cardiac anatomy physiology

By anatomy, 30 November, 2009, No Comment

cardiac anatomy physiology
can someone PLEASE help me with these anatomy and physiology questions?

1. What is the relationship between the anatomical arrangement of muscle and supporting connective tissue to the skeletal system and the body as a whole?

2. How does the body produce muscle contractions at a molecular level?

3. What diseases might affect muscle system function and how does that impact muscle contraction at a molecular level>

4. What are the similarities and differences between skeletal muscle, smooth muscle, and cardiac muscle?

Please help me answer these as thorough as possible! esp. #2 and 4!

These are BIG questions. I’ll answer #2.

The nervous system ‘communicates’ with muscle via neuromuscular junctions. These junctions work very much like a synapse between neurons. In other words:

* the impulse arrives at the end bulb,
* chemical transmitter is released from vesicles (each of which contains 5,000 – 10,000 molecules of acetylcholine) and diffuses across the neuromuscular cleft,
* the transmitter molecules fill receptor sites in the membrane of the muscle & increase membrane permeability to sodium,
* sodium then diffuses in and the membrane potential becomes less negative,
* and, if the threshold potential is reached, an action potential occurs, an impulse travels along the muscle cell membrane, and the muscle contracts.

Some muscles (skeletal muscles) will not contract unless stimulated by neurons; other muscles (smooth & cardiac) will contract without nervous stimulation but their contraction can be influenced by the nervous system. Thus, the nervous and muscle systems are closely interconnected.

In each sarcomere, thin myofilaments extend in from each end. Thick myofilaments are found in the middle of the sarcomere and do not extend to the ends.

Thick myofilaments are composed of a protein called MYOSIN. Each MYOSIN molecule has a tail which forms the core of the thick myofilament plus a head that projects out from the core of the filament. These MYOSIN heads are also commonly referred to as CROSS-BRIDGES.

The MYOSIN HEAD has several important characteristics:

* it has ATP-binding sites into which fit molecules of ATP. ATP represents potential energy.
* it has ACTIN-binding sites into which fit molecules of ACTIN. Actin is part of the thin myofilament and will be discussed in more detail shortly.
* it has a “hinge”at the point where it leaves the core of the thick myofilament. This allows the head to swivel back and forth, and the “swivelling” is, as will be described shortly, what actually causes muscle contraction.

Thin myofilaments are composed of 3 types of protein: ACTIN, TROPONIN, and TROPOMYOSIN.

The actin molecules (or G-actin as above) are spherical and form long chains. Each thin myofilament contains two such chains that coil around each other. TROPOMYOSIN molecules are lone, thin molecules that wrap around the chain of ACTIN. At the end of each tropomyosin is an TROPONIN molecule. The TROPOMYOSIN and TROPONIN molecules are connected to each other. Each of these 3 proteins plays a key role in muscle contraction:

* ACTIN – when actin combines with MYOSIN HEAD the ATP associated with the head breaks down into ADP. This reaction released energy that causes the MYOSIN HEAD to SWIVEL.

* TROPOMYOSIN – In a relaxed muscle, the MYOSIN HEADS of the thick myofilament lie against TROPOMYOSIN molecules of the thin myofilament. As long as the MYOSIN HEADS remain in contact with TROPOMYOSIN nothing happens (i.e., a muscle remains relaxed).

* TROPONIN – Troponin molecules have binding sites for calcium ions. When a calcium ion fills this site it causes a change in the shape and position of TROPONIN. And, when TROPONIN shifts, it pulls the TROPOMYOSIN to which it is attached. When TROPOMYOSIN is moved, the MYOSIN HEAD that was touching the tropomyosin now comes in contact with an underlying ACTIN molecule.

Muscle contraction

1 – Because skeletal muscle is voluntary muscle, contraction requires a nervous impulse. So, step 1 in contraction is when the impulse is transferred from a neuron to the SARCOLEMMA of a muscle cell.

2 – The impulse travels along the SARCOLEMMA and down the T-TUBULES. From the T-TUBULES, the impulse passes to the SARCOPLASMIC RETICULUM.

3 – As the impulse travels along the Sarcoplasmic Reticulum (SR), the calcium gates in the membrane of the SR open. As a result, CALCIUM diffuses out of the SR and among the myofilaments.

4 – Calcium fills the binding sites in the TROPONIN molecules. As noted previously, this alters the shape and position of the TROPONIN which in turn causes movement of the attached TROPOMYOSIN molecule.

5 – Movement of TROPOMYOSIN permits the MYOSIN HEAD to contact ACTIN.

6 – Contact with ACTIN causes the MYOSIN HEAD to swivel.

7 – During the swivel, the MYOSIN HEAD is firmly attached to ACTIN. So, when the HEAD swivels it pulls the ACTIN (and, therefore, the entire thin myofilament) forward. (Obviously, one MYOSIN HEAD cannot pull the entire thin myofilament. Many MYOSIN HEADS are swivelling simultaneously, or nearly so, and their collective efforts are enough to pull the entire thin myofilament).

8 – At the end of the swivel, ATP fits into the binding site on the cross-bridge & this breaks the bond between the cross-bridge (myosin) and actin. The MYOSIN HEAD then swivels back. As it swivels back, the ATP breaks down to ADP & P and the cross-bridge again binds to an actin molecule.

9 – As a result, the HEAD is once again bound firmly

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