Systemic Arterial Pressure Levels Research Articles

Pathogenesis of chronic disorders of cerebral circulation

Chronic disorders of cerebral circulation are a common syndrome, in the pathogenesis of which the important role play structural and functional alterations in large and small arteries, autoregulation of cerebral circulation and the level of systemic arterial pressure. Drugs that increase cerebral blood flow and restore the ability to its autoregulation are used, among others, in treatment of patients with CRMC. The possibility of using nicergoline (sermion) for the treatment of patients with CRMK is considered.

Novel FBLN5 Mutation of Congenital Autosomal Recessive Cutis Laxa With Isolated Right Ventricular Non-Compaction (RVNC): New Findings on Echocardiographic Speckle-Tracking Strain Imaging of RVNC

: We report on a novel mutation in a two-year-old child with autosomal recessive cutis laxa with severe generalized laxity of the skin, prematurely aged appearance, conjunctival chalasia, episodes of severe rectal prolapse, isolated right ventricular non-compaction, (RVNC), significant pulmonary hypertension at the systemic arterial pressure level, severe tricuspid regurgitation, corpulmonale secondary to recurrent pulmonary infections, and mixed pulmonary fibrosis and emphysema. Next generation sequencing of cutis laxa genes identified a novel homozygous mutation in the FBLN5 gene (homozygous sequence alteration of c.907C > T [p. Gin303*] FBLN5 [ENS0342058]). Despite severe and generalized disorder in the patient’s connective tissues, she had no primary valvar or vascular abnormalities in the heart. Complete speckle-tracking strain imaging (SI) by two-dimensional echocardiography showed decreased systolic longitudinal and transverse strain in the involved segment of the right ventricle (RV).

Neural Reflex Hypotension Induced by Very Small Dose of Hypertonic NaCl Solution in Rats

Although the precise mechanisms of transient hypotension after intravenous infusion of hypertonic saline (HTS) are not yet clarified, a rapid infusion of HTS is widely used as the initial therapy of hypovolemia. We investigated the effect of the intravenous infusion of a small dose of 0.97-9.7% NaCl solutions in anesthetized rats. Intravenous infusion of HTS at a rate of 0.3 ml/kg/min for 1 min produced the transient hypotension lasting for several minutes. The depressor response to HTS was not abolished by bilateral cervical vagotomy. The HTS infusion into the femoral vein evoked the depressor response with a larger magnitude and a shorter latency than that into the aortic arch. While the arterial baroreceptor pressure was kept constant at the baseline level of systemic arterial pressure, HTS-induced hypotension was significantly augmented. The gain factor of the arterial baroreflex was reduced by intravenous HTS. Pretreatment with bretylium tosylate completely abolished the depressor response without affecting the baseline level of arterial pressure. These results suggest that the depressor response to the very small dose of intravenous HTS is the sympathosympathetic neural reflex with cardiopulmonary afferents and vasomotor efferents.

Modeling cerebral autoregulation and CO2 reactivity in patients with severe head injury.

The mathematical model presented in a previous work is used to simulate the time pattern of intracranial pressure (ICP) and of blood velocity in the middle cerebral artery (VMCA) in response to maneuvers simultaneously affecting mean systemic arterial pressure (SAP) and end-tidal CO2 pressure. In the first stage of this study, a sensitivity analysis was performed to clarify the role of some important model parameters [cerebrospinal fluid (CSF) outflow resistance, intracranial elastance coefficient, autoregulation gain, and the position of the regulation curve] during CO2 alteration maneuvers performed at different SAP levels. The results suggest that the dynamic "ICP-VMCA" relationship obtained during changes in CO2 pressure may contain important information on the main factors affecting intracranial dynamics. In the second stage, the model was applied to the reproduction of real ICP and velocity tracings in neurosurgical patients. Ten distinct tracings, taken from six patients during CO2 changes at different mean SAP levels, were reproduced. Best fitting between model and clinical curves was achieved by minimizing a least-squares criterion function and adjusting certain parameters that characterize CSF circulation, intracranial compliance, and the strength of the regulation mechanisms. A satisfactory reproduction was achieved in all cases, with parameter numerical values in the ranges reported in clinical literature. It is concluded that the model may be used to give reliable estimations of the main factors affecting intracranial dynamics in individual patients, starting from routine measurements performed in neurosurgical intensive care units.

Nitric oxide and sympathoexcitatory cardiovascular neurons of the ventrolateral medulla in cats

In acute experiments on cats, the effects of injections of nitric oxide (NO) donors and an inhibitor of its synthesis into the sympathoexcitatory neuronal structures in the ventrolateral medulla (VLM) were studied to examine their effects on the peripheral mechanisms of the cardiovascular control. Unilateral injections of NO donors, nitroglycerine (1.3–5.2 nmol) or sodium nitroprusside (1.1–4.6 nmol) into the sites of the sympathoexcitatory neurons residing in the VLM induced the lowering of the systemic arterial pressure (SAP) in a dose-depended fashion. Two types of the hypotensive responses have been distinguished. In the first type responses, lowering of the SAP level was mainly due to a decrease in the peripheral vascular resistance (PVR), while the heart rate (HR) and stroke volume (SV) were only slightly reduced. In the second type responses, the drop in SAP level resulted mainly from a decrease in the HR and myocardial contractivity. These effects were induced by the limitation of the descending excitatory influences to the heart and vessels from the VLM sympathoexcitatory systems. An increase in the NO concentrations in the neuronal structures located 2.5–4.5 mm caudally to the trapezold bodies resulted in the first type responses, while that in the sites immediately adjacent to the caudal sympathoinhibitory area (0.5–1.5 mm rostrally to the XIIth cranial nerve roots) was associated with the second type of reactions. Stimulation of the endogenous NO release from the neurons after injections of L-arginine induced the same cardiovascular shifts as exogenic NO did, and attenuation of NO synthesis following injections of NO antagonist L-NMMA into the VLM neuronal structures evoked hemodynamic shifts of a reverse direction. Injections of NO donors inhibited the reflex responses induced by the activation of the carotid sinus receptors. Our data give further evidence for NO involvement in the inhibitory control of the cardiac activity and vascular tone through those VLM sympatoexcitatory neurons, which are involved in the system of central neurogenic cardiovascular control and the activity of which prevent the development of hypertension.

Nitric oxide influences ventrolateral medullary mechanisms of vasomotor control in the cat

In acute experiments on cats changes in the background sympathetic activity in the renal nerve, chosen as a model of vaso-constrictor nerve, together with arterial pressure shifts have been found following injections of nitric oxide (NO) containing drugs into the ventrolateral medulla. This is the first report of evidence that both sodium nitroprusside, which produces NO spontaneously and thus mimics endothelium-derived relaxing factor (EDRF), and l-arginine, being a precursor for NO, as well as l-N G-monomethyl- l-arginine ( l-NMMA) which inhibits synthesis of NO, induce remarkable changes in the background activity of the renal nerve and systemic arterial pressure (SAP) level shifts, following unilateral injections of drugs examined into the rostral (RVLM) and caudal (CVLM) ventrolateral medulla. These sites are essential for the maintenance of arterial pressure level and vascular tone control. Injections of NO-containing drugs in the RVLM induce attenuation of the renal nerve sympathetic activity and lower the SAP level, while injections in the CVLM reverse these effects. After previous application of Methylene blue on the ventral medullary surface we failed to induce any of the effects following NO injections in the sites examined. Our results raise the possibility that NO influences mechanisms of the neurogenic vasomotor control, realized by neurons within the RVLM and the CVLM via activation of the guanylate cyclase.

Changes in blood flow: hematocrit relationship in larger blood vessels.

We assessed the red blood cell concentration (by estimating the cell number and hematocrit) in blood samples taken from the rabbit common carotid artery. This parameter was found to be dependent upon the blood flow velocity in the artery: reduction of the velocity to mean 62% of the initial value (100%), produced by partial obstruction of the artery, resulted in the decrease of red cell concentration by 1/4 to 1/7, despite the same systemic arterial pressure level and absence of appreciable changes in the blood taken from the control (contralateral) carotid artery. The relationship of the red cell number and hematocrit in the carotid artery was linear (r = 0.76). We conclude therefore, that changes in the local blood flow: hematocrit relationship induced by separation of red cells and plasma in vascular bifurcations occur not only in the microvascular beds, but in the entire arterial branching sequence, including the largest arteries.

Effect of arterial pressure on left ventricular O 2 consumption, coronary blood flow, and reserve capacity following coronary occlusion

The effect of mean systemic arterial pressure ( SAP) on myocardial O 2 consumption (MV̇O 2) coronary blood flow (CBF) and the reduction of left ventricular (LV) reserve capacity resulting from coronary artery occlusion was studied in 25 open-chest pentobarbital anesthetized dogs with fixed cardiac output and controlled heart rate (HR) and SAP . In all animals, baseline MV̇O 2 and CBF were obtained and LV reserve capacity was determined by identifying the HR and SAP level which raised mean left atrial pressure to 12 mm. Hg. After uniform placement of a pericoronary snare, the dogs were randomized to five equal groups, and SAP was set at 40, 70 (two groups), 100, and 130 mm. Hg. MV̇O 2 and CBF were redetermined and the coronary artery was ligated in all except one group (70 mm. Hg) which served as sham control. Thirty minutes after coronary occlusion, MV̇O 2, CBF, and LV reserve capacity were determined again. Percent of nonperfused myocardium did not differ among groups (27.6 ± 1%). MV̇O 2 bore a linear relationship to SAP setting whereas CBF bore a curvilinear relationship. Coronary occlusion did not modify these relationships. Significant, but similar decreases in tolerated HR (23.1 ± 4.7 min. −1) and SAP (41.9 ± 6.2 mm. Hg) from control values were observed in all four groups regardless of SAP setting. We concluded that the impact of coronary ligation on MV̇O 2, CBF, the loss of functional reserve capacity, and possibly the extent of ischemic injury of the left ventricle, is not modified by afterload changes. However, optimal O 2 supply-to-demand ratio appears at SAP of about 100 mm. Hg.

Effects of hemorrhagic hypotension on the cerebral circulation. II. Electrocortical function.

The effects of graded hemorrhagic hypotension on electrocortical function was investigated in 12 cats anesthetized with alpha-chloralose. Cerebral function was assessed both in terms of spontaneous activity (EEG) and the somatosensory evoked response. No significant changes in the EEG trace or in the amplitude of the positive/negative waves of the primary evoked response were observed at mean arterial pressures of between 120 mm Hg and 40 mm Hg. At levels of systemic arterial pressure of less than 40 mm Hg cortical rhythms became slower as pressure was decreased and an isoelectric EEG was recorded in the pressure range 10--30 mm Hg. The earliest sign of any change in the amplitude of the primary evoked responses was observed at arterial pressures of approximately 35--40 mm Hg. Below this value the amplitude decreased with decreasing systemic pressure and became zero in the pressure range 15--25 mm Hg.