Search PubMed⌕ Search

Biomedical subjects

B Chernow

Publications and source records attributed to B Chernow.

At least 127 records · Page 7Linked to original sources
PubMed1984

Increased circulating plasma norepinephrine concentrations in noncardiac causes of pulmonary hypertension.

Sympathetic nervous system (SNS) activity and circulating norepinephrine (NE) levels may play roles in the elevated pulmonary vascular resistance (PVR) found in patients with pulmonary hypertension. To study the relationship between plasma NE levels, pulmonary NE metabolism, and pulmonary hypertension, we studied 9 patients, suspected of having noncardiac causes of pulmonary hypertension, before and after vasodilator therapy with phentolamine, nitroglycerin, isoproterenol, or hydralazine. Patients were admitted to the ICU and studied using pulmonary artery thermodilution catheters. Seven of 9 patients had noncardiogenic pulmonary hypertension whereas 2 patients did not have hemodynamic evidence of pulmonary hypertension. Simultaneous pulmonary and radial artery samples were analyzed for plasma NE and epinephrine (EPI) content before and after various vasodilator agents. Baseline pulmonary artery (PA) and radial artery NE concentrations correlated (r = .72) with PVR, PA pressures, and PA minus pulmonary capillary wedge (WP) pressures and were increased compared to the 2 patients with normal pulmonary pressures (p less than .01). The normal pulmonary extraction of circulating NE was absent in the 7 patients with pulmonary hypertension. PVR decreased significantly in all 7 patients with each vasodilator (p less than .05); however, the decrease was independent of any change in plasma NE concentration and therapy had no effect on the pulmonary extraction of circulating NE. These data indicate that elevations in plasma NE are coincident with the presence of noncardiogenic pulmonary hypertension and that acute pharmacologic reduction of PVR does not normalize the loss of pulmonary NE metabolism.

Adult↗
PubMed1984

Urine glucose testing in the critically ill: a comparison of two enzymatic test strips.

The urine glucose concentration is commonly used to monitor indirectly the degree of hyperglycemia in critically ill patients and to adjust insulin dosage. Most commercially available urine glucose reagent test strips measure the urine glucose concentration from 0% to 2%. When the urine glucose is at the 2% level, the blood glucose concentration may vary over a wide range. We compared a new urine glucose test strip which measures the urine glucose concentration from 0% to 5% versus a conventional strip (0% to 2%) in the analysis of double-voided urine specimens from 285 patients with diabetes mellitus. Both types of test strips were insensitive in detecting hyperglycemia and showed a wide range of blood glucose values for each estimated urine glucose concentration. However, the new test strips which gave measurements at the 3% and 5% urine glucose concentrations allowed for more specificity (99%) in detecting blood glucose levels above 250 mg/dl. We conclude that: (a) test strips measuring from 0% to 5% are superior to conventional 0% to 2% test strips because the 3% and 5% urine glucose readings allow for a high level of specificity in detecting severe hyperglycemia (greater than 250 mg/dl); (b) urine glucose testing is insensitive and nonspecific in detecting hyperglycemia when urine glucose values are 2% or less.

Blood Glucose↗
PubMed1984

Dexamethasone causes less steroid-induced alkalemia than methylprednisolone or hydrocortisone.

Corticosteroid-induced metabolic alkalemia is an important ICU problem because many of these patients may compensate by alveolar hypoventilation. The effects of 3 commonly used steroids on arterial pH, PaCO2, and serum bicarbonate concentrations were studied in 24 healthy male baboons randomly divided into 3 groups. Each group of 8 animals received 7-day dose-equivalent courses of either hydrocortisone (300 mg daily), methylprednisolone (60 mg daily), or dexamethasone (15 mg daily). Treatment with either hydrocortisone or methylprednisolone increased arterial pH (p less than .05) and serum bicarbonate levels (p less than .01) and the animals receiving hydrocortisone showed significant (p less than .05) compensatory alveolar hypoventilation. Dexamethasone therapy did not cause any of these steroid-induced changes.

Acid-Base Imbalance↗
PubMed1984

Sympathetic nervous system sensitivity to hemorrhagic hypotension in the subhuman primate.

The endogenous catecholamine response to hemorrhagic hypotension is poorly defined since most data have been derived from experiments in lower animal species. To clarify this situation we studied the plasma norepinephrine (NE) and epinephrine (Epi) responses to hemorrhagic hypotension in ten healthy male baboons (Papio anubis). After an overnight fast, animals were tranquilized with 100 mg of ketamine hydrochloride after which femoral artery and vein catheters were inserted. The animals then underwent phlebotomy of 20 ml/kg over 60 minutes with retransfusion of the autologous blood over the next 30 minutes. Plasma specimens for catecholamines were collected at 5, 15, 30, and 60 minutes during phlebotomy and again at 15 and 30 minutes during retransfusion. Plasma NE and Epi concentrations were measured by a radioenzymatic technique. Mean arterial blood pressure (MAP) decreased (p less than 0.01) and heart rate (HR) increased (p less than 0.01) within 15 minutes of phlebotomy, and these variables returned to baseline with retransfusion. Plasma NE and Epi levels increased (p less than 0.025) within 5 minutes of the onset of 'hemorrhage' and within 15 minutes plasma NE concentrations were 56% above baseline, whereas plasma Epi levels were six times greater than baseline. With retransfusion, plasma NE and Epi levels returned to baseline concentrations. We conclude: 1) in a primate species, the sympathetic nervous system responds rapidly to hemorrhage; 2) contrary to prior studies in rats, plasma NE increases as rapidly as Epi but not to the same degree; 3) plasma NE and Epi concentrations rapidly return to baseline levels with fluid resuscitation; and 4) there is little justification for the use of exogenous synthetic catecholamines in hemorrhagic hypotension where fluid resuscitation remains the treatment of choice.

Animals↗
PubMed1984

Psychopharmacology in the intensive care unit.

The task of the psychopharmacologist in the ICU does not stop with a recommendation of the best drug and dosage. The clinical course of patients in ICUs is often stormy. With each change, the appropriateness of the chosen psychopharmacologic treatment may be questioned. Is the patient experiencing a side effect? Should the drug be discontinued or the dosage altered? Nonpsychiatrists are often unfamiliar and uncomfortable with psychotropic medications and are not as likely to accurately assess side effects or therapeutic progress. Try to anticipate the more likely complications in the progress notes without being too lengthy, and attempt to verbally communicate impressions and recommendations. Finally, stay abreast of the patient's progress, and make it clear that you are available for consultation and advice. In this way you may assure that the patient will be best able to tolerate and benefit from ICU treatment.

Antidepressive Agents↗
PubMed1984

Effect of antihypertensive therapy on sympathetic nervous system activity in patients with essential hypertension.

The sympathetic nervous system (SNS) plays a major role in blood pressure regulation. Although the exact relationship of the SNS to the etiology of hypertension remains undetermined, many of the agents used to treat hypertension interfere with this system. Clonidine, methyldopa, guanethidine, and reserpine decrease SNS tone whereas hydralazine, minoxidil, and hydrochlorothiazide increase it. Most evidence suggests that beta-adrenergic blocking agents decrease SNS activity. The effect of prazosin and captopril on the SNS requires further study. The appropriate use of these antihypertensive agents requires a knowledge of their sites of action and the physiological reflexes they induce. Efficacy, toxicity, and effective drug combinations can be predicted based on their mechanism of action and effect on SNS activity.

Antihypertensive Agents↗
PubMed1984

Endogenous opioid peptides: critical care implications.

The recent evolution of our understanding of endogenous OPs has led to important new insights into the pathophysiology of many disease states. Opiate antagonism may provide the critical care physician with yet another lifesaving weapon. Opiate antagonists are not approved for human use in the various conditions discussed in this article; their use is strictly experimental and should be restricted to controlled trials. We look forward to continued research and clinical trials involving these agents.

Animals↗
PubMed1984

Glucagon: hormone or therapeutic agent?

Glucagon is an important therapeutic agent in critical care medicine. Although its endogenous hormonal functions have been well described, its clinical uses are rarely discussed. Glucagon is effective in the treatment of hypoglycemia, cardiogenic shock and heart failure, propranolol overdose, esophageal meat impaction, ureteral colic due to calculi, and acute diverticulitis. It may prove useful in the treatment of endotoxin and hypovolemic shock as well as toxicity due to excesses of procainamide, quinidine, or ouabain.

Cardiotonic Agents↗
PubMed1984

Diagnostic dosages of protirelin (TRH) elevate BP by noncatecholamine mechanisms.

While performing thyroid function tests, we noticed that protirelin (TRH) raised BP, and, therefore, we investigated the effect of diagnostic dosages of protirelin (500 micrograms) on plasma catecholamine levels and cardiovascular function in eight patients one day before, one day after, and four weeks following heart surgery. Mean arterial pressure (MAP), heart rate (HR), plasma norepinephrine (NE), epinephrine (EPI), dopamine (DA), thyroid hormone (triiodothyronine [T3], thyroxine), and thyrotropin (TSH) levels were measured before and after the intravenous injection of protirelin. Protirelin increased MAP transiently from 88 +/- 2 to 103 +/- 3 mm Hg (before surgery), 86 +/- 4 to 102 +/- 4 mm Hg (one day after surgery), and 86 +/- 4 to 104 +/- 5 mm Hg (four weeks after surgery). There were no notable changes in HR or plasma NE, EPI, or DA levels. The T3 and TSH response to protirelin was normal on all three study days. Protirelin raised MAP by an effect on systemic vascular resistance (SVR) rather than an increase in cardiac output. We conclude the following: (1) diagnostic dosages of protirelin transiently elevate MAP and SVR by a noncatecholamine mechanism, (2) clinicians who perform protirelin tests should be aware of protirelin's transient pressor effects.

Adult↗
PubMed1984

Epinephrine absorption after intratracheal administration.

Tracheal intubation during cardiopulmonary resuscitation often precedes establishment of an intravenous route for the administration of drugs. To determine the efficacy of intratracheal administration of drugs during cardiopulmonary resuscitation we measured plasma catecholamine levels and hemodynamic responses to intratracheal epinephrine (EPI) administration using a double-blind, randomized crossover design in 7 male baboons (Papio anubis), each studied twice, who received 5 ml of 1:10000 EPI on one day and 5 ml of 0.9% NaCl on another day. Arterial blood samples for measurement of plasma EPI and norepinephrine (NE) concentrations were collected, and heart rate (HR) and mean arterial blood pressure (MAP) were measured before and 1, 2, 4, 8, 16, and 30 min after intratracheal drug administration. Intratracheal EPI significantly (P less than 0.05) elevated HR to 120 +/- 6 from 105 +/- 6 beats/min, MAP to 120 +/- 4 from 112 +/- 5 mm Hg, and plasma EPI to 8882 +/- 2143 from 928 +/- 209 pg/ml within 1 min of administration, and these effects persisted for 30 min. Plasma NE levels did not change after intratracheal EPI administration. None of the four variables changed after intratracheal saline was given. We conclude that in subhuman primates, intratracheal EPI is rapidly absorbed and is an effective pressor agent when given by this route; and that these data lend support to the clinical practice of intratracheal EPI administration during cardiac arrest or in the treatment of shock.

Absorption↗
PubMed1984

Plasma catecholamine levels in normal subjects and in patients with secondary hypertension.

We compared normal values for human venous norepinephrine (NE) and epinephrine (E) as reported in the literature with values determined in this laboratory and we measured and contrasted NE levels in patients with primary and secondary hypertension. Analysis of published data from many laboratories involving more than 800 supine, resting, healthy subjects indicated an average circulating level of venous NE of 260 pg/ml and of E, about 35 pg/ml. Supine levels of NE normally double when normal subjects stand for 5 min. This simple test provides one assessment of overall sympathetic nervous system integrity. Levels of catecholamines have been extensively studied in essential hypertension but much less so in secondary hypertension. Of the groups we studied with secondary hypertension (diabetes mellitus, primary hyperaldosteronism, polycystic kidney disease, chronic bilateral renal parenchymal disease, and unilateral renal arterial stenosis), only the group with renal parenchymal disease had supine NE levels significantly higher than the control group. Patients with essential hypertension and diabetes had a blunted increase in NE on standing. Plasma levels of NE do not reliably differentiate these groups of secondary hypertension from one another or from patients with primary hypertension.

Adolescent↗
PubMed1984

Hypomagnesemia is a common complication of aminoglycoside therapy.

Normal therapeutic dosages of aminoglycosides can cause hypomagnesemia in more than one-third of patients. Hypomagnesemia occurs early in therapy, results in renal Mg++ wasting and may produce hypocalcemia and hypokalemia. Patients who are NPO, eating poorly or not receiving supplemental Mg++ are at high risk for hypomagnesemia. Hypomagnesemia, hypocalcemia and hypokalemia respond to Mg++ replacement therapy. We recommend serial monitoring of serum Mg++ levels in patients receiving aminoglycoside therapy.

Aminoglycosides↗
PubMed1983

Prevalence of increased intraocular pressure in Graves' disease--evidence of frequent subclinical ophthalmopathy.

Graves' exophthalmos is frequently associated with elevated intraocular pressure on upgaze. Eighty patients with Graves' disease were evaluated prospectively by applanation tonometry to assess the prevalence of ophthalmopathy in this disorder. Whereas 21 (26 per cent) of the 80 patients had exophthalmos, 61 (76 per cent) had abnormal intraocular pressure (delta greater than or equal to 3 mm Hg). All patients with exophthalmos had elevated intraocular pressure on upgaze; 40 (68 per cent) of 59 patients without proptosis had abnormal pressure readings. The mean interval between the onset of Graves' disease and this study was 6.3 +/- 1.0 years (S.E.M.) for those patients who had exaggerated positional changes in intraocular pressure, as compared with 3.0 +/- 1.0 years for those with normal intraocular pressure (P less than 0.005). All but 1 of 15 patients in whom the diagnosis of Graves' disease had been documented 10 or more years earlier had increased intraocular pressure on upgaze. We conclude that Graves' ophthalmopathy is more common than is recognized clinically and that eye involvement is an inevitable complication of the disease.

Adult↗
PubMed1983

Local dental anesthesia with epinephrine. Minimal effects on the sympathetic nervous system or on hemodynamic variables.

To define the hemodynamic effects of local dental anesthesia, we measured the mean arterial pressure (MAP), heart rate, and plasma catecholamine responses for 60 minutes following an inferior alveolar nerve block with epinephrine-and nonepinephrine-containing lidocaine hydrochloride anesthesia in 14 men using a randomized double-blind crossover trial. Lidocaine alone caused no significant change in MAP or heart rate and only slight, transient changes in plasma catecholamine concentrations when compared with baseline values. Lidocaine with epinephrine caused significant, sustained (60 minutes) increases in plasma epinephrine concentrations (mean +/- SEM, 27 +/- 4 to 94 +/- 13 pg/mL) and a slight, but transient (two-minute) increase in heart rate from 68 +/- 3 to 70 +/- 3 beats per minute. Lidocaine with epinephrine caused no significant change in MAP. There is no significant hemodynamic response to lidocaine dental anesthesia (with or without epinephrine) in healthy young men.

Anesthesia, Dental↗
PubMed1983

Sympathetic nervous system function in XYY subjects.

Initial reports of males with the XYY sex chromosome anomaly indicated that these individuals excessively exhibit impulsive, aggressive, and criminal behavior. Central nervous system (CNS) defects, including low intelligence, in certain XYY subjects may be associated with these antisocial behaviors. The sympathetic nervous system (SNS) is activated in stressful conditions of "fight or flight" upon standing up from a supine posture, with physical exercise, and with aggressive behavior. Norepinephrine (NE) is the principal neurotransmitter of the SNS, and plasma levels of NE and dopamine-beta-hydroxylase are indices of SNS function. We questioned the integrity of SNS function in XYY subjects for two reasons: (1) their inferred propensity for aggressive behavior and the association of this behavior with increased NE levels; and (2) their potential for CNS dysfunction, which could be reflected in abnormal SNS regulation by the CNS. In the current study plasma levels of NE in XYY subjects are nonsignificantly higher than in normal volunteers. Additionally, XYY patients have a normal NE half-life indicating normal SNS activity and metabolism. Thus, we are unable to document with confidence any abnormality in SNS function in these XYY subjects.

Adolescent↗
PubMed1983

T3 may be a better agent than T4 in the critically ill hypothyroid patient: evaluation of transport across the blood-brain barrier in a primate model.

Thyroid hormone transport across the blood brain barrier in hypothyroid patients is clinically important yet poorly understood. To study this question, 200 micrograms of thyroxine (T4), 100 micrograms of 3,5,3'-triiodothyronine (T3) and 100 micrograms of 3,3',5'-triiodothyronine (reverse T3) were administered separately to 3 baboons, first iv and at a later date intrathecally (IT). Six animals were used. Three received the iv injections and three received the IT injections. In each of the 18 experiments, cerebrospinal fluid (CSF) and serum specimens were collected serially for 6 h after injection. Mean maximal elevations from baseline in CSF iodothyronine levels were 100 +/- 10 ng/dl after iv T4, 3921 +/- 293 ng/dl after iv T3 and 31 +/- 17 ng/dl after iv reverse T3. When given IT in the same dosages, the mean maximal increases in serum iodothyronine concentrations were: 1670 +/- 600 ng/dl for T4, 806 +/- 405 ng/dl for T3, and 210 +/- 43 ng/dl for reverse T3. In every animal studied, rapid bidirectional transfer of T3 from serum to CSF and CSF to serum occurred, whereas iv T4 resulted in delayed minimal increments in CSF T4 concentration. Isotopic experiments were also performed and the results analyzed using a kinetic model. When 125I-T3 was given iv, the equilibrium point in CSF was observed within 90 min with 1.7% of the administered dose/L able to be counted in CSF at any moment in time. When labeled T4 was given iv, only 0.6% of the administered dose/L was counted in CSF and the equilibrium point was not reached until 360 min. These data suggest: (a) T4, T3, and reverse T3 are all capable of bidirectional transfer across the blood brain barrier, (b) T3 may be a better agent than T4 in treating patients with myxedema coma because T3 crosses more rapidly and more completely from serum to CSF.

Animals↗
PubMed1983

Sympathetic nervous system "switch off" with severe hypothermia.

Hypothermia occurs frequently in the critically ill patient, yet little is known about the endogenous catecholamine response to this stress. To study this problem, we measured heart rate (HR), mean arterial blood pressure (MAP), and plasma levels of norepinephrine (NE) and epinephrine (Epi) in subhuman primates (baboons) during progressive hypothermia from 37 degrees to 29 degrees C and then during rewarming to 37 degrees C. As the core temperature decreased from 37 degrees to 33 degrees C, HR and MAP increased significantly (p less than 0.05), but as core temperature further decreased from 33 degrees to 29 degrees C, the HR and MAP fell to prehypothermic levels. Plasma concentrations of NE and Epi increased significantly (p less than 0.01) as core temperature fell from 37 degrees to 31 degrees C, but as core temperature dropped from 31 degrees to 29 degrees C, plasma NE and Epi levels decreased towards prehypothermic concentrations. These findings indicate that the sympathetic nervous system (SNS) responds quickly to hypothermia but may be "switched off" at a threshold temperature of about 29 degrees C. We speculate that hypotensive patients with temperatures less than or equal to 29 degrees C may benefit from infusions of exogenous catecholamines, especially if there have been only minimal benefits achieved with conventional therapy such as fluids, and an increase in ambient temperature.

Animals↗