Interrupted IVC with Azygos Vein Continuation
(Right supracardinal vein > Azygos vein)
Bilateral IVC
Both images above are from Netter's Atlas
(From Tal Geva. Anomalies of Systemic Veins chapter in Moss & Adams 8th ed. Page 856)
Showing posts with label Development. Show all posts
Showing posts with label Development. Show all posts
11/16/2017
11/18/2015
Development: Heart Tube & Looping
Images are from
An Introduction to Human Embryology for Medical Students by Inderbir Singh (5th ed).
MacMillan India Limited, Madras 1995.
(This 3rd figure is intentionally rotated to show in the same orientation as rest of the figures)
3/22/2010
Basic Sci: Calcium Regulation (Adult vs. Newborn Cardiac Myocyte)
(Images & text below are from "Balaguru et al. Curr Probl Pediatr 2000;30:5-30").
Excitation-Contraction Coupling: This is the mechanism by which electrical depolarization (excitation), results in contracton in a cardiac myocyte. Calcium acts as the secondary messenger making that coupling.
Adult Cardiac Myocyte - Calcium Regulation during contraction and relaxation:
In adult cardiac myocyte, sarcoplasmic reticulum (SR) acts as the main store of calcium. Upon depolarization of sarcolemma, a small amount of calcium enters the cell through L-type calcium channels. This small amount of calcium activates calcium release channels (Ryanodine receptors) in junctional SR - causing release of large amount of calcium into the cytoplasm from calcium stores in SR. This is called Calcium-induced Calcium Release (CICR). Increase in cytosolic calcium activates myofibrils to contract. During diastole, the fall in cytosolic calcium concentration occurs through reuptake of calcium into SR stores (~80%), calcium efflux out of the cell via Sodium-Calcium Exchanger (NCX; ~20%) and via sarcolemmal calcium pump (Ca2+-ATPase).
Neonatal cardiac myocyte - Calcium regulation during contraction and relaxation:
In neonatal cardiac myocyte, SR is sparsely developed and poorly organized. So, CICR can not fully function/support cardiac contraction in the newborn. Therefore, neonatal cardiac myocytes depend on trans-sarcolemmal influx of calcium (via L-type Calcium channels & NCX). NCX operates in "reverse" direction during systole in this situation and "forwards" during diastole. NCX plays a major role in calcium homeostasis in neonate.
Other components of Excitation-Contraction Coupling:
1) T-tubules: Invaginations of sarcolemma that help to increase the cell surface area for a given cell volume. T-tubules bring more of the sarcolemmal L-type Calcium Channels in proximity to ryanodine receptors of the SR. Thus, T-tubules enhance the efficiency of CICR. However, in neonatal cardiac myocyte, the T-tubules are absent, which impose a substantial impediment to sarcolemma to SR coupling.
2) Sodium-Pottasium Pump (Na,K-ATPase): This pump, present in sarcolemma maintains an appropriate Na gradient across the membrane. This pump exists in different isoforms. Different isoforms have different senstivity and response to cardiac glycosides - which may explain the relatively high tolerability of neonates and infants to Digoxin.
3) Calsequestrin: Major calcium storing protein inside SR. Activity of calsequestrin increases progressively with development.
4) Actin and Myosin have different isoforms for heavy and light chains - which increase in sensitivity to calcium with increasing maturity, thus influencing inotropy and lusitropy of the cardiac myocyte.
Excitation-Contraction Coupling: This is the mechanism by which electrical depolarization (excitation), results in contracton in a cardiac myocyte. Calcium acts as the secondary messenger making that coupling.
Adult Cardiac Myocyte - Calcium Regulation during contraction and relaxation:
In adult cardiac myocyte, sarcoplasmic reticulum (SR) acts as the main store of calcium. Upon depolarization of sarcolemma, a small amount of calcium enters the cell through L-type calcium channels. This small amount of calcium activates calcium release channels (Ryanodine receptors) in junctional SR - causing release of large amount of calcium into the cytoplasm from calcium stores in SR. This is called Calcium-induced Calcium Release (CICR). Increase in cytosolic calcium activates myofibrils to contract. During diastole, the fall in cytosolic calcium concentration occurs through reuptake of calcium into SR stores (~80%), calcium efflux out of the cell via Sodium-Calcium Exchanger (NCX; ~20%) and via sarcolemmal calcium pump (Ca2+-ATPase).Neonatal cardiac myocyte - Calcium regulation during contraction and relaxation:
In neonatal cardiac myocyte, SR is sparsely developed and poorly organized. So, CICR can not fully function/support cardiac contraction in the newborn. Therefore, neonatal cardiac myocytes depend on trans-sarcolemmal influx of calcium (via L-type Calcium channels & NCX). NCX operates in "reverse" direction during systole in this situation and "forwards" during diastole. NCX plays a major role in calcium homeostasis in neonate.
1) T-tubules: Invaginations of sarcolemma that help to increase the cell surface area for a given cell volume. T-tubules bring more of the sarcolemmal L-type Calcium Channels in proximity to ryanodine receptors of the SR. Thus, T-tubules enhance the efficiency of CICR. However, in neonatal cardiac myocyte, the T-tubules are absent, which impose a substantial impediment to sarcolemma to SR coupling.
2) Sodium-Pottasium Pump (Na,K-ATPase): This pump, present in sarcolemma maintains an appropriate Na gradient across the membrane. This pump exists in different isoforms. Different isoforms have different senstivity and response to cardiac glycosides - which may explain the relatively high tolerability of neonates and infants to Digoxin.
3) Calsequestrin: Major calcium storing protein inside SR. Activity of calsequestrin increases progressively with development.
4) Actin and Myosin have different isoforms for heavy and light chains - which increase in sensitivity to calcium with increasing maturity, thus influencing inotropy and lusitropy of the cardiac myocyte.
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