On Aerodynamic Models for Flutter Analysis: A Systematic Overview and Comparative Assessment

This work reviews different analytical formulations for the time-dependent aerodynamic load of a thin aerofoil and clarifies numerical flutter results available in the literature for the typical section of a flexible wing; inviscid, two-dimensional, incompressible, potential flow is considered in all test cases. The latter are investigated using the exact theory for small airflow perturbations, which involves both circulatory and non-circulatory effects of different nature, complemented by the p-k flutter analysis. Starting from unsteady aerodynamics and ending with steady aerodynamics, quasi-unsteady and quasi-steady aerodynamic models are systematically derived by successive simplifications within a unified approach. The influence of the aerodynamic approximations on the aeroelastic stability boundary is then rigorously assessed from both physical and mathematical perspectives. All aerodynamic models are critically discussed and compared in the light of the numerical results as well, within a comprehensive theoretical framework in practice. In all cases, results accuracy depends on the aero-structural arrangement of the flexible wing; however, simplified unsteady and simplified quasi-unsteady aerodynamic approximations are suggested for robust flutter analysis whenever the wing’s elastic axis lies ahead of the aerofoil’s control point.

The Circulatory Effects of Increased Hydrostatic Pressure Due to Immersion and Submersion

Increased hydrostatic pressure as experienced during immersion and submersion has effects on the circulation. The main effect is counteracting of gravity by buoyancy, which results in reduced extravasation of fluid. Immersion in a cold liquid leads to peripheral vasoconstriction, which centralizes the circulation. Additionally, a pressure difference usually exists between the lungs and the rest of the body, promoting pulmonary edema. However, hydrostatic pressure does not exert an external compressing force that counteracts extravasation, since the increased pressure is transmitted equally throughout all tissues immersed at the same level. Moreover, the vertical gradient of hydrostatic pressure down an immersed body part does not act as a resistance to blood flow. The occurrence of cardiovascular collapse when an immersed person is rescued from the water is not explained by removal of hydrostatic squeeze, but by sudden reinstitution of the effect of gravity in a cold and vasoplegic subject.

Centrally acting cholecystokinin induces depressor circulatory effects in haemorrhage-shocked rats

WstępCholecystokinina (CCK) należy do hormonów peptydowych układu pokarmowego regulujących trawienie lipidów i białek, a ponadto jest ośrodkowym neurotransmiterem/neuromodulatorem. Po podaniu dożylnym wywołuje efekt resuscytacyjny u szczurów we wstrząsie krwotocznym. Ze względu na fakt, iż CCK może wpływać bezpośrednio i pośrednio na czynność ośrodka sercowo-naczyniowego, celem pracy było zbadanie działania pochodnej siarczanowej oktapeptydu CCK (CCK-8) podawanej do komory bocznej mózgu (<i>intracerebroventricularly</i> – icv) w fazie hamowania czynności układu współczulnego we wstrząsie krwotocznym.Materiał i metodyBadania przeprowadzono u samców szczurów szczepu Wistar w znieczuleniu ogólnym (ketamina [100 mg/kg]/ksylazyna [10 mg/kg]), u których wywołano nieodwracalny wstrząs krwotoczny (0% przeżycia 2 h) ze średnim ciśnieniem tętniczym (<i>mean arterial pressure</i> – MAP) 20–25 mmHg. W 5 min krytycznej hipotensji szczurom podawano icv CCK-8 (5, 15 nmol) lub 0,9% roztwór NaCl (5 μl).WynikiKrwotok prowadził do obniżenia ciśnienia tętna (<i>pulse pressu</i>re – PP), częstości rytmu serca (<i>heart rate</i> – HR) oraz wzrostu nerkowego (<i>renal vascular resistance</i> – RVR) i krezkowego oporu naczyniowego (<i>mesenteric vascular resistance</i> – MVR). W grupie kontrolnej nie stwierdzono wzrostu badanych parametrów układu krążenia, a średni czas przeżycia wynosił 32,5 ± 5,1 min. CCK-8 wywoływała zależne od dawki spadki MAP, PP i HR ze wzrostem RVR i MVR, a także skracała czas przeżycia w porównaniu ze zwierzętami kontrolnymi.WnioskiOśrodkowo działająca CCK-8 wywołuje działanie depresyjne na układ krążenia u szczurów we wstrząsie krwotocznym.

Relaxation of Goat Detrusor Muscle by L-arginine Involves NO-dependent but Guanylyl Cyclase Independent Activation of KCa Channels

Background: Urinary incontinence is a major problem both in man and animals particularly dogs. L-arginine, the precursor of NO, relaxes coronary artery smooth muscle by opening of KATP channels. L-arginine has beneficial circulatory effects in patients with essential and secondary hypertension. However, not much is known about the role of L-arginine on bladder physiology. In view of this, the present work investigated the functional role of L- arginine on detrusor smooth muscle of goat. Methods: Detrusor strips of goat, collected from local abattoir were mounted in a thermostatically controlled (37° ± 0.5°C) organ bath (20 ml capacity) containing physiological solution. After 1 hr of equilibrium, carbachol (CCh) (10-5 M) was used to induce sub-maximal contraction. L-arginine (10-3 M) was added at the plateau of contraction to see any observable effect in absence and presence of modulators of NO and ion channels. Result: L- arginine (10-3 M) reversed the contractions induced by CCh (10-5 M) on detrusor tissues. Methylene blue (MB) (10-5 M), the non-specific guanylyl cyclase inhibitor, failed to attenuate the relaxant response of L-arginine but, the NO synthase inhibitor L-NAME (3 x 10-6 M) inhibited the relaxant response of L-arginine. The KATP channel blocker glibenclamide (10-6 M) failed to inhibit the relaxation induced by L-arginine while KCa channel blocker tetraethylammonium (TEA) (10-3 M) inhibited the relaxant response of L-arginine. The results of the present study suggest that L-arginine produces relaxation of goat detrusor muscle and the L-arginine-elicited relaxation is NO-dependent but guanylyl cyclase independent which activates KCa channels.

Effect of sevoflurane on systemic and cerebral circulation, cerebral autoregulation and CO2 reactivity

Background: Sevoflurane is one of the most frequently used inhaled anesthetics for general anesthesia. Previously it has been reported that at clinically used doses of sevoflurane, cerebral vasoreactivity is maintained. However, there are no data how sevoflurane influences systemic and cerebral circulation in parallel. The aim of our study was to assess systemic and cerebral hemodynamic changes as well as cerebral CO2-reactivity during sevoflurane anesthesia. Methods: 29 patients undergoing general anesthesia were enrolled. Anesthesia was maintained with 1 MAC sevoflurane in 40% oxygen. Ventilatory settings (respiratory rate and tidal volume) were adjusted to reach and maintain 40, 35 and 30 mmHg EtCO2 for 5 minutes respectively. At the end of each period, transcranial Doppler and hemodynamic parameters using applanation tonometry were recorded. Results: Systemic mean arterial pressure significantly decreased during anesthetic induction and remained unchanged during the entire study period. Central aortic and peripherial pulse pressure and augmentation index as markers of arterial stiffness significantly increased during the anesthetic induction and remained stable at the time points when target CO2 levels were reached. Both cerebral autoregulation and cerebral CO2-reactivity was maintained at 1 MAC sevoflurane. Discussion: Cerebral autoregulation and CO2-reactivity is preserved at 1 MAC sevoflurane. Cerebrovascular effects of anesthetic compounds have to be assessed together with systemic circulatory effects. Doppler Trial Registration: The study was registered at http://www.clinicaltrials.gov, identifier: NCT02054143, retrospectively registered. Date of registration: February 4, 2014.

Effect of sevoflurane on systemic and cerebral circulation, cerebral autoregulation and CO2 reactivity

Background: Sevoflurane is one of the most frequently used inhaled anesthetics for general anesthesia. Previously it has been reported that at clinically used doses of sevoflurane, cerebral vasoreactivity is maintained. However, there are no data how sevoflurane influences systemic and cerebral circulation in parallel. The aim of our study was to assess systemic and cerebral hemodynamic changes as well as cerebral CO2-reactivity during sevoflurane anesthesia. Methods: 29 patients undergoing general anesthesia were enrolled. Anesthesia was maintained with 1 MAC sevoflurane in 40% oxygen. Ventilatory settings (respiratory rate and tidal volume) were adjusted to reach and maintain 40, 35 and 30 mmHg EtCO2 for 5 minutes respectively. At the end of each period, transcranial Doppler and hemodynamic parameters using applanation tonometry were recorded. Results: Systemic mean arterial pressure significantly decreased during anesthetic induction and remained unchanged during the entire study period. Central aortic and peripherial pulse pressure and augmentation idex as markers of arterial stiffness significantly increased during the anesthetic induction and remained stable at the time points when target CO2 levels were reached. Both cerebral autoregulation and cerebral CO2-reactivity was maintained at 1 MAC sevoflurane. Discussion: Cerebral autoregulation and CO2-reactivity is preserved at 1 MAC sevoflurane. Cerebrovascular effects of anesthetic compounds have to be assessed together with systemic circulatory effects. The study was registered at http://www.clinicaltrials.gov, identifier: NCT02054143, retrospectively registered.

Effect of sevoflurane on systemic and cerebral circulation, cerebral autoregulation and CO2 reactivity

Background: Sevoflurane is one of the most frequently used inhaled anesthetics for general anesthesia. Previously it has been reported that at clinically used doses of sevoflurane, cerebral vasoreactivity is maintained. However, there are no data how sevoflurane influences systemic and cerebral circulation in parallel. The aim of our study was to assess systemic and cerebral hemodynamic changes as well as cerebral CO2-reactivity during sevoflurane anesthesia. Methods: 29 patients undergoing general anesthesia were enrolled. Anesthesia was maintained with 1 MAC sevoflurane in 40% oxygen. Ventilatory settings (respiratory rate and tidal volume) were adjusted to reach and maintain 40, 35 and 30 mmHg EtCO2 for 5 minutes respectively. At the end of each period, transcranial Doppler and hemodynamic parameters using applanation tonometry were recorded. Results: Systemic mean arterial pressure significantly decreased during anesthetic induction and remained unchanged during the entire study period. Central aortic and peripherial pulse pressure and augmentation idex as markers of arterial stiffness significantly increased during the anesthetic induction and remained stable at the time points when target CO2 levels were reached. Both cerebral autoregulation and cerebral CO2-reactivity was maintained at 1 MAC sevoflurane. Discussion: Cerebral autoregulation and CO2-reactivity is preserved at 1 MAC sevoflurane. Cerebrovascular effects of anesthetic compounds have to be assessed together with systemic circulatory effects. Key words: sevoflurane; cerebral blood flow, cerebral autoregulation; CO2-reactivity, applanation tonometry; transcranial Doppler The study was registered at http://www.clinicaltrials.gov, identifier: NCT02054143, retrospectively registered.