How and why Matthew may have edited Mark’s Gospel.

 

Explain how and why Matthew may have edited Mark’s Gospel. Use the following two sets of passages to support your claim.

According to course materials (Bible, textbook, digital materials linked below, etc.):

1. How and why would Matthew have edited Mark 6:45-52 contrasted with Matthew 14:25-27,32-33?

2. How and why would Matthew have edited Mark 9:2-10 contrasted with Matthew 17:1-13?

Sample Solution

How and why Matthew may have edited Mark`s Gospel

The Gospel of Matthew, like the others in the New Testament, evidently is based on sources that were in existence for some time. The two sources on which most of the material is based are Mark and the Logia. A close analysis of the Book of Mathew and that of Mark reveal that Matthew wrote his gospel from Mark`s point of view, however, he did not copy paste. He seem to have edited by either rearranging the verses, reducing or expanding them. By doing so, Matthew made the gospel to fit to his agenda.

Afterload is the pressure or resistance the ventricles need to overcome to eject blood during systole and is assessed by the mean arterial pressure. According to Figueroa & Peters (2006), afterload represents three factors that are impaired in CHF patients; vascular resistance, wall tension, and intrathoracic pressure. (Osborn, 2014 p901-903)
When cardiac output action is compromised, the sympathetic nervous system and renin-angiotensin-aldosterone system is activated. The activation of the sympathetic nervous system releases norepinephrine, which causes vasoconstriction in an attempt to increase ventricular preload. Myocardial contractility and heart rate increases to increase cardiac output. Circulating levels will increase fluid retention by increasing sodium absorption of the kidney. The increased intravascular volume will improve blood pressure and cardiac output. An additional function of norepinephrine allows renal vasoconstriction that maintains the glomerular filtration at a stable rate despite decreased renal perfusion. However, these mechanisms cannot be maintained extensively because it causes cardiac wall stress by constantly increasing pressure. Effects of long term maintenance include,” ..hypertrophy of the heart(cardiomegaly), chamber dilation, increased myocardial oxygen consuming, worsening myocardial ischemia, and pulmonary and systemic congestion (Osborn, 2014 p1029).”
The renin-angiotensin-aldosterone system activates in response to decreased renal perfusion. A series of hormones is released in this system to increase preload, cardiac output, and blood pressure. Renin is released from the kidneys to convert angiotensin I to angiotensin II. Angiotensin II is a strong vasoconstrictor that increases afterload and stimulates the secretion of aldosterone. Aldosterone is a hormone that causes sodium and fluid retention of the kidneys to increase intravascular volume. Like the activation of the sympathetic nervous system, this system has long term effects that will lead to heart failure. These long-term effects include,” inc

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