SUMMARY1. The cardiac and respiratory responses shown by muskrats in both unrestrained and restrained dives have been compared with responses elicited by stimulation of a number of cardio-depressant receptor inputs, in an attempt to determine which are most important in initiating and maintaining diving bradyeardia.2. In unrestrained voluntary dives heart rate fell from 310 + 3 to 54+3 beats min-in 1 to 2 sec, which was significantly below that seen in dives by restrained unanaesthetized or anaesthetized animals. 3. Pouring water on the external nares during maintained artificial ventilation caused heart rate to decline to 76 + 12 beats minm-after 1 sec. Flowing water through the internal nares caused apnoea, in the expiratory position, and bradycardia within one third of a second. Heart rate fell to 20 + 2 beats min-, 1 sec after the start of water flow. Substituting saline for water reduced both the apnoeic and cardiac responses. Bilateral section of the maxillary branch of V and the inferior laryngeal (X) nerves completely abolished the cardiac and respiratory response to water flow.4. Artificial ventilation throughout periods of nasal stimulation with water or saline reduced the bradycardia, although even the saline driven response could not be completely abolished. Lung deafferentation eliminated any direct effect of artificial ventilation on heart rate during nasal stimulation.5. Lung deflation caused bradycardia within 0-97 + 0-17 sec, heart rate falling from 268 + 7 to 59 + 4 beats min-. Bradyeardia also occurred during maintained lung inflation but it was delayed for a period which varied from 6-8 + 1-8 sec at an inflation pressure of 0-5 kPa to 35 + 7 sec at 1-5 kPa.6. Bradyeardia caused by nasal water flow or lung deflation was unaffected by bilateral section of the sinus nerve.7. Artificial ventilation of paralysed muskrats with 5 % CO2 in N2 caused bradycardia when Pa°2 reached 8-4+0-8 kPa and heart rate declined to 76+7 beats min-at 4 kPa. Bilateral section of the sinus nerve delayed bradycardia until Pa o, reached 4-5 + 0-5 kPa.8. These results suggest that the cardiac response to submergence could be the expression of input from three groups of receptors, nasal, lung and carotid chemoreceptors, although it is not clear how they interact with one another to generate the cardiac responses displayed by unrestrained animals during submergence.

The objective of this study was to perform lookback study in recipients of blood components from human T-lymphotropic virus (HTLV) seropositive donors. HTLV-1/2 may be transmitted by blood transfusion. Brazil is an endemic area for the virus and its screening in blood donors is mandatory since 1993. Hemominas Foundation (HF) is the public transfusion centre in Minas Gerais, Brazil. Data on HTLV-1/2 seropositive donors and recipients from 1993 to 2004 were obtained at HF and 24 contracting hospitals. From 1993 to 2004, HTLV-1/2 enzyme immunoassay (EIA) was performed in 918 678 donations of approximately 422 600 blood donor candidates. Of these, 456 donors (0.1%) were reactive and confirmed by Western blot (WB): 449 HTLV-1 and 7 HTLV-2. Sixty-six (14.5%) were repeat donors and had 194 blood cellular components produced from their previous donations. Of the distributed components, 119/146 (81.5%) had the recipient traced, with a total of 114 individuals. Of these, only 13 recipients were tested: six (46%) were HTLV-1 positive (four recipients of red cell units, two of platelets) and seven (54%) were negative (six of red cell units and one of platelets). Eleven did not respond and 62/114 (54.0%) were deceased. Another 28/114 (25.0%) could not be located. All six seropositive HTLV-1 recipients identified had no symptoms suggestive of HTLV-1-associated diseases. Acellular components, when used alone, were not associated with HTLV seropositivity. HTLV-1 transmission by cellular blood components occurred before screening for the virus was introduced. Haemovigilance was difficult to perform due to unavailability of computer systems before 1999 and to inadequate medical records at hospitals.

The effect of the stress of forced submergence in the laboratory on a number of cardiovascular adjustments to diving was examined. Free muskrats, diving in large holding tanks, always displayed bradycardia and heart rate fell from a predive rate of 320 ± 6 to 34 ± 3 beats∙min−1 after 20 s submergence. In the laboratory this degree of bradycardia was only seen during whole-body submergence of anesthetized animals; restrained unanesthetized muskrats showed significantly less bradycardia. Forced submergence of only the head caused about half the bradycardia seen during whole-body submergence in both unanesthetized restrained and anesthetized muskrats. Decerebrated animals gave identical responses to those of anesthetized muskrats. Cardiac output was redistributed in forced diving to favour the heart and brain even when diving heart rate was three times that in free dives. However, many other tissues still received a significant proportion of cardiac output and must have placed a drain on the blood oxygen store which restricted apnoeic tolerance. Struggling during forced submergence was frequent and has a reflex or unconscious component since even decerebrated animals struggled during a dive. The present data suggest that the additional stresses imposed on muskrats during forcible submergence in the laboratory reduce rather than potentiate the cardiovascular adjustments to diving.

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