitation of the patients of both groups improved prostatic microcirculation, raised activity of the antioxidant system resulting in better mobility and viability of spermatozoa. In group 2 the results were better showing the efficacy of local peloid therapy.

Changes of cerebral blood flow during the secondary expansion of a cortical contusion assessed by 14C-iodoantipyrine autoradiography in mice using a non-invasive protocol.

Although changes of cerebral blood flow (CBF) in and around traumatic contusions are well documented, the role of CBF for the delayed death of neuronal cells in the traumatic penumbra ultimately resulting in secondary contusion expansion remains unclear. The aim of the current study was therefore to investigate the relationship between changes of CBF and progressive peri-contusional cell death following traumatic brain injury (TBI). CBF and contusion size were measured in C57Bl6 mice under continuous on-line monitoring of (ETp)CO2 before, and at 15 min and 24 h following controlled cortical impact by 14C-iodoantipyrine autoradiography (IAP-AR; n = 5-6 per group) and by Nissl staining, respectively. Contused and ischemic (CBF < 10%) tissue volumes were calculated and compared over time. Cortical CBF in not injured mice varied between 69 and 93 mL/100mg/min depending on the anatomical location. Fifteen minutes after trauma, CBF decreased in the whole brain by approximately 50% (39 +/- 18 mL/100mg/min; p < 0.05), except in contused tissue where it fell by more than 90% (3 +/- 2 mL/100mg/min; p < 0.001). Within 24 h after TBI, CBF recovered to normal values in all brain areas except the contusion where it remained reduced by more than 90% (p < 0.001). Contusion volume expanded from 24.9 to 35.5 mm3 (p < 0.01) from 15 min to 24 h after trauma (+43%), whereas the area of severe ischemia (CBF < 10%) showed only a minimal (+13%) and not significant increase (22.3 to 25.1 mm3). The current data therefore suggest that the delayed secondary expansion of a cortical contusion following traumatic brain injury may not be caused by a reduction of CBF alone.

Alpha adrenoceptor agonist-induced microcirculatory oscillations are reduced in diabetic neuropathy.

In diabetic patients small fiber neuropathy has been associated with impairment of 0.1 Hz microvascular vasomotion. The aim of this study was (1) to investigate whether vasoconstriction-induced microvascular oscillations in the skin are reduced in diabetic patients with peripheral and/or autonomic neuropathy, and (2) whether this method could be used as a non-invasive surrogate marker to assess diabetic small fiber neuropathy. Four matched groups were studied: diabetic patients without neuropathy (D), with peripheral neuropathy (DPN), with peripheral and autonomic neuropathy (DAN), and non-diabetic controls (Ctrl). All participants were evaluated for peripheral and autonomic neuropathy, microvascular endothelial function, and metabolic syndrome indicators. Laser Doppler flowmetry was used to measure oscillations after iontophoresis of the alpha one selective agonist phenylephrine. approximately 0.1-Hz oscillations recorded at the foot were significantly attenuated in diabetic patients with peripheral and/or autonomic neuropathy (DPN and DAN groups) compared to diabetic patients without neuropathy or non-diabetic controls. In the forearm, microvascular oscillations were significantly reduced only in patients with autonomic neuropathy (DAN). Oscillation measures correlated significantly (P<0.001) with all markers of peripheral neuropathy but not with markers of measurements of microvascular endothelial function, or metabolic syndrome markers. In a logistic regression model, reduced microvascular oscillations at the foot were a strong predictor for the presence of peripheral neuropathy. The measurement of phenylephrine-induced approxiamtely 0.1-Hz microvascular oscillation may represent a useful non-invasive tool with which to study the effects of treatment strategies on the diabetic small fiber neuropathy.

Improvement in circulation and in cardiovascular risk factors with a proprietary isotonic bioflavonoid formula OPC-3.

This study investigated the efficacy of isotonic bioflavonoid supplementation, OPC-3 on 61 individuals presenting with risk factors meeting the criteria for metabolic syndrome. Subjects were supplemented with a proprietary isotonic bioflavonoid OPC-3 or placebo over 2 months. Plasma oxidative stress status was significantly lowered by 10.1% with OPC-3. All major cardiovascular risk factors were improved with blood pressure, total cholesterol, and fasting blood glucose lowered. OPC-3 significantly improved endothelial function as evaluated by increased vasorelaxation in reactive hyperemia and enhanced diastolic carotid artery flow. Cardiac ultrasound scanning revealed a significant increase of left ventricular ejection fraction. Skin microcirculation was enhanced, and better tissue perfusion led to significantly increased transcutaneous oxygen partial pressure and decreased pCO(2). With OPC-3 a dramatic and significant plasma C-reactive protein decrease by 52.1% occurred. Individuals may improve key cardiovascular risk factors by daily supplementation with the bioflavonoid OPC-3 as an important part of a healthier lifestyle.

Management of petrosal veins during microvascular decompression for trigeminal neuralgia.

OBJECTIVE: Venous compression might be the main cause of incomplete decompression and symptom recurrence after microvascular decompression (MVD) in patients with trigeminal neuralgia. Although it can be killed in most cases, cutting the vein sometimes has the potential risk arising from venous congestion. To maneuver the vein safely, we introduced a temporary occlusion test of the vein. METHODS: Among 407 consecutive MVD cases, 48 (11.8%) offending and 157 block veins were encountered. The vein was cut directly in 147 (71.7%). Owing to the potential risk following killing of the vein, 58 (28.3%) patients underwent venous occlusion test with neurophysiologic monitoring during the operation. The temporal occlusion should be ceased immediately as soon as any changes in brainstem auditory evoked potential (BAEP) or trigeminal evoked potential (TEP) wave figuration turn up; otherwise, it would last for 15 minutes. RESULTS: The occlusion test was negative in 53 (91.4%), while positive in five patients (8.6%). According to the results, we cut the vein in test-negative patients, which made the operation easy and offered a satisfactory decompression. Among the five positive cases, the vein was finally saved in two and cut in three cases. Yet, all the three patients developed a severe ipsilateral cerebellar edema and brainstem shift after the vein was sacrificed. Despite those patients were reoperated on immediately for posterior fossa decompression, they remained equilibrium disorder with numbness in ipsilateral face and mind hemiparesis in contralateral extremities post-operatively. The residual two patients had an incomplete pain relief. CONCLUSION: This venous occlusion test could help the surgeon in making a right decision before manipulation of the petrosal veins during MVD.

Acute basilar artery occlusion: topographic study of infarcts.

OBJECTIVE: To determine the ischemic lesions distribution and extension of patients with basilar artery thrombosis by the means of magnetic resonance imaging (MRI). METHODS: In 17 patients with thrombosis of the basilar artery, MRI was performed, including T2-weighted, magnetic resonance angiography (MRA) and diffusion-weighted imaging (DWI) sequences in the short-term phase (<48 hours). The shapes of ischemic lesions were obtained by graphic software and overlapped on a representative layer outline background. RESULTS: The MRA showed basilar artery occlusion in all cases and the DWI revealed different patterns of ischemic lesions. Most patients showed multiple lesions within the posterior circulation territory. Lesions more often occurred in pontes, cerebellums and mesencephalons than medullas, thalami and occipital lobes. Basilar pons, cerebral crus and cerebellum hemisphere were more susceptible than pontine tegmentum, vermis, midbrain tegmentum and tectum. CONCLUSIONS: When the basilar artery is occluded, basilar pons, cerebral crus and cerebellum hemisphere were most susceptible. The branches with smaller lumen of basilar artery, which are easier to be affected, are thought to be the cause of such a phenomenon.