Madanmohan, Department of Physiology, Jawaharlal Institute of Postgraduate Medical Education and Research, Pondicherry, India; e-mail: drmadanmohan123 at rediffmail dot com
Referring to the recent review by E Harper in MPO [1], it may be fruitful to compare the effects of physiotherapy, slow pranayams and fast pranayams in multiple sclerosis. I guess that slow pranayams will be more valuable and they are easier to perform. The effect may be apparent in 3 weeks.
Conflict of interests: none
Reference:
Harper E. Premature skeletal muscle fatigue in multiple sclerosis and its implications for exercise therapy. Medical Physiology Online [Serial Online] article 7; volume 1: 2008. Available from http://www.medicalphysiologyonline.org
Showing posts with label Letter to the Editor. Show all posts
Showing posts with label Letter to the Editor. Show all posts
07 July 2008
11 May 2008
Reply to Pavithran's question: Which is more important in the genesis of tetany: CSF hypocalcemia or serum hypocalcemia and alkalosis?
E.S.Prakash, Editor, Medical Physiology Online, e-mail: medicalphysiologyonline@gmail.com
I refer to Pavithran's question [1]: Which is more important in the genesis of tetany: CSF hypocalcemia or serum hypocalcemia and alkalosis?
The study by Mullin et al [2] specifically investigated the effects of directly lowering CSF calcium levels without altering serum ionized calcium or pH on neuromuscular responses. In these experiments, the authors note that the tetanic phenomena in the animals could have been caused by calcium levels in the CSF as low as 0.1 mM (normally CSF [Ca] is 1.2 mM). They also observed that exposing the lower spinal cord to a calcium poor solution did not produce a noticeable change in muscular tension indicating that the low concentration of calcium in brain interstitial fluid bathing cell bodies of neurons (and not plasma ionized calcium) was the cause for the increased neuromuscular excitability in these experiments. I do not know of clinical states in which CSF calcium levels would reduce to this extent without changes in serum calcium.
Edmonson and colleagues [3] compared the effects of rapid intravenous infusion of ethylene glycol tetraacetate (EGTA) alone versus hypocapnic alkalosis in thyroparathyroidectomized animals and the interaction between hypocalcemia and alkalosis on the "onset of tetany". Their data indicate that hypocapnic alkalosis reducing arterial PCO2 to between 10-20 mmHg alone is associated with tetany even if it is not accompanied by a significant lowering of ionized calcium in serum. However, in the presence of significant hypocalcemia (serum ionized calcium between 0.5 and 0.9 mM) induced by rapid infusion of EGTA, tetanic symptoms are evident at a slightly higher PCO2 (20-30 mmHg). There is a clear time lag of the order of hours for equilibration of calcium ions across the blood brain barrier. In contrast, changes in minute ventilation produce changes in CSF pH instantly. The authors also note that ventilation with a gas containing 5% CO2 was a more rapid and effective means of terminating tetany produced by EGTA and thyroparathyroidectomy than administration of calcium. Thus, this study by Edmonson et al [3] provides clear evidence of an interaction between serum hypocalcemia and respiratory alkalosis in the genesis of tetany and that CSF pH is a key modulator of neuronal excitability.
Conflict of interests: none
Note: This submission was not peer reviewed.
References:
[1] Pavithran P. Which is more important in the genesis of tetanus and tetany: CSF hypocalcemia or serum hypocalcemia and alkalosis? Medical Physiology Online [serial online] article 3.7, volume 1, 2008, available from http://medicalphysiologyonline.blogspot.com
[2] Mullin FJ, Hastings AB, and Lees WM. Neuromuscular responses to variations in calcium and potassium concentrations in the cerebrospinal fluid. Am J Physiol 1938; 121: 719-727
[3] Edmondson JW, Brashear RE, Li TK. Tetany: quantitative interrelationships between calcium and alkalosis. Am J Physiol 1975; 228: 1082-1086
I refer to Pavithran's question [1]: Which is more important in the genesis of tetany: CSF hypocalcemia or serum hypocalcemia and alkalosis?
The study by Mullin et al [2] specifically investigated the effects of directly lowering CSF calcium levels without altering serum ionized calcium or pH on neuromuscular responses. In these experiments, the authors note that the tetanic phenomena in the animals could have been caused by calcium levels in the CSF as low as 0.1 mM (normally CSF [Ca] is 1.2 mM). They also observed that exposing the lower spinal cord to a calcium poor solution did not produce a noticeable change in muscular tension indicating that the low concentration of calcium in brain interstitial fluid bathing cell bodies of neurons (and not plasma ionized calcium) was the cause for the increased neuromuscular excitability in these experiments. I do not know of clinical states in which CSF calcium levels would reduce to this extent without changes in serum calcium.
Edmonson and colleagues [3] compared the effects of rapid intravenous infusion of ethylene glycol tetraacetate (EGTA) alone versus hypocapnic alkalosis in thyroparathyroidectomized animals and the interaction between hypocalcemia and alkalosis on the "onset of tetany". Their data indicate that hypocapnic alkalosis reducing arterial PCO2 to between 10-20 mmHg alone is associated with tetany even if it is not accompanied by a significant lowering of ionized calcium in serum. However, in the presence of significant hypocalcemia (serum ionized calcium between 0.5 and 0.9 mM) induced by rapid infusion of EGTA, tetanic symptoms are evident at a slightly higher PCO2 (20-30 mmHg). There is a clear time lag of the order of hours for equilibration of calcium ions across the blood brain barrier. In contrast, changes in minute ventilation produce changes in CSF pH instantly. The authors also note that ventilation with a gas containing 5% CO2 was a more rapid and effective means of terminating tetany produced by EGTA and thyroparathyroidectomy than administration of calcium. Thus, this study by Edmonson et al [3] provides clear evidence of an interaction between serum hypocalcemia and respiratory alkalosis in the genesis of tetany and that CSF pH is a key modulator of neuronal excitability.
Conflict of interests: none
Note: This submission was not peer reviewed.
References:
[1] Pavithran P. Which is more important in the genesis of tetanus and tetany: CSF hypocalcemia or serum hypocalcemia and alkalosis? Medical Physiology Online [serial online] article 3.7, volume 1, 2008, available from http://medicalphysiologyonline.blogspot.com
[2] Mullin FJ, Hastings AB, and Lees WM. Neuromuscular responses to variations in calcium and potassium concentrations in the cerebrospinal fluid. Am J Physiol 1938; 121: 719-727
[3] Edmondson JW, Brashear RE, Li TK. Tetany: quantitative interrelationships between calcium and alkalosis. Am J Physiol 1975; 228: 1082-1086
10 May 2008
Reply to Dineash Kumar's Question: When ECF volume is measured, is transcellular fluid volume also measured?
Reply to Dineash Kumar: When ECF volume is measured, is transcellular fluid volume also measured?
E.S.Prakash, Editor, Medical Physiology Online, e-mail: medicalphysiologyonline@gmail.com
To quote C.J.Lote [1], "the markers used to measure extracellular fluid volume do not penetrate into transcellular fluids, or do so extremely slowly. Consequently, transcellular fluid volume is not measured when ECF volume is measured".
In a study [2] in which sodium selenate containing a radioactive isotope of selenium was used as a marker for measuring ECF volume, the marker was detected in cerebrospinal fluid and vitreous of the eye between 3-12 hr after infusion but later disappeared.
Thus, a single tracer is not available to measure the total volume of all transcellular fluids. Transcellular fluid volume is thus measured only when total body water is estimated.
References:
[1] Lote CJ. Principles of Renal Physiology, Springer, 2000.
[2] Albert SN, Albert CA, Hirsch EF et al. Selenate as a substitute for sulfate in the measurement of extracellular fluid volume. Journal of Nuclear Medicine 1966; 7: 290-303 [Free full text]
Conflict of interests: none
Note: This submission was not peer reviewed.
E.S.Prakash, Editor, Medical Physiology Online, e-mail: medicalphysiologyonline@gmail.com
To quote C.J.Lote [1], "the markers used to measure extracellular fluid volume do not penetrate into transcellular fluids, or do so extremely slowly. Consequently, transcellular fluid volume is not measured when ECF volume is measured".
In a study [2] in which sodium selenate containing a radioactive isotope of selenium was used as a marker for measuring ECF volume, the marker was detected in cerebrospinal fluid and vitreous of the eye between 3-12 hr after infusion but later disappeared.
Thus, a single tracer is not available to measure the total volume of all transcellular fluids. Transcellular fluid volume is thus measured only when total body water is estimated.
References:
[1] Lote CJ. Principles of Renal Physiology, Springer, 2000.
[2] Albert SN, Albert CA, Hirsch EF et al. Selenate as a substitute for sulfate in the measurement of extracellular fluid volume. Journal of Nuclear Medicine 1966; 7: 290-303 [Free full text]
Conflict of interests: none
Note: This submission was not peer reviewed.
Reply to Ravivarma Rao Panirselvam: Is 5% dextrose an effective osmole?
Reply to Ravivarma Rao Panirselvam: Is 5% dextrose an effective osmole?
E.S.Prakash, Editor, Medical Physiology Online, e-mail: medicalphysiologyonline@gmail.com
A 5% dextrose solution in water has roughly the same osmolality (280 mOsm/Kg H20) as that of normal human plasma. When small amounts of 5% dextrose solution are administered intravenously to an individual whose plasma osmolality is within normal limits, initially, there is little change in plasma osmolality; however, dextrose is taken up by cells and metabolized. Thus, the steady state effect is that of adding water which dilutes plasma [1]. Thus, some water would enter cells. This is why a 5% dextrose solution is used for replenishing intracellular fluid volume. In this instance, water flux across the cell membrane is not due to the restriction of dextrose on one side of the cell membrane – in other words, dextrose does not work as an effective osmole.
However in a diabetic with profound hyperglycemia (example, plasma glucose 400 mg/dL), the entry of glucose into cells is limited by the deficiency of insulin. In this instance, glucose in ECF would function as an effective osmole and bring about water shifts into the ECF resulting in intracellular dehydration.
The principle here is that glucose would function as an effective osmole if glucose transport into cells is a rate limiting step [2].
References:
[1] Ganong WF. Review of Medical Physiology, Mc Graw Hill, International edition, 2005.
[2] Davids MR. Lin SH, Edoute Y et al. Hyponatremia and hypoglycemia during laparoscopic surgery. Quarterly Journal of Medicine 2002; 95: 321 – 330.
Conflict of interests: none
This submission was not peer reviewed.
E.S.Prakash, Editor, Medical Physiology Online, e-mail: medicalphysiologyonline@gmail.com
A 5% dextrose solution in water has roughly the same osmolality (280 mOsm/Kg H20) as that of normal human plasma. When small amounts of 5% dextrose solution are administered intravenously to an individual whose plasma osmolality is within normal limits, initially, there is little change in plasma osmolality; however, dextrose is taken up by cells and metabolized. Thus, the steady state effect is that of adding water which dilutes plasma [1]. Thus, some water would enter cells. This is why a 5% dextrose solution is used for replenishing intracellular fluid volume. In this instance, water flux across the cell membrane is not due to the restriction of dextrose on one side of the cell membrane – in other words, dextrose does not work as an effective osmole.
However in a diabetic with profound hyperglycemia (example, plasma glucose 400 mg/dL), the entry of glucose into cells is limited by the deficiency of insulin. In this instance, glucose in ECF would function as an effective osmole and bring about water shifts into the ECF resulting in intracellular dehydration.
The principle here is that glucose would function as an effective osmole if glucose transport into cells is a rate limiting step [2].
References:
[1] Ganong WF. Review of Medical Physiology, Mc Graw Hill, International edition, 2005.
[2] Davids MR. Lin SH, Edoute Y et al. Hyponatremia and hypoglycemia during laparoscopic surgery. Quarterly Journal of Medicine 2002; 95: 321 – 330.
Conflict of interests: none
This submission was not peer reviewed.
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