급성산증 및 알칼리증시 요중 Pco₂의 변화

Abstract

[한글]

체액의 산-염기 평형에 이상이 생겼을 때 호흡계는 호흡량을 변동시켜 일차적인 보상작용을 하나 최종적으로 신장에서 산성 또는 알칼리뇨를 배출하여 각각 알칼리 또는 산을 체내에 보존하므로써 산-염기평형이상을 교정하게 된다.

이런 요의 산성화(또는 알칼리화)기전에는 체액의 PH와 P^^co 2가 많은 영향을 주는 것으로 알려졌다. 그러나 체액에서보다 신조직의 pH나 P^^co 2의 변화와 요의 산성화 과정과의 상호관계를 추구하는 것이 더 바람직하다. 이런 측정은 기술적으로 곤란한 점이 많아 간접적으로 측정되어왔고 근자에 이르러 직접 측정이 시도되었다.

신장조직에서 산소분압(P^^o 2)의 측정은 여러 연구자에 의해 시행되었는데 Rennie등(1958)은 P^^o 2가 신장모세혈관에서 신세뇨관강까지 직선적인 경사도를 유지하고 이 경사도의 크기는 원위세뇨관과 집합관에서 서로 다르다고 하였으며, Leonhardt 및 Landes(1963)는 수질에서 피질쪽으로 감에따라 P^^o 2의 경사도는 직선적인 관계를 유지한다고 하였다. Uhlich등(1968)은 저 신장수질의 직행혈관에서 P^^co 2의 크기를 측정하였다. 간접적으로 신장의 기체분압을 측정한 것으로는 Hills 및 Reid(1970)가 신우뇨의 P^^co 2를 측정하여 이로부터 신장수질의 P^^co 2를 추정하였다. 또한 Kennedy등(1952), Hong등(1960) 및 Sehy등(1978)은 방광에 축적된 P^^o 2 및 P^^co 2를 측정보고하였다.

그러나 상기한 여러 연구자들의 실험성적들은 한정된 생체의 산-염기 상태 즉 정상 산-염기 상태 및 정상 P^^co 2를 유지 시키면서 유발한 대사성 알칼리증시 신장수질내 P^^co 2의 변동을 관찰한데 불과하였다. 또 방광뇨는 요의 수송도중 또는 방광에 체류하는 동

안 주위조직과 기체교환이 있을 것이므로 정화한 신장조직의 기체분압을 대표한다고 볼 수 없다. 따라서 본 실험에서는 각종 산-염기상태 즉 호흡성 및 대사성 산증과 알칼리증의 단독 또는 혼합되어 발생될 때의 신장수질내 P^^co 2의 변동을 측정하여 산-염기평형

변동때 신장에서 일어나는 보상작용기전의 일부를 규명하고자 하였다.

체중 10kg내외의 개를 secobarbital마취 하에 기도에 삽관하고 인공호흡기로 호흡량을 정상의 1/2 또는 2/3배 및 2배로 유지시켜 호흡성 산증 및 알칼리증 등을 유발시켰고, 혈액채취 및 약물 주입을 위하여 고동맥과 고정맥을 노출, 도관을 삽입하였고 대사성 산증

및 알칼리증은 0.6 N HCI 및 0.6N NaHC0^^3를 일정한 속도로 주입 유발시켰다. 신우뇨를 채취하기 위해 양측 수뇨관을 노출, 도관을 삽입하였다. 요량을 증가시키기 위해 5% mannitol을 계속 주입하였으며 혈액 및 요는 mineral oil하에 무기적으로 채취하여 blood gas analyser로 P^^co 2 및 pH를 측정하였으며 HCO^^3-농도는 Henderson·Hasselbalch식에 의거 산출하였다.

이상과 같은 실험방법으로 얻은 실험성적을 요약하면 다음과 같다.

1) 정상상태에서 동맥혈 및 신우뇨의 pH는 각각 7.30±0.03과 6.81±0.18이었으며 P^^co 2는 각각 34.10±0.93, 48.30±1.26mmHg이었고 HCO^^ 3 농도는 각각 16.60±0.29, 11.9

0±0.96mEq/1로 약간 산증의 경향을 보였는데 이는 마취때문에 호흡이 감소되었기 때문이라고 생각된다.

2) 정상상태, 호흡성 산증 및 알칼리증, 대사성 산증 및 알칼리증인 경우 모두 요중의 P^^co 2가 동맥혈의 P^^co 2보다 의의있게 높았다.

3) 호흡성 산-염기 평형 이상시 동맥혈의 P^^co 2가 증가될수록 △(a-u)P^^co 2가 더욱 커지며 대사성 산증의 경우는 동맥혈의 P^^co 2가 감소할수록 △(a-u)P^^co 2가 커지고 대사성 알칼리증의 경우는 동맥혈의 P^^co 2에 무관하게 △(a-u)P^^co 2가 일정하였다.

이상의 결과는 생체에서 각종 산증 및 알칼리증이 유발되었을때 신장에서 각각의 상태에 따라 H**+분비량조절을 쉽게 할 수 있게끔 수질의 P^^co 2가 변동되는 것으로 생각된다.

Changes in Urinary P^^co 2 in Acute Acid-Base Disturbances

Yong Han

Department of Medical Science The Graduate School, Yonsei University

(Directed by Professor Doo Hee Kang, M.D., Ph.D.)

When disturbances of the acid-base balance in body fluid occur, the respiratory

system initiates a compensation for the disturbances by adjusting alveolar

ventilation. However, this compensation is usually not complete. The kidney, in

principle, restores the acid·base status to normal by adjusting the excretion of

acid or alkali in the urine, conserving equivalent amounts of base or acid

respectively in the body. Mechanism of acidification of urine(or alkalinization)

was been known to be influenced by P^^co 2 and pH of body fluid. Therefore the

measurements of P^^co 2 and pH in renal tissue are worthwhile.

Several authors investigated the problem using various methods. Rennie et al.

(1958)reported that oxygen tension in renal capillaries was higher than in tubular

fluid. Leonhardt and Landes(1963) reported that the medulla to cortex P^^o 2

gradient was linearly correlated.

Uhlich(1968) measured P^^co 2 in vasa recta of renal medulla and Hills and

Reid(1970)estimated P^^co 2 in renal medulla from the value of P^^co 2 in pelvic

urine. Kennedy(1952), Hong et al. (1960) and Sehy et al. (1978) measured both P^^o

2 and P^^co 2 in bladder urine.

However, those findings are obtained under limited acid-base states i.e., at

normal or induced metabolic acidosis with a normal P^^co 2 etc. It is also

difficult to take P^^co 2 of bladder urine as being representative of P^^co 2 of

renal tissue, since gas exchanges between the bladder and surrounding tissues take

place. The present experimental studies were conducted to investigate changes in

P^^co 2 of pelvic urine in acutely induced acidotic and alkalotic dogs.

Either male or female dogs weighing around 10kg were anesthetized with

secobarbital. An endotracheal tube was inserted and connected to Harvard

respirator. The femoral vein was catheterized and catheter was equipped with a

three-way stopcock for intravenous infusion. The femoral artery was catheterized

for blood sampling. The kidney was exposed and a catheter was inserted into the

ureter and its tip was placed up to the renal pelvis for collection of pelvic

urine. Respiratory acidosis and alkalosis were produced by artificial

hypoventilation (1/2 or 2/3 times of normal ventilation) or hyperventilation (2

times of normal ventilation) with room air.

Metabolic acidosis and alkalosis were induced by infusing an acid(0.6 N HCI) or a

base(0.6 N NaHCO^^3) solution. Throughout the experiment, mannitol(20%) was infused

continuously to increase urinary volume. Arterial blood and urine samples were

collected anaerobically and P^^co 2 and pH of both arterial blood and pelvic urine

were measured by Corning blood gas analyzer. Bicarbonate concentrations were

calculated by means of the Henderson·Hasselbalch equation.

The results obtained are summarized as follows.

1. In normal acid-base status, the mean pH of arterial blood and pelvic urine

were 7.30 ±0.03, 6.81±0.18, P^^co 2 were 34.10±0.93, 48.37±1.26, and

bicarbonate concentrations were 16.60±7.29 and 11.90±0.96 mEq/1, respectively.

Although these values show rather acidotic tendency, this may be 여e to a reduction

in ventilation as a result of anesthesia.

2. Urinary P^^co 2 was found to he significantly higher than arterial P^^co 2

under all experimental conditions i.e., in normal respiratory and metabolic

acidosis and alkalosis.

3. Respiratory acidosis and alkalosis led to an increase in △ (a-u) P^^co 2 as

arterial blood P^^co 2 increases. In contrast, in metabolic acidosis, △ (a-u)

P^^co 2 increases when arterial blood P^^co 2 decreases. However, there were no

differences observed between changes in arterial blood and △ (a-u) P^^co 2 in

metabolic alkalosis.

From the above results, it is postulated that renal medullary P^^co 2 under

various acid-base status changes in such a direction as to promote renal

acidification or alkalization of urine.

[영문]

When disturbances of the acid-base balance in body fluid occur, the respiratory system initiates a compensation for the disturbances by adjusting alveolar ventilation. However, this compensation is usually not complete. The kidney, in principle, restores the acid·base status to normal by adjusting the excretion of acid or alkali in the urine, conserving equivalent amounts of base or acid respectively in the body. Mechanism of acidification of urine(or alkalinization) was been known to be influenced by P^^co 2 and pH of body fluid. Therefore the

measurements of P^^co 2 and pH in renal tissue are worthwhile.

Several authors investigated the problem using various methods. Rennie et al. (1958)reported that oxygen tension in renal capillaries was higher than in tubular fluid. Leonhardt and Landes(1963) reported that the medulla to cortex P^^o 2 gradient was linearly correlated.

Uhlich(1968) measured P^^co 2 in vasa recta of renal medulla and Hills and Reid(1970)estimated P^^co 2 in renal medulla from the value of P^^co 2 in pelvic urine. Kennedy(1952), Hong et al. (1960) and Sehy et al. (1978) measured both P^^o 2 and P^^co 2 in bladder urine.

However, those findings are obtained under limited acid-base states i.e., at normal or induced metabolic acidosis with a normal P^^co 2 etc. It is also difficult to take P^^co 2 of bladder urine as being representative of P^^co 2 of renal tissue, since gas exchanges between the bladder and surrounding tissues take place. The present experimental studies were conducted to investigate changes in P^^co 2 of pelvic urine in acutely induced acidotic and alkalotic dogs.

Either male or female dogs weighing around 10kg were anesthetized with secobarbital. An endotracheal tube was inserted and connected to Harvard respirator. The femoral vein was catheterized and catheter was equipped with a three-way stopcock for intravenous infusion. The femoral artery was catheterized

for blood sampling. The kidney was exposed and a catheter was inserted into the ureter and its tip was placed up to the renal pelvis for collection of pelvic urine. Respiratory acidosis and alkalosis were produced by artificial hypoventilation (1/2 or 2/3 times of normal ventilation) or hyperventilation (2 times of normal ventilation) with room air.

Metabolic acidosis and alkalosis were induced by infusing an acid(0.6 N HCI) or a base(0.6 N NaHCO^^3) solution. Throughout the experiment, mannitol(20%) was infused continuously to increase urinary volume. Arterial blood and urine samples were

collected anaerobically and P^^co 2 and pH of both arterial blood and pelvic urine were measured by Corning blood gas analyzer. Bicarbonate concentrations were calculated by means of the Henderson·Hasselbalch equation.

The results obtained are summarized as follows.

1. In normal acid-base status, the mean pH of arterial blood and pelvic urine were 7.30 ±0.03, 6.81±0.18, P^^co 2 were 34.10±0.93, 48.37±1.26, and bicarbonate concentrations were 16.60±7.29 and 11.90±0.96 mEq/1, respectively.

Although these values show rather acidotic tendency, this may be 여e to a reduction in ventilation as a result of anesthesia.

2. Urinary P^^co 2 was found to he significantly higher than arterial P^^co 2 under all experimental conditions i.e., in normal respiratory and metabolic acidosis and alkalosis.

3. Respiratory acidosis and alkalosis led to an increase in △ (a-u) P^^co 2 as arterial blood P^^co 2 increases. In contrast, in metabolic acidosis, △ (a-u) P^^co 2 increases when arterial blood P^^co 2 decreases. However, there were no differences observed between changes in arterial blood and △ (a-u) P^^co 2 in metabolic alkalosis.

From the above results, it is postulated that renal medullary P^^co 2 under various acid-base status changes in such a direction as to promote renal acidification or alkalization of urine.