Effect Of Arterial Blood Pressure Research Articles

Measuring the effect of thrombosis, thrombus maturation and thrombolysis on clot mechanical properties in an in-vitro model

Changes in acute ischemic stroke thrombi structure and composition may result in significant differences in treatment responsiveness. Ischemic stroke patients are often treated with a thrombolytic agent to dissolve thrombi, however these patients may subsequently undergo mechanical thrombectomy to remove the occlusive clot. We set out to determine if rt-PA thrombolysis treatment of blood clots changes their mechanical properties, which in turn may impact mechanical thrombectomy. Using a design-of-experiment approach, ovine clot analogues were prepared with varying composition and further exposed to different levels of compaction force to simulate the effect of arterial blood pressure. Finally, clots were treated with three r-tPA doses for different durations. Clot mass and mechanical behaviour was analysed to assess changes due to (i) Platelet driven contraction (ii) Compaction force and (iii) Thrombolysis. Clots that were exposed to r-tPA for longer duration showed significant reduction in clot mass (p < 0.001). Exposure time to r-tPA (p < 0.001) was shown to be an independent predictor of lower clot stiffness. A decrease in energy dissipation ratio during mechanical compression was associated with longer exposure time in r-tPA (p = 0.001) and a higher platelet concentration ratio (p = 0.018). The dose of r-tPA was not a significant factor in reducing clot mass or changing mechanical properties of the clots. Fibrinolysis reduces clot stiffness which may explain increased distal clot migration observed in patients treated with r-tPA and should be considered as a potential clot modification factor before mechanical thrombectomy.

The Effects of Acute Intracranial Pressure Changes on the Episcleral Venous Pressure, Retinal Vein Diameter and Intraocular Pressure in a Pig Model

ABSTRACT Purpose Orbital veins such as the retinal veins and episcleral veins drain into the cavernous sinus, an intracranial venous structure. We studied the effects of acute intracranial pressure (ICP) elevation on episcleral venous pressure, intraocular pressure and retinal vein diameter in an established non-survival pig model. Methods In six adult female domestic pigs, we increased ICP in 5 mm Hg increments using saline infusion through a lumbar drain. We measured ICP (using parenchymal pressure monitor), intraocular pressure (using pneumatonometer), episcleral venous pressure (using venomanometer), retinal vein diameter (using OCT images) and arterial blood pressure at each stable ICP increment. The average baseline ICP was 5.4 mm Hg (range 1.5–9 mm Hg) and the maximum stable ICP ranged from 18 to 40 mm Hg. Linear mixed models with random intercepts were used to evaluate the effect of acute ICP increase on outcome variables. Results With acute ICP elevation, we found loss of retinal venous pulsation and increased episcleral venous pressure, intraocular pressure and retinal vein pressure in all animals. Specifically, acute ICP increase was significantly associated with episcleral venous pressure (β = 0.31; 95% CI 0.14–0.48, p < .001), intraocular pressure (β = 0.37, 95%CI 0.24–0.50; p < .001) and retinal vein diameter (β = 11.29, 95%CI 1.57–21.00; p = .03) after controlling for the effects of arterial blood pressure. Conclusion We believe that the ophthalmic effects of acute ICP elevation are mediated by increased intracranial venous pressure producing upstream pressure changes within the orbital and retinal veins. These results offer exciting possibilities for the development of non-invasive ophthalmic biomarkers to estimate acute ICP elevations following significant neuro-trauma.

The Upright Body Position Increases Translaminar Pressure Gradient in Normotensive and Hypertensive Rats

ABSTRACTAim: Several lines of evidence suggest that the pathogenesis of glaucoma may depend on an increased translaminar pressure gradient (TPG), the difference between intraocular and intracranial pressure (ICP), rather than on intraocular pressure (IOP) itself. It has also been suggested that high blood pressure might correlate with the incidence of glaucoma; however, the data are contradictory. Here, we studied the effect of arterial blood pressure and changes in body position on TPG in rats.Methods: Experiments were performed on anesthetized 15- to 16-week-old, male, spontaneously hypertensive rats (hypertensive rats, n = 10) and Wistar–Kyoto rats (normotensive rats, n = 10). Continuous recordings of intracranial and IOPs were performed before, during, and after changing the body position from horizontal to vertical.Results: At baseline, hypertensive rats had a significantly higher arterial blood pressure than normotensive rats, while intraocular and intracerebroventricular pressures and TPG did not differ between the groups. Changing the body position from horizontal to vertical produced a significant decrease in ICP, a nonsignificant decrease in IOP, and a significant increase in the TPG. There was no significant difference between normotensive and hypertensive rats in the pattern of changes in intraocular and intracerebroventricular pressures and TPG.Conclusions: Change in the body position from horizontal to vertical, but not hypertension, causes a significant increase in TPG in rats. If further studies confirm that TPG plays a role in the etiology of glaucoma, a vertical position and changes in the body position might be considered as debilitating factors.

The Effects of Arterial Blood Pressure Reduction on Endocan and Soluble Endothelial Cell Adhesion Molecules (CAMs) and CAMs Ligands Expression in Hypertensive Patients on Ca-Channel Blocker Therapy

Background/Aims: To determine the effect of arterial blood pressure (BP) reduction on endocan and soluble cell adhesion molecules' (sCAM) plasma concentration and expression of their ligands on circulatory leukocyte subpopulations. Methods: 24 hypertensive subjects of both sexes (age: 53±8 yrs) were treated with Ca-channel blocker, amlodipin (5-10 mg/day for 8 weeks; to reach BP≤139/89mmHg). The serum sCAMs and endocan concentrations were determined by ELISA kits. Level of ICAM/VCAM ligands on leukocytes was assessed by flow cytometry. Paired t-test, or t-test were used as appropriate, with Pearson's correlation calculated; p<0.05 was considered significant (SigmaPlot v.11). Results: sICAM-1 and sVCAM-1 were decreased (p≤0.001 and p=0.002, respectively), while E-selectin concentration was increased after amlodipin treatment (P=0.014). CD11a/LFA-1 (ICAM-1 and endocan ligand) was significantly increased in all three cell types with BP decrease. CD15 and CD49d/VLA-4 (VCAM-1 ligand) did not change after the treatment. There was significant positive correlation of systolic and diastolic BP with ICAM-1 and VCAM-1, and significant negative correlation of systolic BP with CD11a/LFA-1. Endocan significantly positively correlated with ICAM-1. Conclusions: The increased expression of ICAM/VACM ligands, together with decrease of sCAMs and endocan suggests the de-activation of endothelium with reduction in BP, decreasing the adherence of circulatory leukocytes to endothelium; subsequently decreasing the risk for development of atherosclerosis.

The Effects of Arterial Blood Pressure on Rebleeding When BleedArrest, Celox and Traumadex are Used in a Porcine Model of Lethal Femoral Injury

Uncontrolled bleeding remains the leading cause of preventable death in trauma. Hemostatic agents are effective in hemorrhage control but often fail following high-volume crystalloid resuscitation. Aggressive fluid resuscitation increases the blood pressure which may dislodge the newly formed clot causing rebleeding. The purpose of this study was to determine the systolic blood pressure (SBP) and the mean arterial pressure (MAP) at which rebleeding occurs when a clot is formed by one of these hemostatic agents (BleedArrest, TraumaDex, or Celox) compared to a control group. This was a prospective, experimental study using male 5 Yorkshire swine per group (BleedArrest, TraumaDex, Celox, or control). The femoral artery and vein were transected to simulate a traumatic injury. Subjects were allowed to bleed for 60 seconds then one of the agents was poured into the wound. The control group underwent the same procedures but without the hemostatic agent. After 30 minutes, dressings were removed and the SBP was increased incrementally using intravenous phenylephrine until rebleeding occurred or until the arterial blood pressure reached 210 mm/Hg. The SBP and MAP were significantly higher in the BleedArrest, TraumaDex, and Celox groups compared to a control group (p < 0.05).

Effect of Arterial Blood Pressure on the Arterial to End-tidal Carbon Dioxide Difference During Anesthesia Induction in Patients Scheduled for Craniotomy

Before obtaining results of arterial blood gas analysis in mechanically ventilated patients undergoing neurosurgery, the volume of ventilation is primarily adjusted according to endtidal CO2 (EtCO2). We characterized the impact of various arterial blood pressure changes on arterial PCO2 (PaCO2) to EtCO2 differences (PaCO2-EtCO2) in patients anesthetized for craniotomy. Seventy-two elective craniotomy patients were enrolled in this prospective study. Noninvasive blood pressure was measured before anesthesia induction. Anesthesia was induced with thiopental, rocuronium or suxamethonium, and fentanyl and was maintained with inhaled anesthetics or propofol and remifentanil. Volume-controlled ventilation was adjusted after intubation according to the clinical judgment. The first arterial blood gas analysis was taken just before the head pinning. Systolic, diastolic, and mean arterial blood pressures (MAP) and heart rate were registered after intubation every 5 minutes until the head pinning. PaCO2-EtCO2 correlated positively with percentage difference between MAP awake at arrival in operating room and during arterial CO2 determination (P=0.0008, r=0.388). In analysis according to a MAP decrease of less than 20% (n=17), 20% to 29% (n=24), 30% to 35% (n=16), and more than 35% (n=15), the mean (SD) PaCO2-EtCO2 was greater in patients with MAP decrease of over 35% or 30% to 35% than in patients with MAP decrease of less than 20%. The mean (SD) absolute values of the PaCO2-EtCO2 were 0.96 (0.43) kPa or 0.85 (0.31) kPa versus 0.55 (0.24) kPa, respectively (P<0.05 between categories). Mean EtCO2 was not different in the various MAP difference categories, but PaCO2 was greatest when MAP decreased more than 35% (P<0.05). There was a positive correlation between PaCO2-EtCO2 and MAP decrease shortly after induction of anesthesia. PaCO2-EtCO2 is recommended to be interpreted together with change in MAP during early phase of neuroanesthesia to guarantee optimal mechanical ventilation.

Overnight Thickness Variation in Diabetic Macular Edema

To study the evening-to-morning variation in retinal thickness in patients with fovea-involving diabetic macular edema. Twelve eyes in 12 patients aged 39 to 78 years (mean, 57) with fovea-involving diabetic macular edema and 14 eyes in 7 healthy volunteers aged 30 to 70 years (mean, 57) were examined by optical coherence tomography, in the evening and in the morning after > or =6 hours of sleep in the recumbent position in darkness followed by 0.5 hour wakefulness in the same position in room light with both eyes open. In patients with diabetic macular edema, macular thickness increased overnight, from 316 +/- 72 microm in the evening to 336 +/- 81 microm in the morning (P = 0.003). Visual acuity decreased from a mean of 41 ETDRS letters (Early Treatment of Diabetic Retinopathy Study; range, 4-61) in the evening, to a mean of 36 letters (range, 2-60) in the morning (P = 0.03). No overall change was found in mean arterial blood pressure (MABP; P = 0.48), blood glucose (P = 0.25), or corneal thickness (P = 0.26). The overnight change in macular thickness correlated directly with the change in MABP (r = 0.65, P = 0.03) but not with baseline MABP or blood glucose. The overnight increase in retinal thickness remained significant after statistical adjustment for the effect of arterial blood pressure (P = 0.002). Healthy subjects demonstrated no significant change in any parameter. In fovea-involving diabetic macular edema, a reduction in visual acuity accompanies overnight retinal thickening, the magnitude being related to the nocturnal change in blood pressure. The results indicate that deficient regulation of retinal capillary filling pressure promotes edema, but the bulk of the overnight increase in macular edema is caused by other mechanisms, of which postural variation in venous blood pressure and increased retinal metabolism in the dark merit further study.

Familial predisposition and susceptibility to the effect of other risk factors for myocardial infarction.

STUDY OBJECTIVES: To assess if familial predisposition to myocardial infarction (MI) is an indicator of increased susceptibility to the effect of other established risk factors. The study assessed whether a...

Effect of arterial blood pressure and ventilation gases on cardiac depression induced by coronary air embolism

In this study the time course of cardiac depression after selective intracoronary injection of air bubbles was investigated in six anesthetized pigs (30 +/- 2 kg) with different mixtures of ventilation gases and different mean arterial blood pressures (MAP). Air bubbles of 150 microns diam were injected into the left anterior descending coronary artery (LADCA) in a volume of 2 microliters/kg body wt. In each animal an injection of air bubbles was applied during ventilation with N2-O2 and a MAP of 77 +/- 3 mmHg (N2-O2/low pressure) or 111 +/- 3 mmHg (N2-O2/high pressure) and during ventilation with pure O2 and a MAP of 77 +/- 3 mmHg (O2/low pressure) or 110 +/- 3 mmHg (O2/high pressure). Systemic hemodynamic variables such as left ventricular pressure, its peak first derivatives, and MAP changed < 10% after injection of air bubbles. During N2-O2/low pressure, systolic segment length shortening in the LADCA region (SS-LADCA) decreased from baseline and did not return to baseline within the 10 min after injection of air bubbles. During N2-O2/high pressure and O2/low pressure, SS-LADCA was decreased between 60 and 120 s, whereas for O2/high pressure this period was from 60 to 90 s. By calculating the time integral of the deviation from baseline of SS-LADCA, it could be demonstrated that the depression of regional myocardial function was less severe during O2/high pressure and O2/low pressure than during N2-O2/low pressure. We conclude that, when coronary air embolism occurs during hypertension and during ventilation with pure O2 instead of a normal N2-O2 mixture, the resulting depression of regional myocardial function is reduced.

Role of arteria baroreceptor input on thirst and urinary responses to intracerebroventricular angiotensin II

Intracerebroventricular (icv) infusion of angiotensin II (ANG II) in rats elicits greater water intake under hypotensive, compared with normotensive, conditions. The present experiments used sinoaortic baroreceptor-denervated (SAD) rats and sham-operated rats to examine if the modulatory effects of arterial blood pressure on water intake in response to icv ANG II are mediated by arterial baroreceptors. Mean arterial blood pressure (MAP) was raised or lowered by intravenous (i.v.) infusions of phenylephrine (1 or 10 micrograms.kg-1 x min-1) or minoxidil (25 micrograms.kg-1 x min-1), respectively. The angiotensin-converting enzyme inhibitor captopril (0.33 mg/min) was infused i.v. to prevent the endogenous formation of ANG II during testing. Urinary excretion of water and solutes was measured throughout. Water intake elicited by icv ANG II was inversely related to changes in MAP. Specifically, rats drank more water in response to icv ANG II when MAP was reduced by minoxidil but drank less water when MAP was elevated by phenylephrine. The influence of changing MAP on the icv ANG II-induced drinking responses was not affected by SAD. These results suggest that the modulatory effects of arterial blood pressure on icv ANG II-induced drinking can occur in the absence of sinoaortic baroreceptor input.

Effect of arterial blood pressure and serum glucose on brain intracellular pH, cerebral and cortical blood flow during status epilepticus in the white New Zealand rabbit

Generalized seizures can induce both hypertension and hyperglycemia which may aggravate preexisting cerebral or medical conditions in patients. In vivo fluorescent imaging of regional cortical blood flow and brain intracellular pH (pH i) was performed in fasted New Zealand rabbits (n=35) in which either mean arterial blood pressure (MABP) or serum glucose was the covaried factor during pentylenetetrazole induced status epilepticus under 1.5% inspired halothane. Baseline brain pH i and regional cortical blood flow were 7.02±0.02 and 51.1±1.7 ml/100 g/min, respectively. Following seizure induction, MABP increased to 105 mm Hg and brain pH i fell to 6.79±0.03 within 15 min and remained at this level for 1 h ( P<0.001). With normalization of MABP during ongoing seizures, there was no worsening in brain pH i despite a significant decrease in regional cortical blood flow. Hyperglycemia decreased pH i to 6.71±0.02 compared to 6.84±0.04 in normoglycemic animals ( P<0.001). Using pH i as a cerebral metabolic index, these data suggest that normalization of MABP does not increase metabolic injury while hyperglycemia does significantly worsen brain acidosis. Therefore, administration of glucose to patients with status epilepticus should be avoided unless there is documented hypoglycemia.

Biomathematics of intracranial CSF and haemodynamics. Simulation and analysis with the aid of a mathematical model.

A mathematical model of the isolated intracranial system including autoregulation of cerebral blood flow with the aid of a variable cerebrovascular resistance is described. The rate of formation of cerebrospinal fluid is assumed to depend on the regional blood flow through the choroid plexuses. This model is extended by cardiovascular components including the left ventricle of the heart, the aorta and the peripheral resistance. Additionally the model contains control circuits to simulate the short-time behaviour of the blood pressure regulation with the aid of the baroreceptor reflex. Disturbances of central regulation of blood pressure are simulated depending on changes of the regional blood flow through the brain stem. The application of the model is demonstrated by the analysis of the influence of arterial blood pressure upon the intracranial pulse pressure relationship (PPR) and upon the pressure response to a volume pressure test. Theoretical considerations and simulations reveal an opposite effect of arterial blood pressure (ABP) and its amplitude upon PPR. The ICP amplitude rises with decreasing ABP or increasing ABP amplitude. Breakpoints and other deviations from a linear PPR over the whole ICP range are studied by the analysis of the transfer function. The application of the model concerning parameter estimation methods is demonstrated and discussed. Simulations of rhythmic phenomena with the aid of the extended model point out possible approaches to quantitative descriptions of disturbances of central regulation.

Hemodynamic determinants of ischemic myocardial dysfunction in the presence of coronary stenosis in dogs.

The effects of arterial blood pressure and heart rate on myocardial contraction were studied in a canine model of coronary stenosis. Systolic thickening of a region of myocardium supplied by a cannulated coronary artery was used as a measure of oxygen shortage. A glass stenosis in an external perfusion circuit that provided blood to the cannulated vessel was used to limit coronary flow. Mean arterial pressure was controlled by a blood reservoir and phenylephrine infusion and stabilized at four levels: 60, 80, 100, and 120 mmHg. At each blood pressure level, heart rate was increased by ventricular pacing in steps from 50 to 150 beats/min. Systolic thickening was measured at each of the resulting 20 combinations of blood pressure and heart rate. Measurements were made before cannulation, to serve as an unstenosed control, and following cannulation in the presence of moderate and severe stenoses. In the presence of the severe stenosis, ischemic dysfunction occurred when mean arterial pressure was decreased to 60 mmHg. At this pressure, dysfunction was most dramatic at rapid heart rates. In contrast, hypertension to a mean arterial pressure of 120 mmHg was well tolerated in these nonfailing hearts. Importantly, no single value of either blood pressure or heart rate was found to be associated with ischemia. The threshold for rate-induced ischemia depended on the coexisting value of blood pressure and vice versa. Ischemia was absent if mean arterial pressure exceeded heart rate, that is, if the pressure-rate ratio exceeded one.

The effects of arterial blood pressure on the regional cerebral blood volume by X-ray fluorescence.

Cerebral blood flow (CBF) remains constant over a wide range of arterial blood pressure. This is thought to be accomplished by changes in the diameter, and therefore the volume, of the cerebral resistance vessels. To test this hypothesis, regional cerebral blood volume (rCBV) was measured in vivo in Rhesus monkeys over a range of mean arterial blood pressures (MABP) of 35 to 200 torr. Multiple measurements were made in each animal by the method of stimulated x-ray fluorescence. A significant linear relationship of rCBV = 6.26 (±0.47 SD) -0.015 (±0.004 SD) MABP was found. For each one torr change in the MABP, there is a change in rCBV of 0.015 cc/100 gm of brain tissue over a range of MABP of 35 to 200 torr. An additional observation of this investigation was that autoregulation of the cerebral blood flow (CBF) is perturbed for a period lasting up to 15 minutes after the intravenous injection of Renografin 76 R .

Dynamic pressures in the pial arterial microcirculation.

Dynamic pressures in the pial arterial microcirculation.

Effects of bilateral vagotomy on renal function in the rat.

Renal function was studied in rats before and after section of the vagus nerves at the level of the common carotid arteries. In the control group of rats, sodium output and volume rate of urine flow increased following vagal section but glomerular filtration rate did not change. This response was not altered in other rats by desoxycorticosterone acetate, vasopressin, or renal nerve section. This response was similar to that seen in rats in which both common carotid arteries had been occluded. The natriuresis following bilateral vagotomy did not occur in rats in which the blood pressure was prevented from rising by means of aortic constriction. It is concluded that a natriuresis does occur following bilateral vagotomy. This natriuresis may be a result of the effect of arterial blood pressure following the vagotomy.