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Biomedical subjects

K Ravi

Publications and source records attributed to K Ravi.

At least 37 records · Page 2Linked to original sources

Outpatient coronary stenting: femoral approach with vascular sealing.

Miniaturized devices and pressures for increased patient convenience and lowered cost have shortened length of stay for coronary interventions. A cohort of 60 patients was recruited to assess the feasibility of outpatient stenting with vascular sealing. Patients with stable and unstable angina or myocardial infarction > 24 hours were considered for this strategy. Mean time to hemostasis, ambulation and discharge were 6.1, 256 and 296 minutes, respectively, for the 6F group, and 11.0, 351 and 489 minutes for the 7 to 8F group. No acute procedural complications occurred, and there were no ischemic complications at 24 hours or 1 month. There was 1 pseudoaneurysm requiring surgical correction, but no other access site requiring treatment. The cost saved using the 6F approach is estimated at $478 and using the 8F approach, $437. Outpatient stenting using vascular sealing is feasible and safe, and may lead to significant nationwide cost reductions in the range of $40,000,000 yearly.

Ambulatory Care↗

Reflex changes in heart rate during chemoreceptor stimulation in monkeys.

The changes in heart rate induced by the stimulation of arterial chemoreceptors by apneic asphyxia and left atrial - intracarotid injections of sodium cyanide were investigated in anesthetized artificially ventilated and paralysed monkeys. Apneic asphyxia and sodium cyanide injection caused tachycardia, bradycardia, or both in monkeys paralysed with decamethonium bromide and tachycardia only, in monkeys paralysed with gallamine. In both groups, the tachycardia was abolished by prior administration of propranolol and the bradycardia, by atropine. Prior ventilation with 100% O2 abolished the heart rate responses produced by apnea. Recording of phrenic efferent activity showed that the neural discharge increased in response to apneic asphyxia and sodium cyanide injections. It remained so during the manifestation of tachycardia, bradycardia, or no change in heart rate, suggesting that even though "higher centres" may have an important influence in the heart rate responses elicited, central respiratory drive may not be the only mechanism. The present results show that in the nonhuman primate, arterial chemoreceptor stimulation elicits both cardioacceleratory and cardioinhibitory reflexes, and the net effect of their stimulation on heart rate depends upon the balance between these opposing mechanisms.

Adrenergic beta-Antagonists↗

Outpatient coronary stenting using the femoral approach with vascular sealing.

PURPOSE: We report here the use of vascular sealing devices in conjunction with the use of small transfemoral guiding catheters to decrease time to ambulation, decrease cost associated with hospitalization and achieve early discharge. METHODS: Fifty patients were enrolled in this pilot project from two busy interventional practices between May 1997 and February 1999. Patients with stable or unstable angina or positive ETT and with recent myocardial infarction greater than 24 hours from the time of the procedure were included. Excluded patients included those who had received glycoprotein IIb/IIIa platelet inhibitors and those with intra-procedure access site complications. RESULTS: Of the 50 patients originally recruited, 49 underwent vascular sealing for hemostasis and 45 were discharged on the same day, as planned. Early home telephone follow-up was available on 41 of the 45 same-day discharge patients, of whom 30 noted no complaints. One patient, who had been re-accessed in the right femoral artery after a previous intervention, developed a pseudoaneurysm requiring surgical repair. One-month follow-up was available on all patients. No patient suffered a late ischemic event or access site complication requiring treatment. There were no instances of stent loss, acute closure or subacute thrombosis. CONCLUSION: Though limited by small numbers, this pilot study shows that selected patients undergoing coronary stenting via the femoral approach can be safely treated on an outpatient basis using vascular sealing devices. Cost savings may be significant using this strategy.

Ambulatory Surgical Procedures↗

Effect of pulmonary lymphatic obstruction on rabbit urine flow.

1. The effects of pulmonary lymphatic obstruction on urine flow, sodium and potassium excretion were examined on anaesthetized, artificially ventilated New Zealand White rabbits. Pulmonary lymphatic obstruction was produced by raising the pressure in a pouch created from the right external jugular vein. The experiments were performed on two groups of rabbits (non-hydrated and hydrated). 2. Pulmonary lymphatic obstruction caused a significant increase in urine flow in both groups of rabbits. After release of the obstruction, the urine flow returned to basal values. Urine flow (ml (10 min)-1) for both groups was initial control, 5.3 +/- 0.9; lymphatic obstruction, 8.9 +/- 1.0; final control, 6.2 +/- 0.7 (means +/- S.E.M.; n = 21, P < 0.025). 3. The increase in urine flow was not accompanied by significant changes in concentration of sodium and potassium in urine. Sodium excretion increased significantly only in the hydrated rabbits. 4. The increase in urine flow was abolished by bilateral cervical vagotomy and by renal nerve sectioning. Cooling the cervical vagi to 8 degrees C also abolished the response. 5. Pulmonary lymphatic obstruction did not produce any significant change in heart rate, mean arterial blood pressure, mean right atrial pressure and peak airway pressure. 6. These findings suggest that obstructing the lymph drainage from the lung results in a reflex increase in urine flow. The afferent pathway for this reflex resides in the myelinated fibres of the vagi and the efferent pathway in the renal nerves. The rapidly adapting receptors of the airways are likely to be the receptors involved.

Animals↗

Substance P contributes to rapidly adapting receptor responses to pulmonary venous congestion in rabbits.

1. This study tested the hypothesis that substance P stimulates rapidly adapting receptors (RARs), contributes to the increase in RAR activity produced by mild pulmonary congestion, and evokes an augmented response from RARs when combined with near-threshold levels of pulmonary congestion. 2. RAR activity, peak tracheal pressure, arterial blood pressure and left atrial pressure were measured in paralysed, anaesthetized and ventilated rabbits. Substance P was given i.v. in one-half log incremental doses to a maximum of 3 micrograms kg-1. Mild pulmonary congestion was produced by inflating a balloon in the left atrium to increase left atrial pressure by 5 mmHg. Near-threshold levels of pulmonary congestion were produced by increasing left atrial pressure by 2 mmHg. 3. Substance P produced dose-dependent increases in RAR activity. The highest dose given increased the activity from 1.3 +/- 0.5 to 11.0 +/- 3.1 impulses bin-1. Increases in left atrial pressure of 5 mmHg increased RAR activity from 3.8 +/- 1.4 to 14.7 +/- 3.9 impulses bin-1. Blockade of NK1 receptors with CP 96345 significantly attenuated RAR responses to substance P and to mild pulmonary congestion. 4. Doses of substance P, which alone had no effect, stimulated the RARs when delivered during near-threshold levels of pulmonary congestion. 5. The findings suggest that substance P augments the stimulatory effect of mild pulmonary congestion on RAR activity, most probably by enhancing hydraulically induced microvascular leak.

Animals↗

Role of vagal lung C-fibres in the cardiorespiratory effects of capsaicin in monkeys.

Apnoea, bradycardia and hypotension were elicited by right atrial injections of capsaicin in anaesthetized monkeys. At the threshold dose (2.5 +/- 0.3 microgram/kg), tachypnoea was elicited (latency 1.6 +/- 0.2 s) which got replaced by apnoea with higher doses of capsaicin. These responses persisted (1) after cooling the cervical vagi to 6-8 degrees C, and (2) after instilling xylocaine into the pericardial sac. Tachypnoea and apnoea were elicited after bilateral cervical vagotomy also, but only with higher doses and after a longer latency (5.0 +/- 0.3 s). Right atrial injection of capsaicin and insufflation of halothane stimulated vagal pulmonary C-fibre receptors with a latency of 1.7 +/- 0.7 s and 0.2 +/- 0.1 s, respectively. Tachypnoea/apnoea, bradycardia and hypotension were elicited by left atrial injection of capsaicin also (threshold dose: 5.0 +/- 1.2 micrograms/kg). The respiratory responses persisted (1) after instilling xylocaine into the pericardial sac, and (2) after bilateral cervical vagotomy suggesting that they were due to stimulation of non-cardiac receptors with sympathetic afferents. It is concluded that the initial respiratory responses elicited by right atrial injection of capsaicin were due to stimulation of pulmonary C-fibre receptors with vagal afferents.

Administration, Inhalation↗

Effect of Diazinon PLUS on rapidly adapting receptors in the rabbit.

The effects of Diazinon PLUS aerosol on the activities of rapidly adapting receptors (RARs) and slowly adapting receptors (SAR) of the airways were investigated in anesthetized rabbits. The effects on both the baseline activity and the responses to stimulation by increasing mean left atrial pressure were examined. Action potentials were recorded from the left cervical vagus nerve. Aerosols (particle size 3 microns) were generated by a Mini-HEART nebulizer. We observed that an aerosol of Diazinon PLUS (1:10 vol/vol dilution in normal saline) decreased the baseline RAR activity (n = 10) significantly (P < 0.05) from 209 +/- 77 to 120 +/- 40 impulses/min. In the post-Diazinon PLUS control period, the RAR activity recovered partially to 185 +/- 75 impulses/min and decreased significantly to 131 +/- 52 impulses/min (P < 0.05) after a second exposure of Diazinon PLUS (undiluted) aerosol. Aerosols of normal saline in the control state did not produce a significant change in the RAR activity. A group of SAR (n = 8) were examined under similar conditions, and it was found that only the exposure to Diazinon PLUS (undiluted) aerosol decreased the activity significantly (P < 0.05) from 1,536 +/- 206 to 1,367 +/- 182 impulses/min. The effect of Diazinon PLUS on the response to increasing mean left atrial pressure was examined in seven RARs. In the control state, RAR activity increased significantly (P < 0.05) during elevation of mean left atrial pressure. This response was abolished after exposure to Diazinon PLUS. These findings suggest that diazinon may interfere with airway defense mechanisms by reducing the activity of RARs.

Action Potentials↗

Properties of rapidly adapting receptors of the airways in monkeys (Macaca mulatta).

The properties of rapidly adapting receptors (RARs) of the airways were examined in anaesthetised, artificially ventilated, paralysed and thoracotomised monkeys. The RARs were identified (i) by their rapid adaptation to a maintained inflation and forced deflation of the lungs and (ii) by their conduction velocity measurements. Right atrial (n = 17) and left atrial (n = 13) injections of histamine (10 micrograms/kg) stimulated the RARs. The stimulation was associated with an increase in peak intratracheal pressure. Right atrial injections of phenyl diguanide (n = 6, 10 micrograms/kg) and 5-hydroxytryptamine (n = 6, 10 micrograms/kg) did not produce a significant stimulation of the RARs. Administration of irritant vapours such as ammonia, (n = 12), cigarette smoke (n = 8), alcohol (n = 10), acetone (n = 10) and ether (n = 7), caused a significant stimulation of the RARs. This stimulation occurred in spite of a significant decrease or no change in peak intratracheal pressure. During mild degrees of pulmonary venous congestion produced by graded increments in mean left atrial pressure (+5 and +10 mmHg), there was a graded increase in RAR (n = 6) activity. The present study shows the existence of the RARs in the airways of the rhesus monkey. These receptors are stimulated (i) by administration of agents which cause bronchoconstriction (ii) by vapours which cause airway irritation and (iii) in conditions which cause an expansion of the extravascular space in airways.

Animals↗

Pulmonary venous congestion augments respiratory motoneuronal responses to cigarette smoke in rabbit.

We examined the effects of cigarette smoke inhaled during subthreshold pulmonary venous congestion (sPVC) on phrenic nerve (PN) and unit activity in the ventral respiratory group in rabbits. sPVC was achieved by inflating a balloon in the left atrium. Inhalation of low-nicotine cigarette smoke produced initial prolonged bursts in 34 (19 bulbospinal) out of 43 inspiratory (I) cells and in PN. Smoke decreased the activity of 29 out of 36 expiratory (E) cells (27 of 32 early E and 2 of 4 late E). The prolonged PN bursts occasionally progressed to doublets superimposed over regularly occurring PN bursts. sPVC augmented the smoke effects: I cells displayed greater increases in spikes/burst (27 vs. 12%; P = 0.02) and burst duration (42 vs. 20%; P = 0.02) and greater decreases in interburst interval (34 vs. 10%; P < 0.02); PN displayed greater increases in I time (40 vs. 27%; P < 0.05), greater decreases in E time (18 vs. 26%; P < 0.05), and a greater incidence and duration of time of PN doublets (29 +/- 9 vs. 9 +/- 4 s; P < 0.03); E cells displayed greater decreases in spikes/burst (43 vs. 29%; P = 0.01) and burst durations (35 vs. 18%; P < 0.01). Smoke-induced respiratory changes may be exaggerated during sPVC.

Animals↗

Effect of pulmonary lymphatic obstruction on respiratory rate and airway rapidly adapting receptor activity in rabbits.

1. The effects on respiratory rate of obstruction of pulmonary lymph flow, reduction of plasma protein concentration and a combination of the two procedures were examined in anaesthetized rabbits. The former was achieved by raising the pressure in a pouch created from the right external jugular vein and the latter by batch plasmapheresis. 2. In spontaneously breathing rabbits, neither pulmonary lymphatic obstruction (n = 6) nor plasmapheresis (n = 5) produced a significant change in respiratory rate. However, their combination (n = 8) produced a significant increase in respiratory rate (P < 0.05). 3. Cooling of the cervical vagi to 8-9 degrees C (n = 4) and vagotomy (n = 7) abolished this response. 4. There was a significant increase in the activity of the airway rapidly adapting receptors (RARs; n = 9) during pulmonary lymphatic obstruction, plasmapheresis and their combination (P < 0.05). 5. It is concluded that in the rabbit, obstruction of lymphatic drainage from the lung after plasmapheresis causes a reflex increase in respiratory rate. The afferent pathway for this reflex response lies in the vagus nerve and the RARs are likely to be the receptors involved in this response.

Action Potentials↗

Pulmonary congestion enhances responses of lung rapidly adapting receptors to cigarette smoke in rabbit.

We examined the effects of low-nicotine cigarette smoke, pulmonary venous congestion, and their combination on the activity of rapidly (RAR) and slowly adapting receptors (SAR) in anesthetized rabbits. Pulmonary venous congestion was achieved by inflating a balloon in the left atrium to increase left atrial pressure. We examined smoke effects on RARs (averaged over 15 breaths) at baseline left atrial pressure and at subthreshold and suprathreshold increases in left atrial pressure. At baseline, smoke significantly increased RAR activity from 12.1 +/- 4.2 to 16.2 +/- 4.2 impulses/breath (P < 0.05). At subthreshold increases in left atrial pressure (2.9 +/- 0.6 mmHg), smoke produced larger increases in RAR activity (12.3 +/- 3.3 to 22.5 +/- 4.1 impulses/breath; P < 0.05). Suprathreshold increases in left atrial pressure (9.2 +/- 1.1 mmHg) alone increased RAR activity from 10.9 +/- 3.2 to 19.8 +/- 5.9 impulses/breath (P < 0.05). Smoke had no additional effect (22.3 +/- 4.8 impulses/breath; P > 0.05). There was, however, a transient increase in RAR activity (1st 3 breaths of smoke) under all three conditions. Of nine SARs examined, only two were stimulated by smoke. We conclude that in the rabbit smoke-induced stimulation of RARs is augmented by mild pulmonary venous congestion. of RARs is augmented by mild pulmonary venous congestion.

Adaptation, Physiological↗

Chest radiographs fail to detect right ventricular enlargement and right atrial enlargement in patients with a pure restrictive ventilatory impairment.

The validity of measurements of the cardiac silhouette on chest radiographs for the evaluation of right ventricular enlargement and right atrial enlargement in patients with a pure restrictive ventilatory impairment was investigated in 19 patients. The forced vital capacity (FVC) percent predicted in these patients was 59 +/- 12 percent (mean +/- SD) (range, 29 to 79 percent). Right ventricular enlargement, by two-dimensional echocardiography, was defined as a right ventricular area > 20.4 cm2 and right atrial enlargement was defined as a right atrial area > 15.3 cm2. Chest radiographic measurements in the posteroanterior (PA) projection included distance from the midline to the farthest point of the right border of the cardiac silhouette, transverse cardiac diameter, and cardiothoracic ratio. Measurements in the lateral projection included the lateral horizontal transverse diameter, ventral portion of the lateral broad diameter, and obliteration of the retrosternal space. Neither the right ventricular area nor the right atrial area correlated with any of these radiographic measurements. There were no differences in these chest radiographic measurements among patients with normal right ventricular and right atrial dimensions, patients with right ventricular enlargement, and patients with right atrial enlargement. We conclude, therefore, that PA and lateral chest radiographs do not reliably detect right ventricular enlargement or right atrial enlargement in patients with a pure restrictive ventilatory impairment.

Cardiomegaly↗

Right ventricular dilatation, right ventricular wall thickening, and Doppler evidence of pulmonary hypertension in patients with a pure restrictive ventilatory impairment.

The purpose of this investigation was to determine the severity of pure restrictive ventilatory impairment that results in right ventricular (RV) dilatation, increased RV wall thickness, and pulmonary hypertension. Two dimensional (2-D) echocardiography, Doppler measurements of pulmonary flow, and spirometry were performed on 26 unselected patients (17 female, 9 male) with a pure restrictive ventilatory impairment. A restrictive ventilatory impairment was defined as a forced vital capacity (FVC) < or = 80 percent predicted with a normal FEV1/FVC ratio (FEV1 = 1 s forced expiratory volume). The patients were grouped according to the severity of the restrictive ventilatory defect: mild (FVC, 65 to 80 percent predicted), moderate (FVC, 51 to 64 percent predicted), and severe (FVC < or = 50 percent predicted). An increased RV area (> 20.4 cm2) was shown in 0 of 10 (0 percent) patients with a mild impairment, 6 of 12 (50 percent) patients with moderate restriction, and 2 of 4 (50 percent) patients with severe restriction. Increased RV wall thickness (> 0.5 cm) was observed in 0 of 10 (0 percent) patients with mild restrictive impairment, 3 of 12 (25 percent) with moderate impairment, and 1 of 4 (25 percent) with severe restrictive impairment. Doppler evidence of pulmonary hypertension (ACT/ET ratio < 0.32) (ACT = acceleration time, ET = ejection time) was shown in 0 of 10 (0 percent) patients with a mild restrictive impairment, 8 of 12 (66 percent) patients with moderate restriction, and 4 of 4 (100 percent) patients with severe restriction (p < 0.01 mild vs moderate and mild vs severe). The RV area by 2-D echocardiography correlated well with the FVC percent predicted (r = 0.90, p < 0.001). The ACT/ET ratio also correlated well with the FVC percent predicted (r = 0.73, p < 0.001). In conclusion, RV enlargement and pulmonary hypertension were seen only in patients with a moderate or severe restrictive ventilatory impairment. These data may be useful in the assessment of the likelihood of subtle RV enlargement in patients with occupational pleuropulmonary disease.

Adult↗

Amino acid functional groups involved in the binding of Escherichia coli ribosomal protein S1 to ribosomes and nucleic acids.

Histidine, arginine, tyrosine, lysine and cysteine residues of protein S1 were modified with diethyl pyrocarbonate & rose bengal, 2,3-butanedione (diacetyl), tetranitromethane, pyridoxal 5-phosphate, and N-ethyl-maleimide, respectively. Modification of the residues and the number of modified residues were determined by either fluorescence or UV spectroscopy. The effect of chemical modification on the function of protein S1 was studied with respect to nucleic acid (poly U and M13 ssDNA) binding and ribosome binding properties of the protein. We tested S1 binding to these two types of polynucleotides because of their reported (Draper et al. (1977) PNAS 74, 4786-4790) binding to two different sites on S1. The results indicate that histidine and lysine residues of S1 play an important role in the binding of S1 to both types of nucleic acids and that histidine and to some extent tyrosine residues are involved in the binding of S1 to ribosomes. The Data indicate the need for a re-evaluation of the two nucleic acid binding-site model.

Amino Acids↗

Ribosomal protein S1 in archaea.

Cell extracts and ribosomes of thermoacidophilic and halophilic archaebacteria were analysed by immunoblotting to detect ribosomal protein S1 homologues. Antisera to E. coli S1, the N-terminal ribosome binding domain (F2a) and the central and COOH-terminal nucleic acid binding domain (S1F1) of the protein were used. The results show that the thermoacidophilic archaebacterium sulfolobus acidocaldarius contains a protein with molecular weight of 66,000 that cross-reacts with anti-S1F1. However, the halophilic archaebacteria Halobacterium halobium, H. cutirubrum and H. salinarum contain a protein of molecular weight of about 100,000 that cross-reacts only with anti-F2a. The results indicate a differential conservation of the structural and functional domains of protein S1 in archaebacteria.

Archaea↗

Effect of bradykinin on respiratory rate in anaesthetized rabbits; role of rapidly adapting receptors.

1. This study was performed in anaesthetized, spontaneously breathing rabbits: (a) to determine the effect of bradykinin administered into the right atrium on the respiratory rate, and (b) to elucidate the potential role of rapidly adapting receptors (RARs) in mediating this effect. The role of RARs was established by graded cooling of the cervical vagi. The respiratory rate was measured from an intrapleural pressure tracing. 2. Dose-response curves relating right atrial injections of bradykinin (0.25, 0.5, 1.0 and 1.5 micrograms/kg) to the respiratory rate were established in the control state (i.e. vagi at 37 degrees C). The respiratory rate increased significantly (P < 0.01, ANOVA) from a control value of 51.3 +/- 6.8 breaths/min by 12 +/- 3, 25 +/- 5, 43 +/- 7 and 58 +/- 11% respectively. At doses of 1.0 and 1.5 micrograms/kg I.V., the increase in rate was preceded by apnoea. 3. The dose-response curves were repeated with bolus injections of bradykinin (0.25, 0.5, 1.0 and 1.5 micrograms/kg) after cooling the cervical vagi to 8-9 degrees C. The increase in respiratory rate was attenuated significantly (P < 0.01 ANOVA). The rate increased from a control value of 27.2 +/- 2.1 breaths/min by 5 +/- 2, 6 +/- 2, 16 +/- 5 and 21 +/- 8% respectively. With vagi cooled, apnoea was increased in duration and occurred at lower doses. On rewarming vagi, the original responses were reestablished. 4. When the study was repeated after bilateral vagotomy, apnoea was abolished but there was a small residual increase in rate. This increase was similar to that seen after cooling the vagi (P > 0.05). 5. RAR (n = 5) activity was recorded from the cervical vagus. Right atrial injections of bradykinin (0.25-1.0 micrograms/kg) stimulated RARs. On cooling the vagi to 8-9 degrees C caudal to the recording site, the increase in activity was blocked. 6. These data support the proposition that bradykinin increases the respiratory rate in rabbits and that this response is, in part, a reflex mediated by RARs. In addition, bradykinin has other secondary effects on respiration: an aponea which is mediated by non-myelinated vagal afferents and a small stimulatory effect on respiration which persists after bilateral vagotomy.

Adaptation, Physiological↗

Responses of airway rapidly adapting receptors to bradykinin before and after administration of enalapril in rabbits.

1. The present study was performed in anaesthetized, artificially ventilated, open-chested rabbits to examine whether (a) the rapidly adapting receptors of the airways were stimulated by exogenously administered bradykinin, and (b) if this sensitivity could be enhanced by the angiotensin-converting-enzyme inhibitor, enalapril. 2. Rapidly adapting receptor activity (n = 8) was recorded from the cervical vagus. Bradykinin was injected intravenously (0.25-1.0 microgram/kg) and a dose-response curve relating receptor activity to bradykinin was elicited. In the control state, the threshold dose of bradykinin required for stimulation of rapidly adapting receptors was 0.53 +/- 0.11 microgram/kg. Five minutes after the administration of enalapril maleate (2 mg intravenously), the dose-response curve was shifted to the left significantly (P < 0.01). 3. In seven other rapidly adapting receptors, enalapril (2 mg) increased the resting activity significantly (P < 0.05) over a period of 60 min. This increase was significantly different from the spontaneous variation in neural activity of rapidly adapting receptors (n = 7) recorded over a period of 60 min. 4. Bradykinin either alone (0.25-1.0 microgram/kg) or in the presence of enalapril did not stimulate the slowly adapting receptors (n = 5) of the airways. 5. These results show that (a) exogenous bradykinin stimulates the rapidly adapting receptors, (b) the sensitivity of rapidly adapting receptors to bradykinin is enhanced by enalapril and (c) enalapril increases the resting activity of rapidly adapting receptors. It is suggested that the cough reported after the administration of enalapril may be due to stimulation of rapidly adapting receptors of the airways.

Action Potentials↗

Dolichol: function, metabolism, and accumulation in human tissues.

Dolichol, a homologous series of alpha-saturated polyisoprenoid alcohols containing 14-24 isoprene units, was first isolated and characterized about 30 years ago. The phosphorylated form, dolichyl phosphate, is required for the biosynthesis of biologically important N-linked glycoproteins. Dolichol itself is synthesized by a common isoprenoid pathway from acetate and synthesis can be inhibited by some of the factors that inhibit cholesterol biosynthesis. It is metabolized very slowly and accumulates in tissues during aging and in certain lipid storage diseases. Dolichyl phosphate and cholesterol also accumulate in tissues during aging, but to a lesser extent than dolichol. Although dolichol and cholesterol have important metabolic functions, their accumulation in tissues can have deleterious effects.

Adult↗