Documento di lavoro per la misura ottica della pressione sanguigna e della rigidità delle arterie.
Premesse
- Sia per la misura ottica della pressione che la caratterizzazione della rigidità delle arterie è indispensabile mettere in relazione il segnale ottico con l’ECG.
- Per il segnale ECG è necessaria una banda passante elevata ed una cura estrema dei filtri.
- Alcune punti caratteristici, come i flessi del gruppo QRS, hanno delle variazioni temporali estremamente piccole.
- La derivata prima del segnale porta con sè indicazioni importanti.
- Le arterie hanno un ruolo attivo nella circolazione che molte volte non è riconosciuto. O meglio si fanno delle semplificazioni non valide.
- Quando il fronte di salita del flusso sanguigno attraversa l’arteria questa si dilata ed assorbe energia. Ma passato il picco del flusso, l’artera restituisce un’energia maggiore di quella assorbita.
- Quando si corre i muscoli riescono a recuperare un quarto dell’energia dell’impatto a terra. Successivamente restituiscono sia tutta l’energia che è stata dissipatata che quella necessaria per il proseguo della corsa.
- Le arterie fanno altrettanto. La contrazione ha ovviamente dei ritardi rispetto al segnale.
- La curva sforzo-dilatazione ha un’isteresi dovuta alla propagazione dei segnali, ma si possono avere anche altri artefatti.
- Per un’analisi accurata è necessario fare le misura ottiche con due o più lunghezze d’onda. In modo da avere sia il volume di sangue che attraversa il canale elettrico interessato, ma anche la saturazione in ossigeno.
- L’uso di lenti sui LED può essere utile per separare le vene dalle arterie. E’ utile un’indagine preliminare dell’ immagine del segnale attraverso il polso.
- Dei filtri ottici passa-basso sui SiPM per eliminare il disturbo della luce visibile sono sicuramente da implementare.
- Usato da tutti è il modello di Moens-Korteweg. Vedi raccomandazione di AHA e sopprattutto la breve sintesi di Wikipedia.
- La grossa limitazione del modello è che non tiene direttamente conto del ruolo attivo della muscolatura delle arterie.
- Ritengo che l’implementazione di un sistema a banda sufficientemente larga e con basso SNR nella banda possa facilmene superare molti problemi.
Il modello di Moens-Korteweg
Misura PPG sincrona all’ECG
 |
| La misura PPG (Photoplethysmography), indicata con la curva a colori, consente la misura del volume di sangue che attaversa l’arteria esaminata. |
- I segnali PPG ed ECG sono stati spostati nel tempo in modo da far coincidere il piede del gruppo QRS del segnale ECG con l’inizio del fronte di salita del segnale PPG.
- Si vede chiaramente che la durata dell’eiezione della gittata cardiaca è di minore durata del tempo fra il piede del fronte PPG ed il notch relativo al punto dicroico (chiusura dell’aorta.
- Si fa notare che la forma dei segnali cambia parecchio in funzione dei filtri utilizzati.
Adv Physiol Educ. 2003 Dec;27(1-4):201-6.
Author information: (1)Department of Physiology, Medical College of Georgia, Augusta, Georgia 30912, USA. cwebb@mcg.edu
This brief review serves as a refresher on smooth muscle physiology for those educators who teach in medical and graduate courses of physiology. Additionally, those professionals who are in need of an update on smooth muscle physiology may find this review to be useful. Smooth muscle lacks the striations characteristic of cardiac and skeletal muscle. Layers of smooth muscle cells line the walls of various organs and tubes in the body, and the contractile function of smooth muscle is not under voluntary control. Contractile activity in smooth muscle is initiated by a Ca(2+)-calmodulin interaction to stimulate phosphorylation of the light chain of myosin. Ca(2+) sensitization of the contractile proteins is signaled by the RhoA/Rho kinase pathway to inhibit the dephosphorylation of the light chain by myosin phosphatase, thereby maintaining force generation. Removal of Ca(2+) from the cytosol and stimulation of myosin phosphatase initiate the process of smooth muscle relaxation.
PMID: 14627618 [PubMed - indexed for MEDLINE]
Smooth muscle contraction and relaxation.
Webb RC(1).Author information: (1)Department of Physiology, Medical College of Georgia, Augusta, Georgia 30912, USA. cwebb@mcg.edu
This brief review serves as a refresher on smooth muscle physiology for those educators who teach in medical and graduate courses of physiology. Additionally, those professionals who are in need of an update on smooth muscle physiology may find this review to be useful. Smooth muscle lacks the striations characteristic of cardiac and skeletal muscle. Layers of smooth muscle cells line the walls of various organs and tubes in the body, and the contractile function of smooth muscle is not under voluntary control. Contractile activity in smooth muscle is initiated by a Ca(2+)-calmodulin interaction to stimulate phosphorylation of the light chain of myosin. Ca(2+) sensitization of the contractile proteins is signaled by the RhoA/Rho kinase pathway to inhibit the dephosphorylation of the light chain by myosin phosphatase, thereby maintaining force generation. Removal of Ca(2+) from the cytosol and stimulation of myosin phosphatase initiate the process of smooth muscle relaxation.
PMID: 14627618 [PubMed - indexed for MEDLINE]
J Smooth Muscle Res. 2004 Oct;40(4-5):155-67.
Author information: (1)Department of Pharmacology, School of Pharmacy, Hoshi University, Shinagawa-ku, Tokyo 142-8501, Japan. chiba@hoshi.ac.jp
Smooth muscle contraction is mediated by Ca2+-dependent and Ca2+-independent pathways. The latter Ca2+-independent pathway, termed Ca2+ sensitization, is mainly regulated by a monomeric GTP binding protein RhoA and its downstream target Rho-kinase. Recent studies suggest a possible involvement of augmented RhoA/Rho-kinase signaling in the elevated smooth muscle contraction in several human diseases. An increased bronchial smooth muscle contractility, which might be a major cause of the airway hyperresponsiveness that is a characteristic feature of asthmatics, has also been reported in bronchial asthma. Here, we will discuss the role of RhoA/Rho-kinase-mediated Ca2+ sensitization of bronchial smooth muscle contraction in the pathogenesis of airway hyperresponsiveness. Agonist-induced Ca2+ sensitization is also inherent in bronchial smooth muscle. Since the Ca2+ sensitization is sensitive to a RhoA inactivator, C3 exoenzyme, and a Rho-kinase inhibitor, Y-27632, the RhoA/Rho-kinase pathway is involved in the signaling. It is of interest that the RhoA/Rho-kinase-mediated Ca2+ sensitization of bronchial smooth muscle contraction is markedly augmented in experimental asthma. Moreover, Y-27632 relaxes the bronchospasm induced by contractile agonists and antigens in vivo. Y-27632 also has an ability to inhibit airway hyperresponsiveness induced by antigen challenge. Thus, the RhoA/Rho-kinase pathway might be a potential target for the development of new treatments for asthma, especially in airway hyperresponsiveness.
PMID: 15655303 [PubMed - indexed for MEDLINE]
The role of RhoA-mediated Ca2+ sensitization of bronchial smooth muscle contraction in airway hyperresponsiveness.
Chiba Y(1), Misawa M.Author information: (1)Department of Pharmacology, School of Pharmacy, Hoshi University, Shinagawa-ku, Tokyo 142-8501, Japan. chiba@hoshi.ac.jp
Smooth muscle contraction is mediated by Ca2+-dependent and Ca2+-independent pathways. The latter Ca2+-independent pathway, termed Ca2+ sensitization, is mainly regulated by a monomeric GTP binding protein RhoA and its downstream target Rho-kinase. Recent studies suggest a possible involvement of augmented RhoA/Rho-kinase signaling in the elevated smooth muscle contraction in several human diseases. An increased bronchial smooth muscle contractility, which might be a major cause of the airway hyperresponsiveness that is a characteristic feature of asthmatics, has also been reported in bronchial asthma. Here, we will discuss the role of RhoA/Rho-kinase-mediated Ca2+ sensitization of bronchial smooth muscle contraction in the pathogenesis of airway hyperresponsiveness. Agonist-induced Ca2+ sensitization is also inherent in bronchial smooth muscle. Since the Ca2+ sensitization is sensitive to a RhoA inactivator, C3 exoenzyme, and a Rho-kinase inhibitor, Y-27632, the RhoA/Rho-kinase pathway is involved in the signaling. It is of interest that the RhoA/Rho-kinase-mediated Ca2+ sensitization of bronchial smooth muscle contraction is markedly augmented in experimental asthma. Moreover, Y-27632 relaxes the bronchospasm induced by contractile agonists and antigens in vivo. Y-27632 also has an ability to inhibit airway hyperresponsiveness induced by antigen challenge. Thus, the RhoA/Rho-kinase pathway might be a potential target for the development of new treatments for asthma, especially in airway hyperresponsiveness.
PMID: 15655303 [PubMed - indexed for MEDLINE]
Am J Physiol Heart Circ Physiol. 2005 Nov;289(5):H2048-58. Epub 2005 Jul 8.
Author information: (1)Computational Biomechanics, Graz Univ. of Technology, Schiessstattgasse 14-B, 8010 Graz, Austria. gh@biomech.tu-graz.ac.at
At autopsy, 13 nonstenotic human left anterior descending coronary arteries [71.5 +/- 7.3 (mean +/- SD) yr old] were harvested, and related anamnesis was documented. Preconditioned prepared strips (n = 78) of segments from the midregion of the left anterior descending coronary artery from the individual layers in axial and circumferential directions were subjected to cyclic quasi-static uniaxial tension tests, and ultimate tensile stresses and stretches were documented. The ratio of outer diameter to total wall thickness was 0.189 +/- 0.014; ratios of adventitia, media, and intima thickness to total wall thickness were 0.4 +/- 0.03, 0.36 +/- 0.03, and 0.27 +/- 0.02, respectively; axial in situ stretch of 1.044 +/- 0.06 decreased with age. Stress-stretch responses for the individual tissues showed pronounced mechanical heterogeneity. The intima is the stiffest layer over the whole deformation domain, whereas the media in the longitudinal direction is the softest. All specimens exhibited small hysteresis and anisotropic and strong nonlinear behavior in both loading directions. The media and intima showed similar ultimate tensile stresses, which are on average three times smaller than ultimate tensile stresses in the adventitia (1,430 +/- 604 kPa circumferential and 1,300 +/- 692 kPa longitudinal). The ultimate tensile stretches are similar for all tissue layers. A recently proposed constitutive model was extended and used to represent the deformation behavior for each tissue type over the entire loading range. The study showed the need to model nonstenotic human coronary arteries with nonatherosclerotic intimal thickening as a composite structure composed of three solid mechanically relevant layers with different mechanical properties. The intima showed significant thickness, load-bearing capacity, and mechanical strength compared with the media and adventitia.
PMID: 16006541 [PubMed - indexed for MEDLINE]
Determination of layer-specific mechanical properties of human coronary arteries with nonatherosclerotic intimal thickening and related constitutive modeling.
Holzapfel GA(1), Sommer G, Gasser CT, Regitnig P.Author information: (1)Computational Biomechanics, Graz Univ. of Technology, Schiessstattgasse 14-B, 8010 Graz, Austria. gh@biomech.tu-graz.ac.at
At autopsy, 13 nonstenotic human left anterior descending coronary arteries [71.5 +/- 7.3 (mean +/- SD) yr old] were harvested, and related anamnesis was documented. Preconditioned prepared strips (n = 78) of segments from the midregion of the left anterior descending coronary artery from the individual layers in axial and circumferential directions were subjected to cyclic quasi-static uniaxial tension tests, and ultimate tensile stresses and stretches were documented. The ratio of outer diameter to total wall thickness was 0.189 +/- 0.014; ratios of adventitia, media, and intima thickness to total wall thickness were 0.4 +/- 0.03, 0.36 +/- 0.03, and 0.27 +/- 0.02, respectively; axial in situ stretch of 1.044 +/- 0.06 decreased with age. Stress-stretch responses for the individual tissues showed pronounced mechanical heterogeneity. The intima is the stiffest layer over the whole deformation domain, whereas the media in the longitudinal direction is the softest. All specimens exhibited small hysteresis and anisotropic and strong nonlinear behavior in both loading directions. The media and intima showed similar ultimate tensile stresses, which are on average three times smaller than ultimate tensile stresses in the adventitia (1,430 +/- 604 kPa circumferential and 1,300 +/- 692 kPa longitudinal). The ultimate tensile stretches are similar for all tissue layers. A recently proposed constitutive model was extended and used to represent the deformation behavior for each tissue type over the entire loading range. The study showed the need to model nonstenotic human coronary arteries with nonatherosclerotic intimal thickening as a composite structure composed of three solid mechanically relevant layers with different mechanical properties. The intima showed significant thickness, load-bearing capacity, and mechanical strength compared with the media and adventitia.
PMID: 16006541 [PubMed - indexed for MEDLINE]
Isteresi delle coronarie
Adv Physiol Educ. 2003 Dec;27(1-4):201-6.
Webb RC(1).
Author information: (1)Department of Physiology, Medical College of Georgia, Augusta, Georgia 30912, USA. cwebb@mcg.edu
This brief review serves as a refresher on smooth muscle physiology for those educators who teach in medical and graduate courses of physiology. Additionally, those professionals who are in need of an update on smooth muscle physiology may find this review to be useful. Smooth muscle lacks the striations characteristic of cardiac and skeletal muscle. Layers of smooth muscle cells line the walls of various organs and tubes in the body, and the contractile function of smooth muscle is not under voluntary control. Contractile activity in smooth muscle is initiated by a Ca(2+)-calmodulin interaction to stimulate phosphorylation of the light chain of myosin. Ca(2+) sensitization of the contractile proteins is signaled by the RhoA/Rho kinase pathway to inhibit the dephosphorylation of the light chain by myosin phosphatase, thereby maintaining force generation. Removal of Ca(2+) from the cytosol and stimulation of myosin phosphatase initiate the process of smooth muscle relaxation.
PMID: 14627618 [PubMed - indexed for MEDLINE]
Smooth muscle contraction and relaxation.
Webb RC(1).
Author information: (1)Department of Physiology, Medical College of Georgia, Augusta, Georgia 30912, USA. cwebb@mcg.edu
This brief review serves as a refresher on smooth muscle physiology for those educators who teach in medical and graduate courses of physiology. Additionally, those professionals who are in need of an update on smooth muscle physiology may find this review to be useful. Smooth muscle lacks the striations characteristic of cardiac and skeletal muscle. Layers of smooth muscle cells line the walls of various organs and tubes in the body, and the contractile function of smooth muscle is not under voluntary control. Contractile activity in smooth muscle is initiated by a Ca(2+)-calmodulin interaction to stimulate phosphorylation of the light chain of myosin. Ca(2+) sensitization of the contractile proteins is signaled by the RhoA/Rho kinase pathway to inhibit the dephosphorylation of the light chain by myosin phosphatase, thereby maintaining force generation. Removal of Ca(2+) from the cytosol and stimulation of myosin phosphatase initiate the process of smooth muscle relaxation.
PMID: 14627618 [PubMed - indexed for MEDLINE]
Ruolo di RhoA
La corsa
Il leakage lattacido
- Nella corsa di fondo domanda di energia ed offerta si devono bilanciare.
- Nella corsa lenta, totalmente aerobica, la frequenza cardiaca si mantiene costante ed è tale da fornire ai muscoli ossigeno e zuccheri/grassi per circa 70 Cal/km.
- I mitocondri con l’ausilio di parecchi enzimi, coenzimi, gruppo prostetici per ogni molecola di zucchero generano ben 38 protoni.
- L’energia legata ad ogni protone è modesta, circa 60 meV, ma l’efficienza complessiva delle varie reazioni è di ben il 60%, maggiore delle più efficiente centrali termiche.
- La frequenza cardiaca nella regione completamente aerobica è proporzionale alla sforzo.
- Si può definire quindi un rapporto fra variazione di frequenza cardiaca e variazione dello sforzo (misurato in Cal/ora o meglio in METs, Metabolic Equivalent of Task).
- Richiedendo ai propri muscoli prestazioni sempre superiori, la richiesta può superare il flusso massimo di energia che i mitocomdri possono produrre.
- Superato il limite aerobico le molecole di zucchero si scidono in due al di fuori dei mitocondri con l’aiuto di un enzima, lactate deidrogenase, e generano solo due protoni e due molecole di acidolattico.
- La reazione, il percorso metabolico lattacido, è estremamente inefficace. Inoltre l’acido lattico riducendo il ph del sangue riduce l’assorbimento di ossigeno nei globuli rossi. Quindi anche il ciclo dell’ossigeno diventa meno efficiente.
- La frequenza cardiaca comincia a salire.
- Chiaramente quando si corre si hanno in mente gli obiettivi che si vogliono raggiungere. Per cui di fatto siamo noi che controlliamo il ritmo a cuiaumenta la concentrazione di acidolattico
- L’enzima LDH agisce nella direzione della scissione, ma anche nella direzione inversa.
- Per cui, a meno si stiano correndo gli 800 metri, è possibile raggiungere una situazione di equilibrio fra i due percorsi metabolici.
Accumulo e ricombinazione dell’acido lattico (SIGG 2012)
La variazione della concentrazione di acido lattico nel sangue può essere scritta come: $dC_{la}=k(v-v_a)dt-(\frac{C_{la}}{\tau})dt$ (1)#TODO mathjax$C_{la}$ concentrazione acido lattico
$v$ velocità (è proporzionale alle calorie/ora)
$v_a$ velocità per cui la concentrazione di acido lattico non differisce da quella a riposo
$\tau$ costante di tempo di ricombinazione,
$t$ tempo
Dalla (1) si ottiene: $ \frac{t}{\tau} =ln &frac{k(v−v_a)}{k("v−v_a)−\frac{C_{la}{\tau}} $ (2)
Dalla (2) si ottiene la frequenza cardiaca attraverso due costanti di proporzionalità con la velocità e con la concentrazione dell’acido lattico.
Confronto dati sperimentali ed andamento teorico
La sovrapposizione della curva teorica in rosso con i dati sperimentali consente di ricavare parecchi parametri del modello. Le fasi di recupero danno le due costanti di tempo del recupero del debito lattacido e del debito di acido lattico.
Nessun commento:
Posta un commento