Assessment of Basilar Artery Reactivity in Stroke and Subarachnoid Hemorrhage Using Wire Myograph.

Blood flow regulation of normal cerebral arteries is a critical and important factor to supply the brain tissue with nutrients and oxygen. Stroke insult results in a disruption or reduction in cerebral arteries' blood flow with subsequent brain tissue damage. Hemorrhagic stroke is one type of stroke and accounts for about 13 % of all of stroke insults. In this type of stroke, the cerebral artery breaks open and causes bleeding in or surrounding the brain. Subsequently, this bleeding causes blood vessels to constrict in a process called vasospasm, in which the vessels narrow and impede the blood flow to brain tissue. Hemorrhagic stroke is the major cause of prolonged constriction of cerebral arteries. This leads to partial brain damage and sometimes death in patients with aneurysmal subarachnoid hemorrhage. Among the key delicate techniques to assess small blood vessel functionality is the wire myograph, which can be utilized in several cerebral injury models including stroke. The wire myograph is a device that provides information about the reactivity, stiffness, and elasticity of small blood vessels under isometric conditions. In this book chapter, we describe the techniques involved in wire myography assessment and the different measures and parameters recorded; we describe the utility of this technique in evaluating the effects of subarachnoid hemorrhage on basilar artery sensitivity to different agonists.

Noninvasive assessment of coronary microvascular function in women at risk for ischaemic heart disease.

The primary objective of the current review is to describe the assessment of coronary microvascular function by noninvasive imaging techniques in women at risk for and with ischaemic heart disease (IHD). The search criteria were the analyses of the related bibliography published in PUBMED database. Normal or minimal obstructive coronary artery disease (CAD) at angiography is a common finding in women with signs of ischaemia. Up to 50% of them will have coronary microvascular dysfunction, suggesting that the mechanism of ischaemia may be localised at coronary microcirculation level. Noninvasive measurements of coronary microvascular function can be performed by radionuclide techniques. In particular, positron emission tomography (PET) measures myocardial blood flow (MBF) not only relatively but also in absolute units. Thus, PET offers the possibility to uncover microvascular dysfunction even in patients without obstructive CAD. PET-derived estimates of MBF showed an abnormal coronary microvascular function in women with chest pain and non-obstructive CAD and in women with high-risk conditions for CAD. Interestingly, there is a relationship between an abnormal coronary vascular function and adverse cardiovascular outcomes. In particular, this significant relationship was observed with measurements related to endothelial function. Recent evidence suggests that vascular dysfunction plays a central role as an estimator of outcomes in women at risk for or with IHD. Therefore, assessment of coronary vascular function in these women appears to be of clinical relevance. Whether such evaluation may have an impact to reduce cardiac events needs further investigation.

[Effect of enalapril on endotheliun-dependent contractile reactions and oxygen cost of work of the smooth muscles in experimental diabetes mellitus].

The influence of angiotensin-converting enzyme on endotheliun-dependent contractile vascular reactions was investigated on the rat model of streptozotocin-induced diabetes mellitus. It is shown, that the long-term administration of enalapril results in partial restoration of disturbed at diabetes mellitus reactions and also to reduction of oxygen cost of smooth muscles and myocardial work. Thus, after 28-day's of oral administration of this drug the restoration of endotheliun-dependent dilatation of aorta and coronary vessels, increase of stretch-induced contractile responses of vascular smooth muscles, reduction of stiffness of isolated portal vein strips are observed. Possible mechanisms of such changes are following: increase of nitric oxide synthesis (at the expense of constitutive NOS activity) and reduction of oxidative stress, to what the decrease of diene conjugates contents in tissues of animals with diabetes mellitus after long introduction of enalapril testifies.

Functional assessment of human femoral arteries after cryopreservation.

An established method for the cryopreservation of human femoral arteries for subsequent transplantation as allografts has been studied with particular attention to preservation of smooth muscle and endothelium. Human femoral arteries (HFAs) were harvested from multi-organ donors. Two groups were established; a control group of unfrozen HFAs and a group of cryopreserved HFAs. Cryopreservation was performed using RPMI solution containing dimethyl sulfoxide and the rate of cooling was 1 degrees C/min to -40 degrees C and faster thereafter until -150 degrees C was reached. The contraction and relaxation responses of unfrozen and frozen/thawed arteries were assessed by measurement of the isometric force generated by the HFAs in an organ bath. After thawing (warming was at 15 degrees C/min) the maximal contractile response to noradrenaline was 43% of the response of unfrozen HFAs. The endothelium-independent response to sodium nitroprusside was not altered, whereas the endothelium-dependent relaxation response to acetylcholine was slightly altered. The cryopreservation method used provided limited preservation of the contractility of human femoral arteries, and good preservation of both endothelium-independent and endothelium-dependent relaxation responses.

Pathologic assessment of vasculopathies in pulmonary hypertension.

Pulmonary arterial hypertension (PAH) includes various forms of pulmonary hypertension of different etiology but similar clinical presentation and functional derangement. Histopathological vascular changes in all forms of PAH are qualitatively similar but with quantitative differences in the distribution and prevalence of pathological changes in various portions of the pulmonary vascular bed. The documentation of these topographic variations in the response of the pulmonary vasculature to injury may be important to understand the pathogenesis of the various subsets of PAH. To standardize the precise histopathological documentation of the pulmonary vasculopathy in PAH we propose a histopathological classification that includes both the predominant segment of the pulmonary vasculature affected and the possible coexistence of pathological changes in other vascular segments.

[Angio-MR assessment of vasomotor reactivity impairment as a long-term outcome of SAH following intracerebral aneurysm rupture]. / Reaktywnosc naczyn mózgowych w póznym okresie po SAH z peknietego tetniaka sródczaszkowego w badaniu angio-MR.

Studies on long-term outcome of subarachnoid hemorrhage (SAH) have been carried out for many years using various neuroimaging techniques, such as e.g.: SPECT, PET, TCD and XeCT. In our study angio-MRI supplemented with the acetazolamide test was used to assess cerebrovascular reserve impairment in 30 patients within 6 months since clipping an intracranial aneurysm. Severity of the SAH course was evaluated using the WFNS (World Federation of Neurosurgical Societies) scale [3]. The patients' clinical status was assessed at follow-up by means of the Glasgow Outcome Scale (GOS) [8]. Cereberovascular reserve evaluated at the follow-up in hypercapneal conditions was found to be insufficient. The degree of vessel reactivity dysfunction as a long-term outcome of SAH turned out to depend on massiveness of hemorrhage from the ruptured aneurysm.

Continuous assessment of the cerebral vasomotor reactivity in head injury.

OBJECTIVE: Cerebrovascular vasomotor reactivity reflects changes in smooth muscle tone in the arterial wall in response to changes in transmural pressure or the concentration of carbon dioxide in blood. We investigated whether slow waves in arterial blood pressure (ABP) and intracranial pressure (ICP) may be used to derive an index that reflects the reactivity of vessels to changes in ABP. METHODS: A method for the continuous monitoring of the association between slow spontaneous waves in ICP and arterial pressure was adopted in a group of 82 patients with head injuries. ABP, ICP, and transcranial doppler blood flow velocity in the middle cerebral artery was recorded daily (20- to 120-min time periods). A Pressure-Reactivity Index (PRx) was calculated as a moving correlation coefficient between 40 consecutive samples of values for ICP and ABP averaged for a period of 5 seconds. A moving correlation coefficient (Mean Index) between spontaneous fluctuations of mean flow velocity and cerebral perfusion pressure, which was previously reported to describe cerebral blood flow autoregulation, was also calculated. RESULTS: A positive PRx correlated with high ICP (r = 0.366; P < 0.001), low admission Glasgow Coma Scale score (r = 0.29; P < 0.01), and poor outcome at 6 months after injury (r = 0.48; P < 0.00001). During the first 2 days after injury, PRx was positive (P < 0.05), although only in patients with unfavorable outcomes. The correlation between PRx and Mean index (r = 0.63) was highly significant (P < 0.000001). CONCLUSION: Computer analysis of slow waves in ABP and ICP is able to provide a continuous index of cerebrovascular reactivity to changes in arterial pressure, which is of prognostic significance.

Normal sympathetic vasomotor and cardiac parasympathetic activities in patients with primary aldosteronism: assessment by spectral analysis.

The role of the autonomic nervous system in hypertension due to mineralocorticoid excess remains unclear. To address this issue, we performed power spectral analysis of blood pressure (BP) and RR interval oscillations in 20 patients with primary aldosteronism (PA), 54 patients with essential hypertension (EH) and 45 normotensive (NT) subjects. Blood pressure and the degree of organ damage were similar between PA and EH groups. Age did not differ between the three groups. The Mayer wave power spectrum (MWP) of BP (approx. 0.1 Hz), an index of sympathetic vasomotor tone, was smaller in patients with PA than in patients with EH either while subjects were supine (systolic/diastolic; 3.9 +/- 3.2 (SD)/1.5 +/- 1.3 vs. 5.5 +/- 4.2/2.1 +/- 1.6 mmHg2, P < 0.05 for both) or standing (7.6 +/- 6.6/3.0 +/- 3.0 vs. 17.7 +/- 23.7/7.2 +/- 8.3 mmHg2, P < 0.05 for both). Supine respiratory-related power spectrum (RRP) of the RR interval (approx. 0.25 Hz), an index of cardiac parasympathetic tone, was greater in patients with PA than in patients with EH (545 +/- 574 vs. 302 +/- 464 ms2, P < 0.01). The MWP of BP and the RRP of the RR interval were similar between patients with PA and NT subjects. Adrenalectomy reduced the 24-h mean BP (-18 mmHg for systolic BP, P < 0.001; -12 mmHg for diastolic BP, P < 0.01) and increased the 24-h mean heart rate (+8 bpm, P < 0.001). Furthermore, the diastolic MWP increased mildly (+32%, P < 0.05) and the RRP of the RR interval decreased dramatically (-75%, P < 0.01) following adrenalectomy. These results suggest that both vascular sympathetic and cardiac parasympathetic regulatory systems have minor roles in the maintenance of hypertension in patients with PA. The autonomic nervous system contributes more to the maintenance of BP following than prior to adrenalectomy. This information may be useful for the management of hypertension still persists after removal of adrenal adenoma.

Physiological assessment of augmented vascularity induced by VEGF in ischemic rabbit hindlimb.

This study was designed to assess the physiological consequences of augmented vascularity induced by administration of vascular endothelial growth factor (VEGF), an endothelial cell-specific mitogen, in a rabbit model of hindlimb ischemia. Ten days after excision of the common and superficial femoral arteries from one hindlimb of 24 New Zealand White rabbits, VEGF (n = 15) or saline (control; n = 9) was selectively injected into the ipsilateral internal iliac artery. Limb perfusion was evaluated immediately pre-VEGF (baseline) and again at days 10 and 30. A Doppler guide wire was advanced to the internal iliac artery to record flow velocity at rest and at maximum flow velocity provoked by intra-arterial injection of papaverine. At baseline and at day 10, no differences in flow parameters were observed between the control and the VEGF-treated animals. By day 30, however, flow at rest (P < 0.05), maximum flow velocity (P < 0.001), and maximum blood flow (P < 0.001) were all significantly higher in the VEGF-treated group. These physiological findings complement previous-anatomic studies by providing evidence that a single intra-arterial bolus of VEGF augments flow, particularly maximum flow, in the rabbit ischemic hindlimb. These data thus support the notion that VEGF administration represents a potential treatment strategy for certain patients with lower extremity ischemia.

Assessment of venous muscle pump function by ambulatory calf volume strain gauge plethysmography after surgical treatment of varicose veins: a prospective study of 21 patients.

A prospective study of the improvement in leg muscle pump function after radical surgery was performed for treatment of varicose veins. Venous muscle pump function was assessed in 21 patients with primary varicose veins by means of ambulatory strain gauge plethysmography immediately before surgery and 3 months and 60 months after surgical treatment of varicose veins. The physiologic documentation of the operative efficacy was provided by the mean venous reflux, which was reduced by 54% (p less than 0.001), and the mean expelled volume, which was increased by 58% (p less than 0.001). Initially, all patients had improved venous muscle pump function. This improvement was still present 60 months after surgery. At clinical assessment 3 months after surgery, it was noted that 90% of the patients were without residual varicose veins (p less than 0.01). Sixty months after surgery, 71% of the patients were without apparent varicose veins (p less than 0.05). Subjective symptoms had virtually disappeared 3 months after surgery (p less than 0.001) but were found to a variable extent in 80% of the patients at the 60-month control follow-up. It is concluded that ambulatory strain gauge plethysmography may quantitate the effect of surgery in patients with venous valvular incompetence; in addition to measurements of refilling time, it is able to measure the muscle-pump-generated expelled volume because of in-place electrical calibration.

Venous muscle pump function in patients with primary lymphoedema: assessment by ambulatory strain gauge plethysmography.

The musculovenous pump function was assessed by ambulatory strain gauge plethysmography in 11 patients with primary lymphoedema. The venous function was within the normal range regarding both venous reflux and expelled volume. The values were compared with ten patients with chronic venous insufficiency and oedema. The values for venous function were clearly abnormal for the patients with venous insufficiency and different from those with primary lymphoedema. Ambulatory strain gauge plethysmography may be a useful non-invasive method in distinguishing between oedema of lymphatic or venous origin.

Experimental chronic cerebrovascular spasm in the monkey: an assessment of the functional changes in the cerebral arteries and their protection by diltiazem.

The structure and function of cerebral arteries obtained from a monkey model of chronic cerebral vascular spasm 5 days after hemorrhage have been examined. Narrowing of the larger cerebral arteries demonstrated by angiography at all sites of measurement seems to be due primarily to an increased wall rigidity associated with cellular damage, the resultant inflammatory response and large, long-lasting spontaneous increases in muscle tone. Changes in agonist sensitivity were extremely variable. The reduction of contractility of the vessel wall to a mean of 30% of control diminished the consequence of any changes in active tone characteristics. Neurogenic control on the side of the lesion was remarkably depressed. When treated with diltiazem, beginning 1 day before induction of hemorrhage and continuing to the time of sacrifice, arterial diameter was reduced at only 1 of the 6 standard sites of measurement and then by only a small amount. Neurologic effects invariably seen in the untreated monkeys were prevented by diltiazem. Many of the changes in the artery wall, including structural alterations, were diminished by the drug. Abnormal spontaneous myogenic tone was present but was less in the diltiazem-treated group; however, nerve damage and its functional consequences were not prevented. It is concluded that diltiazem, presumably by preventing the accumulation of intracellular calcium within the cell, prevents the initial events in the evolution of chronic cerebrovasospasm or narrowing. This is probably achieved by a diminishing of the direct vasoconstrictor effects and the toxicity of putative spasmogens released from blood clots, nerves and the brain on the vascular smooth muscle, thus interrupting the sequence leading to pathologic change.