Carotid artery injuries and their management.

BACKGROUND: Major vascular injuries in the region of the neck are most frequently the result of penetrating trauma. Evaluation and management of patients with injury to Zone II of the neck remains highly controversial. Most studies involve small number of patients with a lack of standardization of the nature of the injury in reporting outcome. It is the purpose of this study to propose a grading scale for vascular injuries in the neck that would allow for more uniform reporting of such injuries. EXPERIMENTAL DESIGN: A retrospective review of all patients treated for penetrating trauma to the neck was performed and the subset of patients with major vascular injuries identified. Data from this group of patients are presented. SETTING: Level II urban trauma center. PATIENTS AND INTERVENTIONS: During the period July 1984 to June 1994, 107 patients were treated for penetrating neck trauma. Injuries to the major arteries of the neck were present in 18 of the 107 patients (16.8%). All injuries were graded on the developed scale. Management protocol was based on the grade of the injury. Grade 1 injuries were managed non-operatively with systemic anticoagulation and low molecular weight dextran. Grade 2 injuries were treated with primary repair. Injuries of Grades 3 and 4 were treated by primary repair or interposition graft. Exceptions were isolated injuries of the external carotid artery, which were treated by ligation alone. RESULTS: Of the 18 patients with carotid artery injuries, 2 had injuries of the external carotid artery, treated with ligation alone. The internal carotid artery was injured in 7 cases. An interposition saphenous vein/PTFE graft was used in all cases. In 9 cases the common carotid artery was injured. Repair was accomplished by a combination of either a primary repair or interposition graft. Overall mortality was 3/16 (16.6%). No new or worsening of neurologic deficit occurred in any patient. CONCLUSIONS: Carotid artery injuries occur in about 17% of patients with penetrating neck trauma. Data regarding management and prognosis in these patients are at best concflicting, in part, due to lack of a standardized classification system. The proposed grading scale is designed to overcome this problem.

Gallbladder hypokinesia: an unusual cause of duodenal obstruction.

Gallbladder hypokinesis is an uncommon condition and a potential etiologic factor in the formation of gallstones and the development of cholecystitis. It is associated with a number of different conditions, but gallbladder hypokinesia as a cause of small bowel obstruction is unreported. In the case presented below, we saw a postoperative partial upper small bowel obstruction due to hypokinesia of the gallbladder. The investigations, management, and subsequent recovery are described. A review of the literature failed to reveal any similar occurrence.

Advantage of surgery and adjuvant chemotherapy in the treatment of primary gastrointestinal lymphoma.

BACKGROUND: Surgery has been the mainstay of treatment for gastrointestinal (GI) lymphoma. The role of adjuvant chemotherapy to surgery has not been clearly elucidated. METHODS: The review covered 100 patients who were diagnosed with primary GI lymphoma and treated from 1980 to 1993 at Providence Hospital (Southfield, MI), and Hartford and St. Francis Hospitals (Hartford, CT) with a median follow-up of 5 years. Forty-two patients were treated with surgery alone; 31 patients with surgery and adjuvant chemotherapy; 23 patients with primary chemotherapy, and 4 patients received no treatment. RESULTS: The 5-year actuarial survival based on the above treatments calculated by life-table analysis were 57%, 76%, 58%, and 0%, respectively. This series showed that surgery with adjuvant chemotherapy significantly improved the 5-year actuarial survival of patients with primary GI Lymphoma and that primary chemotherapy showed comparable survival to surgery alone. There was no difference in prognosis when comparing patients with different stage, grade, or location of disease in the GI tract. CONCLUSIONS: We recommend surgery when feasible with adjuvant chemotherapy as the mainstay of treatment for primary GI lymphoma. However, if a patient presents with comorbid factors, primary chemotherapy offers an effective alternative.

NMDA receptor-blocker ketamine protects during acute carbon monoxide poisoning, while calcium channel-blocker verapamil does not.

Levine-prepared, female, Sprague-Dawley rats were used to investigate the possible protective effects of the NMDA receptor-blocker anesthetic ketamine and the Ca2+ channel-blocker verapamil (0.4 mg kg-1 'low dose', and 1.0 mg kg-1 'high dose') in rats during acute 2400 ppm carbon monoxide (CO) poisoning. Blood glucose and lactate concentrations, heart rate, mean arterial blood pressure (BP), body temperature (BT), neurological function and cerebral cortical water content were measured. In most cases glucose increased after 45 min and then fell to initial values after 90 min. Lactate concentration increased sharply during CO exposure in the saline and in the low- and high-dose verapamil groups, while the lactate increase in rats given ketamine at 40 mg kg-1 was significantly lower than with saline. Lactate was also significantly lower in these rats after 90 min than in the high-dose verapamil group. Lactate was normal in all four groups after 2 and 4 h of air recovery. Ketamine significantly lowered the heart rate prior to CO exposure, and the heart rate remained significantly below values for the saline and for the low- and high-dose verapamil groups throughout CO exposure. The BP decreased in all groups during CO exposure, and the BP recovery which took place in all four groups was significantly more rapid in the ketamine group. Recovery from CO-induced hypothermia was similar in the ketamine and saline groups, whereas rewarming tended to occur more slowly and less completely in the two verapamil-treated groups. There were no significant differences in neurological function among the four groups, as assessed after 4 h of recovery. However, cerebral edema was significantly reduced by treatment with 40 mg kg-1 ketamine as compared with saline. Verapamil at neither the low nor the high doses was of significant benefit in this regard. No rat in the 40 mg kg-1 ketamine group died during CO exposure, whereas all deaths in the other groups took place during CO exposure. The use of higher and lower doses of ketamine suggest 40-80 mg kg-1 as most effective in suppressing lactate production; 40 mg kg-1 ketamine may be optimal with regard to survival. The results suggest that ketamine is beneficial, when administered before and during acute severe CO poisoning, in reducing blood lactate and cerebral edema and in improving BP recovery and survival. Verapamil, in contrast, appears to provide no benefits in these respects.

Metabolic, cardiovascular, and neurologic aspects of acute cyanide poisoning in the rat.

Acute cyanide (CN) toxicity was investigated in the Sprague-Dawley rat. Conscious, loosely restrained rats received sodium CN solution at varying dose rates through a jugular cannula (low CN, 0.077-0.155 mg/kg/min; high CN, 0.157-0.204 mg/kg/min). Blood glucose concentration was significantly increased 45 min after initial CN treatment in both the low and the high CN groups compared to the saline controls. Blood lactate concentration was significantly increased only in the high CN group after 45 min. Lactate increased directly with CN dose rate in surviving high CN rats. In rats that succumbed during CN infusion, lactate concentration reached nearly 150 mg/dl. Body temperature decreased modestly at low CN dose rates, but increased markedly at high CN dose rates. Heart rate was relatively constant in the low CN group, but decreased rapidly in the high CN group with increasing CN dose rate. In rats surviving CN treatment, no significant alterations in either cerebral cortical water content or neurologic status were detected. This contrasts with another potent poison, carbon monoxide, which produces marked neurologic deficit and cerebral edema in this animal model. The mean lethal CN dose was 4.6 mg/kg (range 4.25-4.90 mg/kg). Expressed on the basis of CN infusion rate, the lethal zone was from 0.16 to 0.21 mg/kg/min, a surprisingly narrow range. Assuming that extrapolations are possible to other species, the data provide strong evidence that greatly elevated blood lactate may be a useful marker for CN poisoning very near or within the lethal zone.

Cyanide poisoning in animals and humans: a review.

Cyanide (CN) is a deadly poison which animals and humans encounter from a number of sources. The following article briefly reviews many of the major studies of CN toxicology in animals and humans. The discussion focuses on sources, body levels, metabolic changes, physiopathology, experimental antidotal studies and the diagnosis and management of CN poisoning in humans.

Coronary vessel alterations following chronic carbon monoxide exposure in the adult rat.

Adult male rats were exposed to 500 ppm CO continuously for 30 days, while litter-mate controls remained in room air (AIR). Heart weight-to-body weight ratio and hematocrit were increased significantly. Right ventricle (RV) free wall thickness was increased significantly as was right to left heart diameter and average heart diameter. Cross-sectional areas of the left ventricle (LV) free wall, interventricular septum (S) and RV midway between the apex and base were increased significantly. Morphometric analysis of the CO-exposed and AIR hearts revealed no significant differences in the number of small (27-114 microns) or larger (> 114 microns) blood vessels in any region; however, there was a trend towards an increased number of the smaller vessels, both arterioles and venules, in the CO-exposed rats. The larger arteries in the S and RV were significantly larger in the CO-exposed rats. There was a significant overall effect of CO on larger artery diameter across all heart regions, consistent with the appearance of heart radiographs taken. There were no differences in the diameter of the small vessels in any region of the heart between the CO-exposed and AIR rats. The vessel cross-sectional area of the larger vessels tended to be increased in all regions of the heart. The cross-sectional area of the large arteries in the LV was increased significantly. Arterial wall thickness was decreased significantly in RV and there was a significant overall effect of CO in decreasing wall thickness and the ratio of wall thickness-to-vessel luminal diameter in these vessels. No vascular pathology was observed. The results of this study suggest changes in coronary vessel architecture during chronic CO-induced cardiac hypertrophy and are consistent with earlier hemodynamic and morphometric studies of CO-exposed hearts.

Stethoscope acoustics and cervical auscultation of swallowing.

Frequency response characteristics of six popular stethoscopes are reported for the higher frequency range (to 3000 Hz) to supplement equivalent measurements for the lower frequencies (35-1000 Hz) published previously. Spectra of the sounds of swallowing from the throat, transduced with an accelerometer, demonstrate important frequency composition in this higher range. Two stethoscope models were found to have superior transmission characteristics for use in cervical auscultation of swallowing sounds.

Pulmonary vascular responsiveness in rats following neonatal exposure to high altitude or carbon monoxide.

Exposure of adult and neonatal rats to high altitude increases pulmonary vascular responsiveness during the exposure. A study was undertaken to determine if a short exposure of neonatal rats to either high-altitude or carbon monoxide (CO) hypoxia would cause persistent alterations in pulmonary vascular responsiveness postexposure. One-day-old male Sprague-Dawley rats were obtained as 16 litters of 10-12 pups each. At 2 days of age, 4 litters were exposed to CO (500 ppm) for 32 days, and 4 litters were exposed to ambient air (AIR) in Detroit (200 m). Another 4 litters were exposed to 3500 m altitude (ALT) in a chamber for 32 days, and 3 litters were exposed to ambient conditions in Fort Collins (CON, 1524 m). After the exposures, all rats were maintained at 1524 m. At 2, 40, 76, and 112 days postexposure, lungs were isolated and perfused with Earle's salt solution (+Ficoll, 4 g%). Pulmonary vascular responsiveness was assessed by dose responses to angiotensin II (AII, 0.025-0.40 micrograms) and acute hypoxia (3% O2 for 3 min). AII responses were higher in ALT vs CON rats at all ages, but no differences were noted between CO and AIR rats. Acute hypoxic responses were higher in ALT versus CON rats at 2 and 40 days postexposure, but no differences were noted between CO and AIR rats. Baseline pulmonary vascular resistance and pulmonary arterial pressure (in isolated lungs) were higher in ALT rats at all four ages compared to the other three groups. Both the ALT and CO rats displayed hypertrophy of the right ventricle (RV) and the left ventricle (LV) at the termination of treatment and elevated hematocrit. LV hypertrophy and polycythemia regressed with time, but RV hypertrophy remained significant in the ALT rats through 112 days postexposure. The results indicate that neonatal exposure to ALT, but not CO, causes a persistent increase in pulmonary vascular responsiveness and RV hypertrophy for at least 112 days after termination of the exposure.

Structural and functional myocardial responses to chronic treatment with the Ca2+ blocker verapamil (Calan-SR) in hypertensive patients.

We wished to determine whether prolonged therapy with the Ca2+ channel blocker verapamil has beneficial structural and functional cardiac effects. Nine hypertensive outpatients [systolic blood pressure (SBP) 164 +/- 4 and diastolic BP (DBP) 103 +/- 4 mm Hg: men and women, blacks and whites, mean age 48.6 years] received 240-480 mg slow-release verapamil (Calan-SR) a day. BP, left ventricle (LV) wall thickness and mass, and mitral flow characteristics on echocardiography, and plasma catechols and renin were determined at 0, 5, 10, and 15 months. Patients were compared with 10 normotensive controls, of similar group composition (SBP 130 +/- 3 and DBP 82 +/- 1 mm Hg; age 47.2 years). In the hypertensive patients, SBP and DBP decreased significantly (p < 0.05), by 14 and 12 mm Hg, respectively, but remained well above that of controls and > 140/90 mm Hg. Diastolic LV septal thickness decreased from 15.3 +/- 0.6 to 14.5 +/- 1.1 mm (not significant), while diastolic LV posterior wall thickness (PWTd) decreased significantly (p < 0.05) from 15.7 +/- 0.6 to 14.1 +/- 0.7 mm after 8 months, but not to the value of the controls. LV diastolic and systolic and left atrial dimensions remained constant. Normalized LV mass, initially 60% greater than the controls, decreased slightly (11%) but nonsignificantly and remained above that of controls. Neither LV mass nor LV posterior wall thinning was correlated with reduction in BP. Patient peak systolic wall stress was initially significantly lower than that of controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Electrocardiographic responses to carbon monoxide and cyanide in the conscious rat.

Carbon monoxide (CO) and cyanide (CN), commonly found in exhaust fumes and smoke, act as hypoxic agents in eliciting morbid and lethal effects. This study explored the effects of these two toxicants on the ECG in a controlled and well-characterized animal model. Levine-prepared awake female rats were treated with 1500 and 2400 ppm CO for 90 min, CN at 4 mg/kg, or 1500 ppm CO plus 4 mg/kg CN. As in past studies, CO initially induced hyperglycemia and many-fold increases in blood lactate concentration, and rebound increases in blood glucose during recovery. CN produced hyperglycemia, however, there was no glucose rebound, nor was there a significant increase in lactate. CN plus 1500 ppm CO produced glucose changes similar to that of CO alone. CO exposure also induced hypothermia and hypotension, while CN produced little change in these parameters. CO increased heart rate, while CN tended to decrease heart rate. PR interval was increased significantly 4.5-17.0 ms by exposure to CO, with or without combination with CN, while CN alone produced minimal change in the PR interval. QT interval was increased up to 20 ms by exposure to CO, with or without combination with CN. CN alone produced no change in the QT interval. T wave duration was increased up to 22.5 ms by exposure to 1500 ppm CO, with or without combination with CN. CN alone produced minimal changes in T wave duration. There were no changes in duration of the (Q)RS complex or of the R wave. QT interval lengthening was positively correlated with the decrease in systolic blood pressure (0-30 min, r = 0.657, P < 0.05; 0-60 min, r = 0.704, P < 0.05). Hypothermia was correlated with increase in lactate concentration (r = 0.73, P < 0.05) and with decrease in blood pressure (r = 0.69, P < 0.05). No correlation between body temperature and QT interval was observed. The results indicate that CO at the concentrations used in the Levine-prepared rat has major effects on the ECG in slowing AV conduction and ventricular repolarization. In contrast, CN at 4 mg/dl has little or no effect on either conduction or repolarization in this animal model. These findings are discussed in light of past animal and human studies.

Chronic carbon monoxide exposure in young rats alters coronary vessel growth.

The goal of this study was to determine whether chronic monoxide exposure in the developing heart produces long-lasting coronary vasculature alterations. One-day-old male rat pups were exposed to 500 ppm CO continuously for 30 d, while littermate controls remained in room air (AIR). At 61 and 110 d of age hearts were removed, perfusion fixed, x-rayed, and processed for analysis of coronary vessel architecture. Body weight (BW) and heart weight (HW) increased with age; the ratio of HW/BW decreased. There were no differences in HW and ventricular dimensions at either age due to prior CO exposure. Morphometric analysis of the fixed hearts from CO-exposed and AIR rats revealed no significant individual group differences in the number of small (27-114 microns) or larger (> 114 microns) vessels in any heart region. The septum (S) in CO rats was an exception: There were more small veins at 61 d of age and more larger veins at 110 d of age. There was a significant increase in the number of small arteries at both ages in the CO rats across all heart regions, and in the smaller veins at 61 d of age. The large vessels in the S at 61 d of age had a significantly greater diameter in CO compared to AIR rats. This was also true for the large arteries in the S and right ventricle (RV) of the 110-d-old rats. Taking all heart regions together, the large arteries in CO rats were larger than in AIR rats. Previous CO exposure significantly increased large artery and total cross-sectional area in the S and RV at 61 d of age, and in RV at 110 d of age. Total cross-sectional area of veins in the S was also increased. Taking all heart regions together, CO significantly increased small artery cross-sectional area at 61 d of age, and small, large, and total artery cross-sectional area at 110 d of age. With one exception (small veins, 110 d of age), there was no effect of CO on vein cross-sectional area. These changes resulted in the percentage of total cross-sectional area contributed by the larger vessels being increased. Pathological examination showed nothing abnormal. The results suggest profound and persistent changes in coronary vessel architecture following chronic neonatal CO exposure.

Carbon monoxide-induced cardiac hypertrophy is not reduced by alpha- or beta-blockade in the rat.

The stimulus for carbon monoxide-induced cardiac hypertrophy was investigated. Two experiments were carried out in which adult male Sprague-Dawley rats were exposed continuously to 700 ppm CO for 30 days (CO) or inhaled room air (Air). In each experiment, 2/3s of the rats received either the beta-1-adrenergic blocker, atenolol, or the alpha-1 adrenergic blocking agent, prazosin, in the food daily, at low and high doses. Systolic blood pressure (SBP) was significantly lowered (20-25 mmHg) by CO alone. Atenolol alone lowered SBP, but only at the high dose. Low dose and particularly high dose atenolol, lowered SBP even more in the CO rats. Prazosin lowered SBP, particularly at the high dose and further lowered SBP in the CO rats. Heart rate was significantly lowered by atenolol and prazosin alone at both doses in the Air rats. Heart rate remained the same or was slightly elevated by CO exposure. Heart rate in the presence of CO was significantly depressed by prazosin, but not by atenolol. Carbon monoxide alone resulted in 30-43% and 18-25% weight increases in right ventricle free-wall (RV) and left ventricle + septum (LV+S), respectively, relative to untreated controls. Neither low nor high dose prazosin significantly decreased RV and LV+S weights in the CO rats. Low dose atenolol failed to alter RV and LV+S weights in the CO rats; however, high dose atenolol, significantly (P < 0.01) increased RV weight in the CO rats. Right ventricle weight was positively correlated with SBP lowering by CO and/or atenolol, or prazosin. Carbon monoxide exposure increased lung/body weight ratio; atenolol, but not prazosin, attenuated this effect. Hematocrit increased from 50% in the Air to 77% in the CO rats; it was unaltered by prazosin or atenolol treatment. Thus, CO-induced cardiac hypertrophy develops in spite of lowered SBP (i.e. lowered LV afterload), and the blockade of either alpha or beta-1 receptors. It is suggested that the increased ventricular preload caused by atenolol and prazosin is directly responsible for the cardiac hypertrophy, regardless of the ameliorating effects of decreased inotropicity and heart rate produced by the adrenergic blocking agents. The results suggest the potentially powerful role of enhanced preload in driving myocardial hypertrophy.

Acute carbon monoxide poisoning in an animal model: the effects of altered glucose on morbidity and mortality.

An animal model in which the common carotid artery and the jugular vein serving one side of the brain are occluded by indwelling catheters has been used during the past few years to investigate acute carbon monoxide (CO) poisoning. This article reviews the recent research examining the pattern of changes in blood glucose concentration which results from CO exposure, and the manner in which altered glucose concentration alters neurologic outcome and mortality. At present it appears that either greatly depressed glucose or greatly elevated glucose during and/or after CO exposure increases morbidity and mortality. Cyanide (CN) poisoning, in contrast to CO, produces a different pattern of changes in blood glucose and lactate, and unlike CO, fails to slow cardiac AV conduction and ventricular repolarization. Through the use of magnetic resonance imaging and spectroscopic techniques, cerebral cortical edema and the changes in brain phosphagens have been assessed following CO poisoning in the rat. The published results as well as data from recent pilot studies are discussed in the light of our current understanding of CO toxicology.

Dibromomethane and carbon monoxide in the rat: comparison of the cardiovascular and metabolic effects.

The goals of this study were to examine the cardiovascular and metabolic responses to a dihalogenated methane and to compare them to inhaled CO. One group of male Sprague-Dawley rats received an i.p. injection of either 3 or 6 mmol kg-1 dibromomethane (DBM) diluted 1:3 with sesame oil. Measurements of carboxyhemoglobin (COHb), rectal body temperature (BT), heart rate, systolic blood pressure (BP) and blood glucose and lactate concentrations were made at times 0, 30, 60, 120, 240, 360, 480, 600, 720, 840, 1020, 1440 and 1680 min. A second group of rats received only sesame oil and was tested in the same manner. A third group of rats breathed 225 ppm CO for 120 min before being tested. Peak COHb levels were 16% 8 h after 3 mmol kg-1 DBM, 18% 12 h after 6 mmol kg-1 DBM and 17% in the CO-exposed group. The sesame oil controls exhibited no elevation in COHb. The BT dropped by ca. 1 degree C in both the DBM- and CO-exposed rats, while there was no BT change in the sesame oil controls. The BT dropped by 1.0 degree C and 1.2 degree C after 6 h in the 3 and 6 mmol kg-1 DBM groups, respectively, and by 0.9 degree C after 120 min in the CO-exposed group. The CO-exposed rats displayed a 12 mmHg decrease in systolic BP, while both doses of DBM failed to produce any significant BP change. The BP in the sesame oil controls remained constant.(ABSTRACT TRUNCATED AT 250 WORDS)

Magnetic resonance imaging of the rat brain following acute carbon monoxide poisoning.

Magnetic resonance (MR) may be used for repeatedly and non-invasively imaging the brain. Until now, no studies have used this approach to study the effects of carbon monoxide (CO) poisoning in a defined animal model. Conscious, Levine-prepared female rats (unilateral carotid artery and jugular vein occlusion) were exposed to 2400 ppm CO for 90 min, with or without the infusion of 50% glucose solution; CO-stimulated increases in blood glucose and lactate occurred in both groups, while blood pressure and body temperature fell. One to four hours following termination of CO exposure, increased cortical pixel intensity, cortical surface area and brain midline shift were observed on the operated side of the brain in some rats of both groups (i.e. responders = R), providing evidence of edema. At sacrifice, 5 h following termination of CO exposure, gross water content was increased on the left side in the corresponding cortical slices in R rats, providing another measure of edema. Significant positive correlations were found between left to right pixel intensity difference and water content difference, and between the extent of midline shift and water content difference. The elevations of blood glucose and lactate concentrations, and the magnitudes of CO-induced hypothermia and hypotension were similar to those in past studies, but appeared to exert no effect on the severity of cortical edema in terms of differences in pixel intensity, surface area, midline shift or gross tissue water content. Thus, the observed differences between the R rats is not explained by the available data.(ABSTRACT TRUNCATED AT 250 WORDS)

Heart and lung alterations in neonatal rats exposed to CO or high altitude.

We wished to determine whether cardiac changes produced by CO are related to the development of pulmonary hypertension and whether they are specific for CO or also occur with high-altitude exposure. Newborn male Sprague-Dawley rats were exposed to 500 ppm CO for 32 days (CO) at Detroit, MI or to 11,500-ft simulated altitude at Fort Collins, CO (barometric pressure 495 Torr; 11K); ambient air controls were maintained at Detroit (657 ft, 200 m; AIR) and at Fort Collins (5,000 ft, 1,524 m; 5K). Rats were maintained at Fort Collins after 34 days of age. Hematocrit was elevated to a greater extent in the CO than in the 11K group 2 days postexposure; however, no differences existed 40, 76, or 112 days postexposure. Right ventricle (RV) and left ventricle plus septum (LV + S) mass in CO rats were increased 38.0 and 37.4%, respectively, relative to the AIR group 2 days after CO exposure; RV and LV + S in the 11K group were increased 55.7 and 9.3%, respectively, relative to the 5K group. Cardiac hypertrophy declined in the CO and 11K groups postexposure but remained significant for the RV, reaching 20.7% above the AIR group (CO) and 29.7% above the 5K group (11K) at 145 days of age. By use of an in vitro preparation, pulmonary vascular resistance (PVR) and pulmonary arterial pressure were significantly increased immediately after altitude but not after CO exposure and remained elevated in adulthood after altitude exposure. PVR was correlated with hematocrit in altitude- but not in CO-exposed rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiovascular, metabolic and neurologic effects of carbon monoxide and cyanide in the rat.

Levine-prepared, female Sprague-Dawley rats were used to investigate the effects of carbon monoxide (CO) and cyanide (CN) on heart rate, blood pressure, hematocrit, body temperature, blood glucose, lactate, and neurologic function. Rats were exposed to either 2400 ppm CO, 1500 ppm CO, 4 mg/kg NaCN, or both 1500 ppm CO and 4 mg/kg NaCN for 90 min, followed by 4 h of room air recovery. Following exposure to 2400 ppm CO, rats exhibited a significant bradycardia which normalized by 2 h of recovery. All groups exhibited an initial hypotension which was either maintained or exaggerated during exposure in all but the rats exposed to CN, and which returned to pre-exposure values by 90 min. All groups experienced a significant hypothermia during the exposure period, with those in the 1500 ppm CO or the CN returning to initial values over the recovery period. The only significant change in hematocrit was due to 2400 ppm CO (4.1% increase). During exposure, all groups experienced an initial surge in glucose concentration which was maintained in all but rats exposed to 2400 ppm CO. The greatest hyperglycemic response resulted from the combination of CO and CN, whereas 2400 ppm CO produced the smallest. CN alone produced no significant rise in lactate concentration. However, lactate concentration in all other groups was significantly elevated during the exposure period, returning to initial values by 4 h of recovery. Lactate concentrations and neurologic deficit in rats exposed to 1500 ppm CO, when added to those rats treated with CN, closely approximated the lactate and neurologic deficit of the combination treatment. Neurologic deficit was greatest in rats exposed to 2400 ppm CO. While in most cases the responses of the rats to CO and CN differed whether the substances were administered alone or in combination, a synergistic relationship is not suggested. An additive or less than additive relationship is more likely.

Comparison of the acoustic properties of six popular stethoscopes.

This study evaluated stethoscope acoustics by using a sound frequency generator and an active artificial ear. Six popular, currently available stethoscopes were compared in their various modes involving bells, diaphragms, etc.: Littmann Classic II, Littmann Cardiology II, Littmann Master Cardiology, Hewlett-Packard Rappaport-Sprague, Tycos Harvey Triple Head, and Allen Medical Series 5A RPS Binaural. The transfer function was measured from 37.5-1000 Hz, the range where nearly all heart and lung sounds are found. Sound in the low-frequency range (37.5-112.5 Hz) was in most cases amplified by the bells and attenuated by the diaphragms; however, there were no significant differences. Both bells and diaphragms attenuated sound transmission in the high range, and this increased with frequency. The Tycos Harvey Triple Head ribbed diaphragm attenuated sound transmission to a significantly greater extent than the other diaphragms (P less than 0.01). The results show that the bell and diaphragm for a given stethoscope usually have different transmission characteristics, particularly at low frequencies. The Littmann Classic II is an exception. The Hewlett-Packard and Tycos Harvey stethoscopes showed the greatest differences in low frequency response between the bell and the diaphragm. While the differences found in sound transmission between stethoscopes were in most cases small, the Littmann Cardiology II, bell and diaphragm, appears to possess the best overall performance by this study design.

Non-coordinate expression of collagen mRNAs during carbon monoxide-induced cardiac hypertrophy.

Collagen gene expression during volume overload-induced cardiac hypertrophy was investigated in adult male rats. Hypertrophy of the left ventricle (22%) and right ventricle (37%) occurred following 27 days continuous exposure to 700 ppm carbon monoxide; hematocrit increased nearly 47%. To examine potential cellular and molecular control of restructuring in the heart, we investigated the expression of two specific procollagen mRNAs for collagen types which have different structural-functional roles [Type I (alpha-1) & Type IV]. Type I (interstitial) mRNA levels increased at least 100% relative to controls within 3 days of initial exposure to 700 ppm CO, then declined afterwards; type IV (basement membrane) mRNA levels increased more modestly at first, and increased further afterwards. The ratio of type I/type IV RNA's also increased initially, then later declined, with the greatest differences in the relative responses of type I and IV mRNAs seen in the right ventricle. These data suggest that types I and IV collagen mRNA expression is not coordinately expressed during this type of volume overload-induced hypertrophy in rat heart.