Biomedical subjects

D G Penney

Publications and source records attributed to D G Penney.

At least 19 recordsLinked to original sources

PubMed2000

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. METHODS 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.

Adolescent↗

PubMed1998

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.

Biliary Dyskinesia↗

PubMed1997

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.

Adolescent↗

PubMed1995

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.

Acidosis, Lactic↗

PubMed1994

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.

Acceleration↗

PubMed1994

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.

Animals↗

PubMed1993

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.

Animals↗

PubMed1993

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.

Animals↗

PubMed1993

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.

Animals↗

PubMed1993

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.

Analysis of Variance↗

PubMed1993

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)

Blood Pressure↗

PubMed1992

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.

Animals↗

PubMed1992

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)

Animals↗

PubMed1992

Blood lactate and catecholamine levels in the carbon monoxide-exposed rat: the response to elevated glucose.

Previous studies have shown that elevated blood glucose is detrimental to the outcome in acute carbon monoxide (CO) poisoning. The present goals were to characterize the blood lactate and catecholamine changes and to determine whether elevated blood glucose results in increases in the levels of these substances. Two groups of adult Sprague-Dawley, Levine-prepared, female rats (n = 22 each) were exposed to 2400 ppm CO for 90 min: one group received nothing (CO alone), while the other group was infused with a 50% glucose solution (4 ml/kg) (CO + glucose). The usual hypothermia, hypotension, bradycardia and hemoconcentration associated with acute severe CO poisoning were observed. Survival rates were 68% and 54% in the CO alone and CO + glucose groups, respectively. Arterial blood pressure tended to decline more in rats that died; the difference was significant in the CO + glucose group. In the CO alone group, plasma glucose concentration was significantly lower after CO exposure in rats that died than in survivors (35 +/- 15 vs. 99 +/- 16 mg/dl). In the CO + glucose group, glucose concentration was significantly higher after 45 min in rats that died (d) than in survivors (s) (447 +/- 29 vs. 324 +/- 31 mg/dl). Elevated blood glucose in the CO + glucose group failed to significantly increase blood lactate; however, lactate tended to be higher in rats that died in both groups [CO alone group: 175 +/- 17 (d) vs. 138 +/- 9 (s); CO + glucose group: 154 +/- 10 (d) vs. 143 +/- 8 (s)]. Plasma epinephrine and norepinephrine increased significantly 6-10-fold and 2-6-fold in each of the two groups, respectively; however, catecholamine levels were not related to either the administration of glucose or survival. With regard to CO poisoning in this animal model, the results do not support the hypotheses that elevated blood glucose exacerbates the increase in blood lactate, that increased catecholamine increases glucose, or that greater CO-induced hypoglycemia results from increased lactate production. The results do show that death is related to abnormally high or low blood glucose, but that it is not due to higher blood lactate or catecholamine levels.

Animals↗

PubMed1992

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.

Animals↗

PubMed1992

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.

Acoustics↗

PubMed1992

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)

Aging↗

PubMed1991

In situ assessment of the rat heart during chronic carbon monoxide exposure using nuclear magnetic resonance imaging.

Ventricular hypertrophy induced in male Sprague-Dawley rats by inhalation of 500 ppm carbon monoxide (40% carboxyhemoglobin level) for 0-62 days was assessed by contiguous 2-mm thick axial cardiac cross-sections, using 32 accumulated averages of ungated fast-scan gradient-recalled nuclear magnetic resonance (NMR) images. Following final imaging, the rats were sacrificed and the hematocrit and heart mass were determined. The mean outside diameter of the left ventricle plus interventricular septum (LV + S) showed a strong correlation (r = 0.73, P less than 0.01) with the duration of CO exposure, while the correlation coefficients for the LV + S lumen diameter and wall thickness were marginally significant. The mean pleural space diameter also increased significantly (r = 0.64, P less than 0.05) with the duration of CO exposure. The ratio of the LV + S wall thickness and the lumen radius was 0.53 in the rats exposed to CO for 0-8 days; this value did not change with longer CO exposure. The LV + S outside and lumen diameter showed significant correlations to the hematocrit (r = 0.72, p less than 0.05 and r = 0.66, P less than 0.05, respectively), and the LV + S outside diameter correlated with the increase in the LV + S mass (r = 0.72, P less than 0.05). The results achieved with NMR imaging are consistent with past morphometric studies of CO-induced ventricular hypertrophy, where heart dimensions were determined in relaxed frozen tissue, and corroborate the eccentric nature of CO-induced ventricular hypertrophy.

Animals↗