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Biomedical subjects

M L Blank

Publications and source records attributed to M L Blank.

At least 73 records · Page 4Linked to original sources
PubMed1985

The adrenergic system and the cardiovascular effects of platelet activating factor (1-0-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine) in SHR and WKY rats.

1-0-Hexadecyl-2-acetyl-sn-glycero-3-phosphocholine (1-hexadecyl-2-acetyl-GPC, platelet activating factor, PAF) was previously shown to produce profound hypotension and sympathetic activation in conscious rats. To determine the role of the sympatho-adrenomedullary system in the cardiovascular responses elicited by 1-hexadecyl-2-acetyl-GPC, the vasoactive phospholipid was administered (1 nmol per 300 g) to a) intact, b) bilaterally demedullated, and c) propranolol- (a beta-adrenoceptor blocker) treated SHR and WKY rats. The hypotensive response to 1-hexadecyl-2-acetyl-GPC was prolonged in demedullated or propranolol-pretreated WKY rats and in propranolol-treated SHR rats. The extreme tachycardia produced by 1-hexadecyl-2-acetyl-GPC in both the WKY and SHR rats was abolished by propranolol pretreatment. Pressor responses to norepinephrine during the 1-hexadecyl-2-acetyl-GPC-induced hypotension in propranolol-pretreated rats were suppressed in both the normotensive and SHR rats. Plasma acetylhydrolase activity, which inactivates PAF, was higher in hypertensive (SHR) rats or demedullated WKY rats than in the normotensive (WKY) rats. These results show that the tachycardia evoked by 1-hexadecyl-2-acetyl-GPC is mediated solely by sympathetic activation and the beta-adrenergic receptors and further indicate the major role of the sympathetic system and beta-adrenoceptors in recuperation from 1-hexadecyl-2-acetyl-GPC-induced shock. The data also suggest that acetylhydrolase in serum is an important regulatory enzyme for controlling PAF levels in the vascular compartment.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed1985

Cardiac output and peripheral vascular resistance during intravenous infusion of 1-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine in conscious normotensive and spontaneously hypertensive rats.

Cardiovascular responses to intravenous 1-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine (56 and 112 pmoles/kg/min) were examined in conscious Wistar-Kyoto (WKY) normotensive rats and spontaneously hypertensive rats (SHR) instrumented with arterial and venous catheters, and an electromagnetic flow probe around the ascending aorta. The results suggest that this compound reduces mean blood pressure via a dose related fall in peripheral vascular resistance and cardiac index in conscious SHR and WKY rats.

Animals↗
PubMed1984

Conversion of 1-alkyl-2-acetyl-sn-glycerols to platelet activating factor and related phospholipids by rabbit platelets.

The metabolic pathway for 1-alkyl-2-acetyl-sn-glycerols, a recently discovered biologically active neutral lipid class, was elucidated in experiments conducted with rabbit platelets. The total lipid extract obtained from platelets incubated with 1-[1,2-(3)H]alkyl-2-acetyl-sn-glycerols or 1-alkyl-2-[3H]acetyl-sn-glycerols contained at least six metabolic products. The six metabolites, identified on the basis of chemical and enzymatic reactions combined with thin-layer or high-performance liquid chromatographic analyses, corresponded to 1-alkyl-sn-glycerols, 1-alkyl-2-acetyl-sn-glycero-3-phosphates, 1-alkyl-2-acyl (long-chain)-sn-glycero-3-phosphoethanolamines, 1-alkyl-2-acetyl-sn-glycero-3-phosphoethanolamines, 1-alkyl-2-acetyl-sn-glycero-3-phosphoethanolamines, 1-alkyl-2-acyl(long-chain)-sn-glycero-3-phosphocholines, and 1-alkyl-2-acetyl-sn-glycero-3-phosphocholines (platelet activating factor). These results indicate that the metabolic pathway for enzymatic activities: choline- and ethanolamine- phosphotransferases, acetyl-hydrolase, an acyltransferase, and a phosphotransferase. The step responsible for the biosynthesis of platelet activating factor would appear to be the most important reaction in this pathway and this product could explain the hypotensive activities previously described for alkylacetyl-(or propionyl)-glycerols. Of particular interest was the preference exhibited for the utilization of the 1-hexadecyl-2-acetyl-sn-glycerol species in the formation of platelet activating factor.

Animals↗
PubMed1984

Novel quantitative method for determination of molecular species of phospholipids and diglycerides.

A novel method is described for the quantitative analysis of subclasses (alk-1-enylacyl, alkylacyl, and diacyl types) and molecular species within each subclass of glycerophosphatides. Diradylglycerols from phospholipase C hydrolysis of the phospholipids are converted to benzoate derivatives, the benzoates are separated into their respective subclasses by thin-layer chromatography, and quantitated by measuring absorbance at 230 nm. Molecular species within individual subclasses are separated using a combination of argentation thin-layer chromatography and reversed-phase high-performance liquid chromatography with direct, on-line quantitation at 230 nm. We applied the method to the analysis of ethanolamine phosphatides from beef brain and were able to quantitate the three diradylglycerol subclasses (alk-1-enylacyl, alkylacyl, and diacyl types) as well as ca. 29 molecular species within each of these subclasses. This new quantitative approach for the analysis of specific molecular species of glycerolipids should be applicable to studies involving a variety of biologically important lipids, such as phosphatidylcholine, phosphatidylinositol, platelet activating factor, plasmalogens, and neutral type glycerolipids including diacylglycerols.

Animals↗
PubMed1984

Liposomal preparations of calcium- or zinc-DTPA have a high efficacy for removing colloidal Ytterbium-169 from rat tissues.

Results from this study demonstrate that liposomes increase the effectiveness of chelating agents in removing heavy metals from contaminated tissues in vivo. We compared the ability of free and liposomal preparations of Ca- and Zn-diethylenetriaminepentaacetic acid (DTPA) to remove 169Yb from tissues of rats previously injected intravenously with either soluble or colloidal forms of 169Yb . Although single injections of liposomal Zn-DTPA were better than the free chelator in reducing the body burden of 169Yb administered in a soluble form (citrate), the liposomal preparations of Zn-DTPA or Ca-DTPA were even more effective in removing the 169Yb that had been injected as the colloidal form. However, a second injection of liposomal Zn-DTPA given 8 days after the initial treatment was not as effective in removing 169Yb as a second injection of the free chelator. Whether injected in the free or liposomal forms, Ca-DTPA was more effective than Zn-DTPA in removing the colloidal 169Yb . Significantly lower amounts of colloidal 169Yb remained in the liver, kidney, muscle, bone, and blood of rats after injection of the liposomal preparations of Ca- or Zn-DTPA than in the corresponding organs of the controls (P less than 0.01). The liposomal preparations were also more efficient in reducing the retention of colloidal 169Yb in bone and blood than the free chelators (P less than 0.01).

Animals↗
PubMed1984

A new class of antihypertensive neutral lipid: 1-alkyl-2-acetyl-sn-glycerols, a precursor of platelet activating factor.

A new type of neutral lipid is described that possesses hypotensive activity in genetic hypertensive (SHR) and normotensive (WKY) rats. 1-Alkyl-2-acetyl-sn-glycerols and 1-alkyl-2-propionyl-sn-glycerols are both equally effective in eliciting the hypotensive response. Requirement for the 1-alkyl and 2-acetyl or 2-propionyl structure of the active isomer was documented by the negative responses obtained with closely related neutral lipid analogs (1-alkyl-2-acyl-, 1-alkyl-3-acetyl-, 1-acyl-2-acetyl-, 1-alkyl-2,3-diacetyl-, and 1-alkyl-glycerols). Although less potent than PAF (1-alkyl-2-acetyl-sn-glycero-3-phosphocholine), the 1-alkyl-2-acetyl-sn-glycerols produce a response of significantly longer duration and may have fewer immediate side effects than PAF. The mechanism for the biological activity is unknown; however, we have demonstrated previously that the enzymatic synthesis of 1-alkyl-2-acetyl-sn-glycerols to PAF occurs via a specific cholinephosphotransferase and therefore the observed blood pressure response might be due to the conversion of the neutral lipid precursor to PAF in vivo.

Animals↗
PubMed1984

[Method for the automated mapping of 35 ECG leads].

The method of recording the ECGs, inputting them into a computer and automatic analysis of 35 ECG leads is described. The proposed method largely diminishes the time expenditure and difficulties in obtaining and analysing 35 ECG lead mapping grams, as the computer makes all measurements and calculations and produces a final document.

Analog-Digital Conversion↗
PubMed1983

Inactivation of 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine by a plasma acetylhydrolase: higher activities in hypertensive rats.

We have partially characterized the properties of a specific acetylhydrolase in plasma from spontaneous hypertensive rats. This enzyme inactivates 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine (a lipid involved in platelet aggregating, hypotensive, and allergic responses) by removal of the acetate group. The extent of acetate hydrolysis was linear with both time and protein concentration, and the enzyme had an apparent Km of 2.5 microM and a Vmax of 2.6 nmol/min/mg protein. As with an intracellular acetylhydrolase previously characterized by us, the plasma activity was not affected by addition of phosphatidylcholine, EDTA, or Ca2+. However, in contrast to the acetylhydrolase activity in the rat kidney soluble fraction, the plasma activity was associated with a higher molecular weight protein resolved on a Sepharose 6B column and the plasma acetylhydrolase was not inhibited by treatment with trypsin, pronase, or subtilisin. We also compared the acetylhydrolase activity in plasma of age-matched spontaneous hypertensive rats and their normotensive controls, and found approximately 20% higher levels of activity in plasma from the hypertensive animals (P less than 0.01).

Animals↗
PubMed1983

Spontaneous and protein-catalyzed transfer of 1-alkyl-2-acetyl-sn-glycero-3-phosphocholine (platelet-activating factor) between phospholipid bilayers.

1-Alkyl-2-acetyl-sn-glycero-3-phosphocholine (platelet-activating factor or alkylacetyl-GPC), a bioactive phospholipid that possesses hypotensive, platelet-aggregating and inflammatory properties, is known to be secreted by a variety of cell types. The biological activity of alkylacetyl-GPC is related to a precise chemical structure that implicates interaction with proteins. We have studied the spontaneous and protein-catalyzed transfer of alkylacetyl-GPC between phospholipid vesicles and have demonstrated the following: 1. There are at least two transferable pools of alkylacetyl-GPC in sonicated phospholipid vesicles. 2. These two pools differ in the rate at which they dissociate from the vesicles; one pool equilibrates between donor and acceptor vesicles instantaneously while the other pool is transferred much more slowly. 3. Dialysis of alkylacetyl-GPC between phospholipid vesicles through the aqueous phase is slow. 4. A protein fraction derived from rat lung cytosol catalyzes the transfer of the nonequilibrating pool of alkylacetyl-GPC between phospholipid vesicles; this transfer is superimposed on the spontaneous transfer and is unchanged in experiments using vesicles from which the rapidly equilibrating pool has been removed.

Kinetics↗
PubMed1983

Antihypertensive effects of I-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine on plasma renin activity and catecholamine responses in spontaneously hypertensive rats.

Fourteen 23 week old male spontaneously hypertensive rats (SHR) were randomly divided into saline control or phospholipid (I-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine) treatment groups. Four weeks of baseline systolic blood pressure (SBP) and heart rate (HR) measurements were determined via tail plethysmography. On week 25 of the baseline period a 1.5 ml blood sample was taken by tail clip for analysis of norepinephrine (NE), epinephrine (E), and plasma renin activity (PRA). On the following week, a single injection of phospholipid (11 ug/kg, s.c.) was given to the experimental animals following baseline SBP and HR determinations. A similar procedure was employed for control subjects, except they received an injection of normal saline (0.5 ml, s.c.). Systolic BP and HR responses were monitored for 24 minutes following the injection. A 1.5 ml blood sample was taken at the end of the 4th minute for NE, E, and PRA assays. A significant drop in SBP (202 +/- 5 mmHg to 124 +/- 6 mmHg) and an increase in HR (431 +/- 17 bpm to 519 +/- 21 bpm) were observed for experimental animals, but not for control subjects. Plasma NE increased significantly (446 +/- 42 pg/ml to 1099 +/- 77 pg/ml), but E remained unchanged following treatment with the phospholipid. Plasma renin activity increased for both groups, but this change was only significant for the experimental group (18.1 +/- 5.7 ng Al/ml/hr to 34.3 +/- 3.6 ng Al/ml/hr). Thus, it appears that I-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine is a potent antihypertensive vasodilating agent which stimulates baroreceptor mediated sympathetic discharge to the heart and kidneys of the SHR.

Animals↗
PubMed1983

Quantitative analysis of ether-linked lipids as alkyl- and alk-1-enyl-glycerol benzoates by high-performance liquid chromatography.

Methodology for the quantitative and qualitative analyses of alkyl- and alk-l-enyl-glycerols derived by Vitride reduction of ether-linked glycerolipids in the presence of an internal standard was developed. The procedure involved preparation of benzoate derivatives that were subsequently analyzed by high-performance liquid chromatography with detection at 228 nm. Separation of the glycerol ether dibenzoates on a C18 reverse-phase column allowed for the simultaneous quantitation and the determination of chain length of both alkyl- and alk-l-enyl-glycerols in a single chromatographic run of less than 15 min. The method was accurate (less than 10% error), reproducible, and sensitive (less than 1 microgram per component). Application of the method to the analysis of phospholipids from L-M cells grown in the presence and absence of elaidic acid demonstrated that the cells incorporated a portion of the trans acid supplement (presumably via the fatty alcohol) into the side chains of both alkyl- and alk-l-enyl-glycerol-containing phosphatides.

Animals↗
PubMed1982

Formation of alkylacyl- and diacylglycerophosphocholines via diradylglycerol cholinephosphotransferase in rat liver.

We found that diacylglycerol and alkylacylglycerol choline phosphotransferase activities exhibited similar pH optima, thermolabilities and inhibitions by Mn2+, and dithiothreitol. The Vmax of diacylglycerol cholinephosphotransferase was higher (approx. 1-2-fold) than the Vmax of alkylacylglycerol cholinephosphotransferase. The Km value for diacylglycerol was somewhat greater than for the alkylacylglycerol, but no differences were found for the Km of CDPcholine with either type of diradylglycerol as the other substrate. Endogenous levels of diacylglycerols in microsomes were 24.3 nmol/mg protein, whereas no detectable amount of alkylacylglycerols was observed. Results from this study indicate that a similar or identical enzyme catalyzes the formation of 1,2-diacyl- and 1-alkyl-2-acyl-sn-glycero-3-phosphocholine and that the availability of diradylglycerols and the turnover rate of ether-linked lipids would appear to be important factors in controlling the level (under 1%) of 1-alkyl-2-acyl-sn-glycero-3-phosphocholine in rat liver.

Animals↗
PubMed1982

Cardiovascular and sympathetic effects of l-O-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine in conscious SHR and WKY rats.

Injections of 1-)-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine (alkylacetyl-GPC, 0.2-5.0 nmol/300 g body weight) induced dose-related hypotension and tachycardia in spontaneous hypertensive (SHR) and normotensive control (WKY) rats. The hypotension that developed was more pronounced in SHR than in WKY rats and was unchanged by indomethacin pretreatment. Plasma norepinephrine (NE) and epinephrine (EPI) levels were markedly increased at the time of maximal hypotension (2 min after injection of alkylacetyl-GPC); plasma EPI (but not NE) was higher in the SHR than in WKY animals. Plasma levels of TXB2, but not 6-keto-PGF 1 alpha, increased in both groups; the increase was more pronounced in SHR than in WKY rats. In pithed SHR rats, alkylacetyl-GPC caused only short lasting hypotension without any effect on heart rate or circulating levels of NE or EPI. These data suggest that there is an increased vascular sensitivity to alkylacetyl-GPC in SHR rats and activation of thromboxane-generating elements in both SHR and WKY rats.

Animals↗
PubMed1982

[Role of the serial determination of myoglobin, enzymes and isoenzymes in the early diagnosis of myocardial infarction].

Seventy-eight patients with myocardial infarction had been admitted to the intensive care unit not later than 5 h after the beginning of illness. The levels of myoglobin, CPK, LDH, AST, ALT, MB CPK and LDH1 were determined in the blood serum of the patients in the time course during the first 24 hours of hospitalization. All patients showed considerable increase of myoglobin level in the blood serum. In myocardial infarction the level of myoglobin is enhanced significantly earlier than all the other indices, and reached its maximum figure also earlier. In the majority of cases its content reverts to normal at the beginning or in the middle of the second day. In 10 patients with the spread of the primary focus of lesion a repeated peak of myoglobin rise was recorded a few hours after the painful attack. In cases complicated during the course of illness by circulatory insufficiency hypermyoglobinemia was observed during a much greater period of time. Hypermyoglobinemia is the most sensitive and the earliest test of myocardial infarction compared to other biochemical tests.

Adult↗