Answer to Question #323117 in Human Anatomy and Physiology for Noah

Question

The third experiment

1. Increase of carbon dioxide concentration in inspired air，how does respiratory movement change? Why?

2. Cut the vagus nerve two sides， how does respiratory movement change? Why?

The fourth experiment

1. How does the amount of urine change after injection of 20% glucose 5ml? How is the mechanism?

2. How does the amount of urine change after injection of Furosemide? How is the mechanism?

The fifth experiment

1. To stimulate the complete depressor nerve(aortic nerve) and the end of the central and peripheral ends, blood pressure, what changes? And why?

2. Injection of 0.01% Noradrenaline 0.3ml, blood pressure, what changes? And why?

 

 

 

Answer 1

III.

1. An increase in the frequency of detection of CO2 up to 4-5% already occurs in patients with increased frequency and increased respiratory rate, tinnitus, and a noticeable pulsation of blood in the temples. However, the presence in the atmosphere, perhaps even up to 6% CO2, is not even dangerous to life or health. In the presence of 8% CO2, there are signs of headaches, dizziness, and general malaise, with the development of development, the identified symptoms appear in more forms, and 10% of people usually have symptoms of consciousness.
2. Transection of the vagus nerve is reflected a large extent on the function of the stomach and intestines, which was observed, in addition to I. P. Pavlov, P. A. Herzen and others. It turned out that one of the terrible symptoms of such an operation is a sharp paresis of the gastrointestinal tract with a violation of motor and secretory functions. In animals, bilateral transection of the vagus almost always led to death due to dysfunction of the stomach and intestines, which was manifested by fermentation and severe intoxication. IP Pavlov, having found this mechanism, came to the conclusion about the expediency of imposing a gastrostomy, through which systematic gastric lavages are performed, preventing the death of the animal. Similar studies were carried out by P. A. Herzen.

IV.

1. The introduction of a 20% glucose solution is carried out only through the central vein. The rate of administration of the solution is up to 30-40 drops/min (1.5-2 ml/min). The maximum daily dose for adults is 500 ml. Usually, glucose is completely absorbed by the body (it is not normally excreted by the kidneys), so the appearance of glucose in the urine may be a pathological sign. From the side of the kidneys and urinary tract, polyuria may appear. Polyuria is a pathological condition characterized by an increase in urine output of more than 3 liters per day. In the general analysis of urine, proteinuria, glucosuria, and ketonuria, an increase in relative density are detected.
2. Furosemide acts throughout the thick segment of the ascending limb of the loop of Henle and blocks the reabsorption of 15–20% of filtered Na + ions. Secreted into the lumen of the proximal renal tubules. Increases the excretion of bicarbonates, phosphates, Ca2+, Mg2+, and K+ ions, and increases urine pH. It has secondary effects due to the release of intrarenal mediators and the redistribution of intrarenal blood flow. Quickly and fairly completely absorbed by any route of administration. Oral bioavailability is usually 60-70%. Plasma protein binding - 91-97%. T1 / 2 0.5–1 h. In the liver, it undergoes biotransformation with the formation of inactive metabolites (mainly glucuronide). It is excreted by 88% by the kidneys and by 12% with bile. The diuretic effect is characterized by significant severity, short duration, and depends on the dose. After oral administration, it occurs after 15-30 minutes, reaches a maximum after 1-2 hours, and lasts 6-8 hours. With an intravenous injection, it manifests itself after 5 minutes, the peak is after 30 minutes, and the duration is 2 hours.

V.

1. The depressor compartment is the center where impulses directly from vascular baroreceptors arrive, under the influence of which its activity increases. The depressor section does not have its own efferent connections with peripheral vessels, and it can only have an effect on blood pressure by inhibiting the activity of the pressor section through inhibitory interneurons, which leads to vasodilation and a decrease in blood pressure. In addition, the depressor region is associated with the cardioinhibitory center of the medulla oblongata, represented by the autonomic nucleus of the vagus. Impulses coming from the baroreceptors, simultaneously with the depressor center, increase the activity of the vagus center, which leads to a decrease in the heart rate, a decrease in its output and a decrease in total arterial pressure.
2. Getting into the blood even at low concentrations, it causes generalized vasoconstriction, with the exception of coronary vessels, which expand due to indirect action (due to increased oxygen consumption), which leads to an increase in the strength and (in the absence of vagotonia) the frequency of myocardial contraction, increasing stroke and minute volume hearts. It causes an increase in blood pressure (BP), both systolic and diastolic, increases total peripheral vascular resistance (OPSS) and central venous pressure. The cardiotropic effect of norepinephrine is associated with its stimulating effect on the ß1-adrenergic receptors of the heart.