Biomedical subjects

L Longerich

Publications and source records attributed to L Longerich.

At least 19 recordsLinked to original sources

PubMed2002

Dietary vitamin E supplementation lowers blood pressure in spontaneously hypertensive rats.

In spontaneously hypertensive rats (SHRs) excess endogenous aldehydes bind sulfhydryl groups of membrane proteins, altering membrane Ca2+ channels and increasing cytosolic free calcium and blood pressure. The thiol compound, N-acetyl cysteine, normalizes elevated blood pressure in SHRs by binding excess endogenous aldehydes. Vitamin E increases tissue glutathione levels--a storage form of cysteine. The aim of the present study was to investigate whether a dietary supplementation of vitamin E lowers blood pressure and prevents renal vascular changes by normalizing tissue aldehyde conjugates and cytosolic [Ca2+] in SHRs. Starting at 12 weeks of age, animals were divided into three groups of six animals each. Animals in the WKY-control group and SHR-control group were given a normal diet and the SHR-vitamin E group a diet supplemented with vitamin E (34 mg/ kg feed) for the next 9 weeks. After 9 weeks, systolic blood pressure, platelet [Ca2+]i, and liver, kidney and aortic aldehyde conjugates were significantly higher in SHR controls as compared to WKY controls and the SHR-vitamin E group. SHR-controls also showed smooth muscle cell hyperplasia in the small arteries and arterioles of the kidney. Dietary vitamin E supplementation in SHRs lowered the systolic blood pressure, cytosolic [Ca2+], tissue aldehyde conjugates and attenuated adverse renal vascular changes.

Administration, Oral↗

PubMed2002

Dietary vitamin E and C supplementation prevents fructose induced hypertension in rats.

In fructose-induced hypertension in Wistar-Kyoto (WKY) rats, excess endogenous aldehydes bind sulfhydryl groups of membrane proteins, altering membrane Ca2+ channels and increasing cytosolic free calcium and blood pressure. The thiol compound N-acetyl cysteine prevents fructose-induced hypertension by binding excess endogenous aldehydes and normalizing membrane Ca2+ channels and cytosolic free calcium. The aim of the present study was to investigate whether dietary supplementation of vitamin E and vitamin C which are known to increase tissue glutathione, a storage form of cysteine, prevents this hypertension and its associated biochemical and histopathological changes. Starting at 7 weeks of age, animals were divided into four groups of six animals each and treated as follows: control group, normal diet and normal drinking water; fructose group, normal diet and 4% fructose in drinking water; fructose + vitamin E group, diet supplemented with vitamin E (34 mg/ kg feed) and 4% fructose in drinking water; fructose + vitamin C group, diet supplemented with vitamin C (1,000 mg/kg feed) and 4% fructose in drinking water. At 14 weeks, systolic blood pressure, platelet [Ca2+]i and kidney and aortic aldehyde conjugates were significantly higher in the fructose group. These animals also displayed smooth muscle cell hyperplasia in the small arteries and arterioles of the kidneys. Dietary vitamin E and C supplementation in fructose-treated WKY rats prevented the increase in systolic blood pressure by normalizing cytosolic [Ca2+]i and kidney and aortic aldehyde conjugates and preventing adverse renal vascular changes.

Animals↗

PubMed2001

Dietary vitamin C supplementation lowers blood pressure in spontaneously hypertensive rats.

In spontaneously hypertensive rats (SHRs) excess endogenous aldehydes bind sulfhydryl groups of membrane proteins, altering membrane Ca2+ channels and increasing cytosolic free calcium and blood pressure. The thiol compound, N-acetyl cysteine, normalizes elevated blood pressure in SHRs by binding excess endogenous aldehydes. Vitamin C can increase tissue cysteine and glutathione levels. The aim of the present study was to investigate whether a dietary supplementation of vitamin C can lower tissue aldehydes and blood pressure and normalize associated biochemical and histopathological changes in SHRs. Starting at 12 weeks of age, animals were divided into 3 groups of 6 animals each. Animals in the WKY-control group and SHR-control group were given a normal diet and the SHR-vitamin C group a diet supplemented with vitamin C (1000 mg/kg feed) for the next 9 weeks. After nine weeks, systolic blood pressure, platelet [Ca2+]i, plasma insulin and liver, kidney and aortic aldehyde conjugates were significantly higher in SHR controls as compared to WKY controls and the SHR-vitamin C group. SHR-controls also showed smooth muscle cell hyperplasia in the small arteries and arterioles of the kidneys. Dietary vitamin C supplementation in SHRs lowered the systolic blood pressure, tissue aldehyde conjugates and attenuated adverse renal vascular changes.

Aldehydes↗

PubMed2000

Dietary alpha-lipoic acid supplementation lowers blood pressure in spontaneously hypertensive rats.

BACKGROUND AND OBJECTIVES: In spontaneously hypertensive rats (SHRs), excess endogenous aldehydes bind sulfhydryl groups of membrane proteins, altering membrane Ca2+ channels and increasing cytosolic free calcium and blood pressure. The thiol compound, N-acetyl cysteine, normalizes elevated blood pressure in SHRs by binding excess endogenous aldehydes and normalizing membrane Ca2+ channels and cytosolic free calcium. The aim of the present study was to investigate whether a dietary supplementation of an endogenous fatty acid, alpha-lipoic acid, another thiol compound that is known to increase tissue cysteine and glutathione, can lower blood pressure and normalize associated biochemical and histopathological changes in SHRs. METHODS AND RESULTS: Starting at 12 weeks of age, animals were divided into three groups of six animals each. Animals in the Wistar- Kyoto (WKY) rat control group and the SHR control group were given a normal diet, and the SHR-lipoic acid group was given a diet supplemented with lipoic acid (500 mg/kg feed) for the next 9 weeks. After 9 weeks, systolic blood pressure, platelet [Ca2+]i, plasma insulin and liver, kidney and aortic aldehyde conjugates were significantly higher in SHR controls as compared with WKY rat controls and the SHR lipoic acid group. SHR controls also showed smooth muscle cell hyperplasia in the small arteries and arterioles of the kidneys. CONCLUSIONS: Dietary alpha-lipoic acid supplementation in SHRs lowered the systolic blood pressure, cytosolic [Ca2+]i, blood glucose and insulin levels, and tissue aldehyde conjugates, and attenuated adverse renal vascular changes.

Aldehydes↗

PubMed2000

Dietary lipoic acid supplementation prevents fructose-induced hypertension in rats.

BACKGROUND AND AIMS: In fructose-induced hypertension in Wistar-Kyoto (WKY) rats, excess endogenous aldehydes bind sulfhydryl groups of membrane proteins, alter membrane Ca2+ channels and increase cytosolic free calcium and blood pressure. The thiol compound N-acetyl cysteine prevents such hypertension by binding these aldehydes and normalizing membrane Ca2+ channels and cytosolic free calcium. The aim of this work was to investigate whether dietary supplementation of an endogenous fatty acid, alpha-lipoic acid, another thiol compound known to increase cysteine and glutathione, prevents this hypertension and its associated biochemical and histopathological changes. METHODS AND RESULTS: Starting at seven weeks of age, animals were divided into three groups of six animals each and treated as follows: control (normal diet and normal drinking water); fructose (normal diet and 4% fructose in drinking water); fructose + lipoic acid (diet supplemented with lipoic acid 500 mg/kg feed and 4% fructose in drinking water). After 14 weeks, systolic blood pressure, platelet [Ca2+]i, plasma glucose and insulin and kidney and aortic aldehyde conjugates were significantly higher in the fructose group. These also displayed smooth muscle cell hyperplasia in the small arteries and arterioles of the kidneys. CONCLUSION: Dietary alpha-lipoic acid supplementation in fructose-treated WKY rats may prevent their increase in systolic blood pressure by normalizing cytosolic [Ca2+], blood glucose and insulin, kidney and aortic aldehyde conjugates and preventing adverse renal vascular changes.

Aldehydes↗

PubMed1999

Antihypertensive effect of low ethanol intake in spontaneously hypertensive rats.

Light to moderate drinking in humans lowers the risk of coronary heart disease and may lower blood pressure. We examined the effect of chronic low daily alcohol consumption on blood pressure, platelet cytosolic free calcium [Ca2+]i, tissue aldehyde conjugates and renal vascular changes in normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). We also examined the effects of the same weekly amount of alcohol consumption over a one day period each week simulating weekend drinking in humans. Animals, age 7 weeks, were divided into six groups of six animals each and were treated as follows: WKY and SHR control, normal drinking water; WKY and SHR, 0.5% ethanol in drinking water; WKY and SHR, 3.5% ethanol in drinking water one day/week. After 14 weeks systolic blood pressure, platelet [Ca2+]i, liver, kidney and aortic aldehyde conjugates were significantly higher (p < 0.05) in untreated SHRs as compared to untreated WKYs. Daily 0.5% ethanol consumption in SHRs significantly (p < 0.05) attenuated these changes and also attenuated smooth muscle cell hyperplasia and narrowing of the lumen in small arteries and arterioles of the kidney. WKY rats treated with 0.5% ethanol had lower aldehyde conjugates without any significant effect on blood pressure and platelet [Ca2+]i as compared to WKY controls. Consumption of 3.5% ethanol one day/week did not affect blood pressure and associated changes in normotensive WKY rats or hypertensive SHRs as compared to their respective controls. These results suggest that chronic daily low ethanol intake lowers blood pressure in SHRs by lowering tissue aldehyde conjugates and cytosolic free calcium.

Alcohol Drinking↗

PubMed1999

Dietary vitamin B6 supplementation attenuates hypertension in spontaneously hypertensive rats.

In spontaneously hypertensive rats (SHRs) excess endogenous aldehydes bind sulfhydryl groups of membrane proteins, altering membrane Ca2+ channels, increasing cytosolic free calcium and blood pressure. N-acetyl cysteine normalizes elevated blood pressure in SHRs by binding excess endogenous aldehydes. It is known that dietary vitamin B6 supplementation can increase the level of endogenous cysteine. Our objective was to investigate whether a dietary supplementation of vitamin B6 can prevent hypertension and associated changes in SHRs. Starting at 7 weeks of age, animals were divided into three groups of six animals each. Animals in WKY-control group and SHR-control group were given a normal vitamin B6 diet; and SHR-vitamin B6 group, a high vitamin B6 diet (20 times the recommended dietary intake; RDA) for the next 14 weeks. After 14 weeks, systolic blood pressure, platelet [Ca2+]i and liver, kidney and aortic aldehyde conjugates were significantly higher in SHR controls compared to WKY controls. These animals also showed smooth muscle cell hyperplasia in the small arteries and arterioles of the kidneys. Dietary vitamin B6 supplementation attenuated the increase in systolic blood pressure, tissue aldehyde conjugates and associated changes. These results further support the hypothesis that aldehydes are involved in increased systolic blood pressure in SHRs and suggest that vitamin B6 supplementation may be an effective antihypertensive.

Aldehydes↗

PubMed1999

Dietary vitamin B6 supplementation prevents ethanol-induced hypertension in rats.

BACKGROUND AND AIMS: All known pathways of ethanol metabolism result in the production of acetaldehyde, a highly reactive compound. Acetaldehyde has been shown to deplete vitamin B6 in chronic alcoholics. It also binds with sulfhydryl groups of membrane proteins, altering membrane Ca2+ channels and increasing vascular cytosolic free calcium, peripheral vascular resistance and blood pressure. The aldehyde-binding thiol compound, N-acetyl cysteine, attenuates elevated blood pressure and associated adverse changes in ethanol-induced hypertensive rats. Vitamin B6 supplementation increases the level of endogenous cysteine. Aim of this work was thus to investigate whether a dietary supplementation of vitamin B6 can prevent ethanol-induced hypertension and associated changes in Wistar-Kyoto (WKY) rats. METHODS AND RESULTS: Starting at 7 weeks of age, WKY rats were divided into three groups of six animals each. The control group received a normal vitamin B6 diet (regular chow) and normal drinking water, the ethanol group, the same diet plus 1% ethanol in the drinking water, and the ethanol + vitamin B6 group a high vitamin B6 diet (20 times normal diet) and 1% ethanol in the drinking water. After 14 weeks, systolic blood pressure, platelet [Ca2+]i and kidney and aortic aldehyde conjugate levels were significantly higher in the ethanol group. These rats also showed smooth muscle cell hyperplasia in the small arteries and arterioles of the kidneys. Dietary vitamin B6 supplementation prevented these changes. CONCLUSIONS: Dietary vitamin B6 supplementation prevented ethanol-induced hypertension and associated changes in WKY rats by normalizing tissue aldehyde conjugate levels.

Analysis of Variance↗

PubMed1998

Role of aldehydes in fructose induced hypertension.

Aldehydes are formed in tissues of humans and animals as intermediates of glucose and fructose metabolism and due to lipid peroxidation. N-acetyl cysteine (NAC), an analogue of the dietary amino acid cysteine, binds aldehydes thus preventing their damaging effect on physiological proteins. We measured systolic blood pressure (SBP), platelet cytosolic free calcium [Ca2+]i and tissue aldehyde conjugates in fructose induced hypertensive Wistar-Kyoto (WKY) rats and examined the effect of NAC in the diet on these parameters. Animals age 7 weeks were divided into three groups of 6 animals each and were treated as follows: WKY-control (chow diet and normal drinking water); WKY-Fructose (chow diet and 4% fructose in drinking water); WKY-Fructose+NAC (1.5% NAC in chow diet and 4% fructose in drinking water). After 11 weeks, systolic blood pressure, platelet [Ca2+]i and kidney aldehyde conjugates were all significantly higher in fructose treated rats. NAC treatment prevented these changes. These results suggest that aldehydes may be the cause of fructose induced hypertension and elevated cytosolic free calcium.

Acetylcysteine↗

PubMed1998

i-STAT hand-held point-of-care analyzer for dialysis units.

The i-STAT hand-held analyzer assays ten tests including electrolytes, gases, urea, glucose, ionized calcium, and hematocrit. Eight different cartridges assay one to eight tests. We have previously confirmed or demonstrated that accuracy and precision for blood assays are comparable to accepted laboratory methods. We now report similar results for hemodialysis dialysate and peritoneal dialysis effluent. The i-STAT analyzer is simple to use, and dialysis nurses produced accurate results with 20 min training. The results are viewed digitally on the analyzer and automatically on a small attachable printer. i-STAT blood analysis is most valuable when results are desired immediately, anywhere, including before, during and after dialysis in hemodialysis units. Hemodialysate analysis using i-STAT can be most valuable for rapidly checking dialysis machine function such as dialysate mixing and conductivity and ramping results and dialysate concentrations prepared in the unit. Peritoneal effluent analysis is useful for rapid evaluation of membrane function.

Calcium↗

PubMed1998

Aldehyde induced hypertension in rats: prevention by N-acetyl cysteine.

Methylglyoxal, a highly reactive endogenous aldehyde is formed in the tissue of humans and animals as an intermediate of glucose and fructose metabolism. N-acetyl cysteine (NAC), an analogue of the dietary amino acid cysteine, binds aldehydes thus preventing their damaging effect on physiological proteins. We measured systolic blood pressure (SBP), platelet [Ca2+]i, circulating nitric oxide levels, tissue aldehyde conjugates and renal vascular changes in chronic methyglyoxal treated Wistar-Kyoto (WKY) rats and examined the effect of NAC in the diet on these parameters. Animals, age seven weeks, were divided into three groups of six animals each and were treated as follows: WKY-control (chow diet and normal drinking water); WKY-methylglyoxal (chow diet and methyglyoxal in drinking water); WKY-methyglyoxal + NAC (1.5% NAC in diet and methylglyoxal in drinking water) for the next 18 weeks. Methylgyoxal in drinking water was given at a concentration of 0.2% during weeks 0-5; 0.4%, weeks 6-10; and 0.8%, weeks 11-18. After 18 weeks systolic blood pressure, platelet [Ca2+]i and kidney aldehyde conjugates were significantly higher and serum nitric oxide levels lower in methylglyoxal treated rats. Methylglyoxal treated rats also showed smooth muscle cell hyperplasia in the small artery and arterioles of the kidney. N-acetyl cysteine, an aldehyde binding thiol compound, prevented these changes.

Acetylcysteine↗

PubMed1995

Ethanol- and threonine-induced hypertension in rats: a common mechanism.

OBJECTIVE: To investigate the effects of oral L-threonine and ethanol, precursor of endogenous acetaldehyde, on systolic blood pressure, cystolic free calcium ([Ca2+]i) and vascular calcium uptake in Wistar-Kyoto (WKY) rats. METHODS: Twenty-four male WKY rats aged eight weeks were divided into four groups of six animals each. Animals were given either water or 5% ethanol, 8% L-threonine or 8% L-glycine in drinking water for 15 weeks, animals were sacrificed, aortic rings were incubated in physiological buffer containing 45Ca2+ and uptake was measured after 20 mins. ([Ca2+]i in platelets was measured with a fluorescence [Ca2+]i indicator, FURA-2. Tissues were processed for morphological investigation. RESULTS: After 15 weeks, systolic blood pressure, platelet [Ca2+]i and aortic calcium uptake were all significantly higher (P < 0.001) in rats given either threonine or ethanol than in control rats given water or glycine. Animals in threonine or ethanol group also showed smooth muscle cell hyperplasia, with some thickening of the wall and narrowing of the lumen in small arteries and arterioles of the kidney. Glycine treatment did not cause any of these changes in rats. CONCLUSION: These results suggest that acetaldehyde may be a common cause of both ethanol- and threonine-induced hypertension.

Animals↗

PubMed1995

N-acetyl cysteine attenuates ethanol induced hypertension in rats.

All known pathways of ethanol metabolism result in the production of acetaldehyde, a highly reactive compound. N-acetyl cysteine, an analogue of the dietary amino acid cysteine, binds acetaldehyde, thus preventing its damaging effect on physiological proteins. This study examined the effect of oral N-acetyl cysteine on the increased blood pressure, platelet cytosolic free calcium, blood acetaldehyde and adverse renal vascular changes induced by chronic ethanol treatment in rats. Twenty-four male Wistar-Kyoto (WKY) rats, age 7 weeks were divided into four groups of six animals each. Animals in group I were given water and group II 5% ethanol in water for the next 14 weeks. Animals in group III were given 5% ethanol + 1% N-acetyl cysteine for 4 weeks followed by 5% ethanol + 2% N-acetyl cysteine for the next 10 weeks. Animals in group IV were given 5% ethanol for 7 weeks; at that time ethanol was withdrawn and animals were placed on water with 2% N-acetyl cysteine for the next 7 weeks. After 14 weeks systolic blood pressure and platelet cytosolic free calcium were all significantly higher (p<0.001) in rats given ethanol as compared to rats in other groups. N-acetyl cysteine treatment, along with ethanol, significantly (p<0.001) attenuated the increased blood pressure and platelet cytosolic free calcium and adverse renal vascular changes. Discontinuation of ethanol treatment for 7 weeks along with N-acetyl cysteine supplementation also significantly lowered the blood pressure and platelet cytosolic free calcium and attenuated adverse renal vascular changes. There was no significant difference in aortic malonaldehyde among four groups. Increase in blood acetaldehyde with ethanol treatment was significantly attenuated with N-acetyl cysteine treatment. These results suggest that acetaldehyde may be the cause of ethanol-induced hypertension and elevated cytosolic free calcium and renal vascular changes.

Acetaldehyde↗

PubMed1994

Fructose-induced hypertension, hypertriglyceridemia and elevated cytosolic calcium in rats: prevention by deuterium oxide.

We examined the effect of 5% deuterium oxide (D20) in drinking water on systolic blood pressure, platelet cytosolic free calcium, aortic calcium uptake and plasma insulin, glucose and triglycerides in rats with fructose-induced hypertension. Eighteen male Wistar-Kyoto (WKY) rats, age 8 weeks, were divided into 3 groups of 6 animals each. Animals in group I were given water; group II, 8% fructose and group III, 8% fructose + 5% D20 as their drinking water for the next 15 weeks. Systolic blood pressure in the fructose treated rats was significantly higher (p < 0.01) than in animals on water after 2 weeks and remained higher throughout the study. At 15 weeks, systolic blood pressure, platelet cytosolic calcium, aortic calcium uptake and plasma glucose, insulin and triglycerides were significantly higher (p < 0.01) in the fructose treated rats compared with rats from other groups. Deuterium oxide given together with fructose prevented development of high blood pressure and the associated increase in platelet cytosolic calcium, aortic calcium uptake and plasma triglycerides. D20 treatment did not prevent fructose induced increases in plasma insulin and glucose. The parallel increase in systolic blood pressure, cytosolic free calcium, and in vascular calcium uptake suggests that an increased cytosolic free calcium is involved in the pathophysiology of hypertension. D20 prevents this hypertension by normalizing cytosolic free calcium.

Animals↗

PubMed1994

Oral treatment with low molecular weight heparin normalizes blood pressure in hypertensive rats.

Increased calcium uptake in vascular tissue, leading to elevated cytosolic free calcium has been implicated in the pathophysiology of hypertension. This study examined the effect of oral low molecular weight heparin (Logiparin) on systolic blood pressure, platelet cytosolic free calcium and aortic calcium uptake in spontaneously hypertensive rats. Starting at age 12 weeks, spontaneously hypertensive rats were divided into three groups of six animals each. The drinking water of groups 1, 2 and 3 was replaced by 100% H2O, 0.5 mg (low dose) or 1 mg (high dose) low molecular weight heparin/ml H2O, respectively, for next 11 weeks. Six normotensive Wistar-Kyoto rats (age 12 weeks) on H2O and six on low dose heparin in H2O were used as controls. At age 23 weeks, increase in systolic blood pressure, platelet cytosolic free calcium and aortic calcium uptake in spontaneously hypertensive rats was significantly lowered by low dose LMW heparin as compared to spontaneously hypertensive rats on H2O, but was significantly higher than Wistar-Kyoto rats on H2O and LMW heparin. This dose of heparin did not have any effect on these parameters in normotensive Wistar-Kyoto rats. High dose LMW heparin normalized the elevated platelet cytosolic free calcium, aortic calcium uptake and systolic blood pressure in spontaneously hypertensive rats, but it had a limited effect on adverse renal vascular changes. Oral low molecular weight heparin did not cause any abnormal hematological, biochemical or pathological changes in rats.

Administration, Oral↗

PubMed1993

Calcium and calcium magnesium carbonate specimens submitted as urinary tract stones.

Of 8,129 specimens submitted as urinary stones from 6,095 patients, 67 from 15 patients were predominantly calcium carbonate or calcium magnesium carbonate (dolomite) by infrared analysis. Detailed study of 1 man and 4 women who submitted 3 or more such specimens showed that all were of aragonite calcium carbonate crystal form in 2 women and all calcite in the man. All 3 patients had a long history of nephrolithiasis preceding submission of calcium carbonate stones. There was frequent and often painful spontaneous passage of many small stones. Medullary sponge kidney was reported in 2 patients. Specimens submitted by the other 2 women included dolomite and quartz artifacts. Of the other 10 patients 4 had calcite and 1 had aragonite (possibly true stones). Five patients had artifacts with dolomite in 3 and mixed specimens in 2. True calcium carbonate kidney stones and calcium carbonate artifacts may be difficult to distinguish, and dolomite and quartz artifacts may require x-ray diffraction for clear-cut diagnosis.

Adult↗

PubMed1993

Deuterium oxide normalizes blood pressure and elevated cytosolic calcium in rats with ethanol-induced hypertension.

This study examined the effect of 10% deuterium oxide (D2O) in drinking water on systolic blood pressure, platelet cytosolic free calcium, aortic calcium uptake and renal vascular changes in rats with ethanol-induced hypertension. Eighteen male Wistar-Kyoto rats, age seven weeks, were divided into three groups of six animals each. Group I was given water and groups II and III, 5% ethanol in drinking water for the next seven weeks. After one week, systolic blood pressure in the ethanol-treated rats was significantly higher (P < 0.01) than in rats drinking water. After seven weeks, animals in group I were continued on water, group II on 5% ethanol, group III on 5% ethanol but with the addition of 10% D2O in their drinking water for the next seven weeks. After 14 weeks, systolic blood pressure, platelet cytosolic free calcium and aortic calcium uptake was significantly higher (P < 0.01) in group II rats (given ethanol for 14 weeks) compared with rats from other groups. Ethanol-treated rats also showed smooth muscle hyperplasia with some thickening of the wall and narrowing of the lumen in small arteries and arterioles of the kidney. D2O given to ethanol-treated rats normalized their blood pressure, platelet cytosolic free calcium, aortic calcium uptake and attenuated renal vascular changes.

Animals↗

PubMed1993

Digoxin-like factors in herbal teas.

Forty-six commercially packaged teas and 78 teas prepared from purchased herbs were assayed for digoxin-like factors (DLF) by their crossreactivity with digoxin antibody (immuno-crossreactive DLF) and by their inhibition of ouabain binding to membrane Na,K-ATPase (NKA inhibitory DLF). Three packaged teas and 3 herbs gave NKA inhibitory DLF values > 30 micrograms digoxin equivalents/cup. Two packaged teas and 3 herbs gave immuno-crossreactive DLF values > .050 micrograms digoxin equivalent/cup. One herb, pleurisy root, had a crossreactive DLF value of 187 micrograms/cup and NKA inhibitory DLF equivalent to 3658 micrograms/cup. Plasma digoxin-like factors were measured after ingestion of the 3 commercially packaged herbal teas with highest values for NKA inhibitory DLF. After ingestion of each of the 3 teas, plasma NKA inhibitory DLF increase, in one case more than 100-fold. Two teas produced a measurable increase in plasma immuno-crossreactive DLF after ingestion. Some digoxin-like factors in human plasma may have a dietary source.

Beverages↗